Posts Tagged serotonin

[WEB PAGE] Neurotransmitters: What they are, functions, and psychology

Neurotransmitters are chemical messengers in the body. Their job is to transmit signals from nerve cells to target cells. These target cells may be in muscles, glands, or other nerves.

The brain needs neurotransmitters to regulate many necessary functions, including:

  • heart rate
  • breathing
  • sleep cycles
  • digestion
  • mood
  • concentration
  • appetite
  • muscle movement

The nervous system controls the body’s organs, psychological functions, and physical functions. Nerve cells, also known as neurons, and their neurotransmitters play important roles in this system.

Nerve cells fire nerve impulses. They do this by releasing neurotransmitters, which are chemicals that carry signals to other cells.

Neurotransmitters relay their messages by traveling between cells and attaching to specific receptors on target cells.

Each neurotransmitter attaches to a different receptor — for example, dopamine molecules attach to dopamine receptors. When they attach, this triggers action in the target cells.

After neurotransmitters deliver their messages, the body breaks down or recycles them.

Key types of neurotransmitters

a person pointing to neurotransmitters on a model of a brain.

Many bodily functions need neurotransmitters to help communicate with the brain.

Neurotransmitters have different types of action:

  • Excitatory neurotransmitters encourage a target cell to take action.
  • Inhibitory neurotransmitters decrease the chances of the target cell taking action. In some cases, these neurotransmitters have a relaxation-like effect.
  • Modulatory neurotransmitters can send messages to many neurons at the same time. They also communicate with other neurotransmitters.

Some neurotransmitters can carry out various functions, depending on the type of receptor that they are connecting to.

The following sections describe some of the best-known neurotransmitters.

Acetylcholine

Acetylcholine triggers muscle contractions, stimulates some hormones, and controls the heartbeat. It also plays an important role in brain function and memory. It is an excitatory neurotransmitter.

Low levels of acetylcholine are linked with issues with memory and thinking, such as those that affect people with Alzheimer’s disease. Some Alzheimer’s medications help slow the breakdown of acetylcholine in the body, and this can help control some symptoms, such as memory loss.

Having high levels of acetylcholine can cause too much muscle contraction. This can lead to seizures, spasms, and other health issues.

The nutrient choline, which is present in many foods, is a building block of acetylcholine. People must get enough choline from their diets to produce adequate levels of acetylcholine. However, it is not clear whether consuming more choline can help boost levels of this neurotransmitter.

Choline is available as a supplement, and taking high doses can lead to serious side effects, such as liver damage and seizures. Generally, only people with certain health conditions need choline supplements.

Dopamine

Dopamine is important for memory, learning, behavior, and movement coordination. Many people know dopamine as a pleasure or reward neurotransmitter. The brain releases dopamine during pleasurable activities.

Dopamine is also responsible for muscle movement. A dopamine deficiency can cause Parkinson’s disease.

A healthful diet may help balance dopamine levels. The body needs certain amino acids to produce dopamine, and amino acids are found in protein-rich foods.

Meanwhile, eating high amounts of saturated fat can lead to lower dopamine activity, according to research from 2015. Also, certain studies suggest that a deficiency in vitamin D can lead to low dopamine activity.

While there are no dopamine supplements, exercise may help boost levels naturally. Some research has shown that regular exercise improves dopamine signaling in people who have early stage Parkinson’s disease.

Endorphins

a laughing senior black woman.

The body may release endorphins during laughter.

One of the best-known ways to boost levels of feel-good endorphins is through aerobic exercise. A “runner’s high,” for example, is a release of endorphins. Also, research indicates that laughter releases endorphins.

Endorphins may help fight pain. The National Headache Foundation say that low levels of endorphins may play a role in some headache disorders.

A deficiency in endorphins may also play a role in fibromyalgiaThe Arthritis Foundation recommend exercise as a natural treatment for fibromyalgia, due to its ability to boost endorphins.

Epinephrine

Also known as adrenaline, epinephrine is involved in the body’s “fight or flight” response. It is both a hormone and a neurotransmitter.

When a person is stressed or scared, their body may release epinephrine. Epinephrine increases heart rate and breathing and gives the muscles a jolt of energy. It also helps the brain make quick decisions in the face of danger.

While epinephrine is useful if a person is threatened, chronic stress can cause the body to release too much of this hormone. Over time, chronic stress can lead to health problems, such as decreased immunity, high blood pressurediabetes, and heart disease.

People who are dealing with ongoing high levels of stress may wish to try techniques such as meditation, deep breathing, and exercise.

Anyone who thinks that their levels of stress could be dangerously high or that they may have anxiety or depression should speak with a healthcare provider.

Meanwhile, doctors can use epinephrine to treat many life threatening conditions, including:

  • anaphylaxis, a severe allergic reaction
  • asthma attacks
  • cardiac arrest
  • severe infections

Epinephrine’s ability to constrict blood vessels can decrease swelling that results from allergic reactions and asthma attacks. In addition, epinephrine helps the heart contract again if it has stopped during cardiac arrest.

GABA

Gamma-aminobutyric acid (GABA) is a mood regulator. It has an inhibitory action, which stops neurons from becoming overexcited. This is why low levels of GABA can cause anxiety, irritability, and restlessness.

Benzodiazepines, or “benzos,” are drugs that can treat anxiety. They work by increasing the action of GABA. This has a calming effect that can treat anxiety attacks.

GABA is available in supplement form, but it is unclear whether these supplements help boost GABA levels in the body, according to some research.

Serotonin

a father and son enjoying a sunny day on a hill.

Exposure to sunlight may increase serotonin levels.

Serotonin plays a role in depression and anxiety. Selective serotonin reuptake inhibitors, or SSRIs, can relieve depression by increasing serotonin levels in the brain.

Seasonal affective disorder (SAD) causes symptoms of depression in the fall and winter, when daylight is less abundant. Research indicates that SAD is linked to lower levels of serotonin.

Serotonin-norepinephrine reuptake inhibitors (SNRIs) increase serotonin and norepinephrine, which is another neurotransmitter. People take SNRIs to relieve symptoms of depression, anxiety, chronic pain, and fibromyalgia.

Some evidence indicates that people can increase serotonin naturally through:

  • being exposed to bright light, especially sunlight
  • vigorous exercise

A precursor to serotonin, called 5-hydroxytryptophan (5-HTP), is available as a supplement. However, some research has found that 5-HTP is not a safe or effective treatment for depression and can possibly make the condition worse.

Summary

Neurotransmitters play a role in nearly every function in the human body.

A balance of neurotransmitters is necessary to prevent certain health conditions, such as depression, anxiety, Alzheimer’s disease, and Parkinson’s disease.

There is no proven way to ensure that neurotransmitters are balanced and working correctly. However, having a healthful lifestyle that includes regular exercise and stress management can help, in some cases.

Before trying a supplement, ask a healthcare provider. Supplements can interact with medications and may be otherwise unsafe, especially for people with certain health conditions.

Health conditions that result from an imbalance of neurotransmitters often require treatment from a professional. See a doctor regularly to discuss physical and mental health concerns.

 

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[WEB PAGE] Dopamine vs. serotonin: Similarities, differences, and relationship

By Jamie Eske, Reviewed by 

Dopamine and serotonin are chemical messengers, or neurotransmitters, that help regulate many bodily functions. They have roles in sleep and memory, as well as metabolism and emotional well-being.

People sometimes refer to dopamine and serotonin as the “happy hormones” due to the roles they play in regulating mood and emotion.

They are also involved in several mental health conditions, including low mood and depression.

Dopamine and serotonin are involved in similar bodily processes, but they operate differently. Imbalances of these chemicals can cause different medical conditions that require different treatments.

In this article, we look at the differences between dopamine and serotonin, their relationship, and their links with medical conditions and overall health.

What is dopamine?

a young woman sat on her bed wondering if its dopamine or serotonin thats helping her feel so awake this morning.

Dopamine and serotonin play an important role in sleep and emotional well-being.

Neurons in the brain release dopamine, which carries signals between neurons.

The body uses dopamine to create chemicals called norepinephrine and epinephrine.

Dopamine plays an integral role in the reward system, a group of brain processes that control motivation, desire, and cravings.

Dopamine levels also influence the following bodily functions:

  • mood
  • sleep
  • learning
  • movement
  • alertness
  • blood flow
  • urine output

What is serotonin?

Serotonin is another neurotransmitter present in the brain.

However, more than 90% of the body’s total serotonin resides in the enterochromaffin cells in the gut, where it helps regulate the movement of the digestive system.

In addition to aiding digestion, serotonin is involved in regulating:

  • the sleep-wake cycle
  • mood and emotions
  • metabolism and appetite
  • cognition and concentration
  • hormonal activity
  • body temperature
  • blood clotting

Differences between dopamine and serotonin

Although both dopamine and serotonin relay messages between neurons and affect mood and concentration, they have some other distinct functions.

Dopamine, for example, relays signals between neurons that control body movements and coordination.

This neurotransmitter also plays a role in the brain’s pleasure and reward center, and it drives many behaviors. Eating certain foods, taking illicit drugs, and engaging in behaviors such as gambling can all cause dopamine levels in the brain to spike.

Higher levels of dopamine can lead to feelings of euphoria, bliss, and enhanced motivation and concentration. Therefore, exposure to substances and activities that increase dopamine can become addictive to some people.

Like dopamine, serotonin can also influence people’s moods and emotions, but it helps regulate digestive functions such as appetite, metabolism, and gut motility.

The relationship between dopamine and serotonin

nicotine withdrawal in stressed and tired man

Overproduction of dopamine may lead to impulsive behavior.

They interact with and affect each other to maintain a careful chemical balance within the body. There are strong links between the serotonin and dopamine systems, both structurally and in function.

In some cases, serotonin appears to inhibit dopamine production, which means that low levels of serotonin can lead to an overproduction of dopamine. This may lead to impulsive behavior, due to the role that dopamine plays in reward seeking behavior.

Serotonin inhibits impulsive behavior, while dopamine enhances impulsivity.

Dopamine and serotonin have opposite effects on appetite; whereas serotonin suppresses it, low levels of dopamine can stimulate hunger.

Which conditions have links to dopamine and serotonin?

Having abnormal levels of either dopamine or serotonin can lead to several different medical conditions.

Both neurotransmitters can affect mood disorders such as depression. Imbalances can also result in distinct conditions that affect different bodily functions.

In the sections below, we cover these conditions in more detail:

Dopamine

Having too much or too little dopamine can impair communication between neurons and lead to the development of physical and psychological health conditions.

Dopamine deficiency may play a significant role in the following conditions and symptoms:

Dopamine also plays a role in motivation and reward driven behaviors.

Although dopamine alone may not directly cause depression, having low levels of dopamine may cause specific symptoms associated with depression.

These symptoms can include:

  • lack of motivation
  • difficulty concentrating
  • feelings of hopelessness and helplessness
  • loss of interest in previously enjoyable activities

The SLC6A3 gene provides instructions for creating the dopamine transporter protein. This protein transports dopamine molecules across neuron membranes.

A medical condition known as dopamine transporter deficiency syndrome, or infantile parkinsonism-dystonia, occurs when mutations in the SLC6A3 gene affect how the dopamine transporter proteins function.

Dopamine transporter deficiency syndrome disrupts dopamine signaling, which impacts the body’s ability to regulate movement.

For this reason, dopamine transporter deficiency syndrome produces symptoms similar to those of Parkinson’s disease, including:

  • tremors, spasms, and cramps in the muscles
  • difficulty eating, swallowing, speaking, and moving
  • impaired coordination and dexterity
  • involuntary or abnormal eye movements
  • decreased facial expression, or hypomimia
  • difficulty sleeping
  • frequent pneumonia infections
  • digestive problems, such as acid reflux and constipation

Serotonin

a man smiling when his daughter greets him with a touch on the shoulder.

Genetics and family history may contribute to a person’s risk of developing a mood disorder.

Similar to dopamine, researchers have linked abnormal levels of serotonin with several medical conditions, especially mood disorders such as depression and anxiety.

Contrary to popular belief, it appears that low serotonin does not necessarily cause depression. Multiple factors beyond biochemistry contribute to depression, such as:

  • genetics and family history
  • lifestyle and stress levels
  • environment
  • additional medical conditions

That said, having low serotonin levels may increase a person’s risk of developing depression. Serotonin medications — such as selective serotonin reuptake inhibitors (SSRIs), which increase the availability of serotonin in the brain — may also help treat depression.

SSRI medications include:

On the other hand, having too much serotonin can lead to a potentially life threatening medical condition called serotonin syndrome.

Serotonin syndrome, or serotonin toxicity, can occur after taking too much of a serotonergic medication or taking multiple serotonergic medications at the same time.

The Food and Drug Administration (FDA) provided a list of serotonergic medications in 2016. Aside from SSRIs, some of these include:

  • serotonin and norepinephrine reuptake inhibitors (SNRIs), such as venlafaxine (Effexor)
  • tricyclic antidepressants (TCAs), such as desipramine (Norpramin) and imipramine (Tofranil)
  • certain migraine medications, including almotriptan (Axert) and rizatriptan (Maxalt)

According to the FDA, opioid pain relievers can interact with serotonergic medications, which can lead to a buildup of serotonin or enhance its effects in the brain.

Summary

The neurotransmitters dopamine and serotonin regulate similar bodily functions but produce different effects.

Dopamine regulates mood and muscle movement and plays a vital role in the brain’s pleasure and reward systems.

Unlike dopamine, the body stores the majority of serotonin in the gut, instead of in the brain. Serotonin helps regulate mood, body temperature, and appetite.

Having too much or too little of either neurotransmitter can cause psychological and physical symptoms.

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[WEB SITE] Prozac vs. Zoloft: What are the differences?

Prozac and Zoloft are common antidepressant drugs. Although they have similar effects on the body, their specific uses, side effects, and dosages are different.

Prozac and Zoloft are both selective serotonin reuptake inhibitors (SSRIs). This class of medication is among the first options for treating major depressive disorder, which people usually call depression.

Fluoxetine is the generic drug name for Prozac, and sertraline is the generic name for Zoloft.

In this article, we discuss the differences between Prozac and Zoloft.

What do they treat?

prozac vs zoloft

Taking either Prozac or Zoloft will increase the levels of serotonin in the brain.

The Food and Drug Administration (FDA) have approved both Prozac and Zoloft for treating:

In addition, the FDA have approved Prozac for the treatment of:

Doctors may also use Zoloft to treat post-traumatic stress disorder (PTSD) and social anxiety disorder.

Some doctors prescribe Prozac for social anxiety disorder in adults, borderline personality disorderRaynaud’s phenomenon, and selective mutism, but the FDA have not approved these uses.

Other SSRIs include:

  • escitalopram (Lexapro)
  • vortioxetine (Trintellix)
  • citalopram (Celexa)
  • fluvoxamine (Luvox)
  • paroxetine (Paxil)
  • vilazodone (Viibryd)

Forms

Both Prozac and Zoloft are available in the forms of a liquid oral solution, a tablet, and a capsule.

The following table lists the different forms of each drug along with the available dosages in milligrams (mg) and milligrams per milliliter (mg/ml).

Prozac Zoloft
Capsule 10 mg, 20 mg, 40 mg, 90 mg 25 mg, 50 mg, 100 mg
Tablet 60 mg 25 mg, 50 mg, 100 mg
Liquid 20 mg/5 ml 20 mg/ml

How to take and dosage

When a person first starts taking antidepressants, they will typically begin on a smaller dosage and increase this over time. Doing this makes it possible to test how well the drug works and monitor its side effects, as the effectiveness and adverse effects can differ among individuals.

American Psychiatric Association guidelines report the following starting dosages and the usual effective dosages when treating MDD:

Prozac Zoloft
Starting dosage 20 mg/day 50 mg/day
Usual effective dosages 20–60 mg/day 50–200 mg/day

Some people may see improvements in their symptoms in the first 1–2 weeks of treatment, whereas it may take 2–4 weeks for others to notice changes.

Some studies have shown that all antidepressants require at least 4–6 weeks before they reach their maximal clinical effectiveness.

There are three phases of MDD therapy:

  • The acute phase. The goal of the acute phase is for the person to recover from depressive symptoms and return to their baseline of functioning. This phase will last about 6–12 weeks.
  • The continuation phase. During the continuation phase, doctors will recommend that people continue treatment for 4–9 months to prevent symptoms from returning.
  • The maintenance phase. Some people may need to continue their medication for longer and complete a maintenance phase. The goal is to protect at-risk people from recurring depressive symptoms.

Doctors will usually recommend a maintenance phase for people with recurrent MDD or chronic depression.

If a person does not have a satisfactory response to medication, the doctor may try increasing the dosage. However, a higher dosage may cause more side effects, so doctors need to evaluate the risks and benefits of increasing it.

Another strategy to increase the effectiveness of the therapy is to add another medicine. A doctor may advise a person to combine Prozac or Zoloft with certain other antidepressants and other types of medication to improve their symptoms.

The doctor will determine which combinations are the most appropriate for each person while keeping in mind the possibility of drug interactions.

Doctors may also adjust medication dosages and regimens for people who are combining medication therapy and psychotherapy.

Side effects

As Prozac and Zoloft are both SSRIs, people may experience similar side effects with these drugs.

Zoloft is more likely than Prozac to cause gastrointestinal tract side effects, such as nausea and diarrhea. Men taking Zoloft may also report more sexual dysfunction side effects, such as failure to ejaculate, than those using Prozac.

However, people taking Prozac more often experience headaches, nervousness, and a lack of energy.

The following table lists the most common side effects of Prozac and Zoloft, which occur in at least 5% of people.

Prozac Zoloft
nausea 22% 26%
diarrhea 11% 20%
constipation 5% 6%
decreased appetite no data available 7%
anorexia 10% no data available
acid reflux 8% 8%
dry mouth 9% 14%
sweating 7% 7%
insomnia 19% 20%
drowsiness 12% 11%
anxiety 12% no data available
agitation no data available 8%
nervousness 13% no data available
dizziness 9% 12%
tremor 9% 9%
headache 21% no data available
weakness/lack of energy 11% no data available
flu-like symptoms 5% no data available
decreased sex drive no data available 6%
failure to ejaculate no data available 8%

Warnings

When people are ready to come off their antidepressant medications, they should do so gradually. Stopping Prozac, Zoloft, or any other antidepressant abruptly can cause discontinuation symptoms.

Discontinuation symptoms may include:

  • dysphoria, or general unease and dissatisfaction
  • irritability
  • agitation
  • dizziness
  • electric shock sensations
  • anxiety
  • confusion
  • headaches
  • lethargy
  • emotional lability, or rapid and exaggerated changes in mood
  • sleeplessness

Several short-term studies have shown that children, adolescents, and young adults under 24 years old have an increased risk of suicidal thoughts and behaviors when taking any antidepressants.

Doctors will monitor people taking Prozac, Zoloft, or any other antidepressant for worsening of depressive symptoms, suicidal thoughts, and unusual behaviors.

People with glaucoma and a history of seizures should use Prozac, Zoloft, and other SSRIs with caution because the drugs can make these conditions worse.

Suicide prevention

  • If you know someone at immediate risk of self-harm, suicide, or hurting another person:
  • Call 911 or the local emergency number.
  • Stay with the person until professional help arrives.
  • Remove any weapons, medications, or other potentially harmful objects.
  • Listen to the person without judgment.
  • If you or someone you know is having thoughts of suicide, a prevention hotline can help. The National Suicide Prevention Lifeline is available 24 hours a day at 1-800-273-8255.

Interactions

SSRIs, including Prozac and Zoloft, have similar drug interactions.

Serotonin syndrome

prozac vs zoloft agitated

Feelings of agitation and restlessness can indicate serotonin syndrome.

Serotonin syndrome is a potentially life-threatening interaction that occurs as a result of combining drugs that increase serotonin in the body.

Doctors should avoid prescribing Prozac, Zoloft, and other SSRIs alongside the following drugs:

  • triptans
  • tricyclic antidepressants (TCAs)
  • fentanyl
  • lithium
  • tramadol
  • tryptophan
  • buspirone
  • amphetamines
  • St. John’s wort
  • monoamine oxidase inhibitors (MAOIs)

Some of the signs and symptoms of serotonin syndrome include:

  • agitation
  • anxiety
  • restlessness
  • disorientation
  • sweating
  • a high body temperature
  • increased heart rate
  • nausea
  • vomiting
  • shaking
  • muscle rigidity
  • overactive reflexes
  • abnormal muscle contractions
  • dilated pupils
  • abnormal eye movements
  • dry mucous membranes
  • flushed skin
  • increased bowel sounds

MAOIs

People cannot take MAOIs, another type of antidepressant, with Prozac, Zoloft, or any other SSRIs because the risk of developing serotonin syndrome is very high.

Anyone taking an MAOI must stop taking it at least 2 weeks before starting SSRI treatment.

QT prolongation

Doctors have reported QT prolongation in people taking Prozac and Zoloft. QT prolongation is a potentially fatal heart rhythm dysfunction.

This heart condition is more common in people who take other drugs that can prolong the QT interval on an electrocardiograph. These include certain antipsychotics, antibiotics, and anti-arrhythmic medications.

Abnormal bleeding

Some people can experience abnormal bleeding when combining Prozac, Zoloft, and other SSRIs with drugs that can increase bleeding, such as:

  • aspirin
  • nonsteroidal anti-inflammatories (NSAIDs)
  • warfarin
  • anticoagulants

Cost

The following table compares the lowest available prices of Prozac and Zoloft:

fluoxetine Prozac sertraline Zoloft
Capsule (30 capsules) 10 mg: $3.00
20 mg: $3.00
40 mg: $3.00
10 mg: $461.85
20 mg: $474.70
40 mg: $947.40
no information available no information available
Tablet (30 tablets) 10 mg: $4.00
20 mg: $26.76
60 mg: $96.35
no information available 25 mg: $3.99
50 mg: $7.17
100 mg: $6.52
25 mg: $313.61
50 mg: $313.61
100 mg: $313.61
Liquid oral solution (1 bottle) 120 ml: $12.81 no information available 60 ml: $25.10 60 ml: $216.18

Can you take Prozac and Zoloft together?

People should not take Prozac and Zoloft together. These drugs are in the same drug class and have the same actions. Taking both drugs will not improve symptoms but can cause additional side effects.

When people are not feeling the intended effects of either Prozac or Zoloft, the doctor may increase the dosage or alter the treatment regimen by adding another antidepressant or antipsychotic drug that has different actions on the brain.

Summary

Prozac and Zoloft are part of the same family of antidepressants, and both raise the levels of serotonin in the brain. Both drugs have FDA approval for the treatment of MDD, and they also have other approved and nonapproved uses.

The safe warnings relating to taking Prozac or Zoloft are similar, as are many of the side effects, although these can vary from person to person. Zoloft may be harsher on the stomach, while Prozac is more likely to cause headaches.

Both drugs are generally effective and safe, but people taking Prozac or Zoloft should follow up with their doctor to discuss their symptoms and side effects to ensure that they are taking the most effective dosage.

If treatment is successful, the doctor will slowly reduce the dosage if possible to eventually stop the medication. People should not abruptly stop taking Prozac or Zoloft.

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[WEB SITE] Amitriptyline: Uses, side effects, warnings, and interactions

Amitriptyline is an antidepressant drug that doctors prescribe to treat depression. It also has off-label uses for other mental and physical health conditions.

Amitriptyline is a drug in the tricyclic antidepressant (TCA) family.

TCAs were introduced in the late 1950s as a treatment for depression. Since then, other less toxic drugs have become available. Among them are selective serotonin reuptake inhibitors, better known as SSRIs.

Doctors prescribe amitriptyline to people with depression who have not responded to other antidepressants. There are additional uses for amitriptyline that the Food and Drug Administration (FDA) have not approved.

Read on to learn more about the uses, side effects, warnings, and potential interactions of amitriptyline.

What is amitriptyline?

amitriptyline

Amitriptyline is a prescription antidepressant drug.

The structure of amitriptyline allows it to attach to receptors in the brain called alpha-adrenergic, histaminic, and muscarinic receptors. This means that amitriptyline can cause more side effects than some other TCAs.

Some examples of other drugs in the TCA class include:

  • clomipramine
  • desipramine
  • doxepin
  • imipramine
  • nortriptyline
  • protriptyline
  • trimipramine

There are six dosages of amitriptyline: 10 milligrams (mg), 25 mg, 50 mg, 75 mg, 100 mg, and 150 mg.

Amitriptyline was once manufactured under the brand Elavil, but only generic forms of the drug are currently available.

Uses

Doctors prescribe amitriptyline to treat depression in adults.

They may also use the drug in ways that the FDA has not approved, known as off-label uses. For example, a doctor may recommend amitriptyline as an off-label treatment for:

amitriptyline headache

Taking amitriptyline can cause dizziness and drowsiness.

Amitriptyline may also cause blurred vision, urinary retention, a rapid heartbeat, and acute-angle glaucoma when it binds to muscarinic receptors in the body.

When amitriptyline attaches to histaminic receptors, it may cause sedation, confusion, and delirium.

People who have seizures should use amitriptyline with caution because it can lower the seizure threshold.

Serious cardiac side effects can occur when amitriptyline binds to alpha-adrenergic receptors in the heart. Low blood pressure upon standing and heart rate fluctuations and irregularities are some of these effects.

How to take and dosage

When treating depression with amitriptyline, doctors usually prescribe a starting dosage of 25 mg per day — at bedtime because it can cause drowsiness. For off-label uses, doctors may prescribe dosages of 10–20 mg per day.

Depending on a person’s response to the medication, the doctor may increase the dosage by 25 mg every 3–7 days. The effective dosage of amitriptyline is one that controls symptoms without causing too many side effects.

The maximum daily dosage of amitriptyline is 150–300 mg per day.

When the dosage is correct, people should notice their symptoms improving within 2–4 weeks. The doctor will recommend maintaining an effective dosage for at least 3 months to prevent symptoms from returning.

If a person wants to stop taking amitriptyline, it is important to develop a tapering schedule with a doctor to prevent withdrawal symptoms. Stopping amitriptyline abruptly can cause side effects.

What happens when you stop taking it?

It is important to gradually reduce the dosage of amitriptyline to prevent withdrawal symptoms.

Withdrawal symptoms can include:

  • nausea
  • headache
  • general discomfort

A doctor will recommend a tapering schedule. An individual approach is key because each person may have a different reaction to stopping the drug.

Keeping track of any symptoms and informing the doctor can help them judge whether to speed up or slow down the tapering.

Warnings

Short-term studies have shown that antidepressants can increase the risk of suicidal thoughts and behaviors in children, adolescents, and young adults. Research has not shown that people older than 24 years experience these or similar effects.

Before prescribing amitriptyline to a child, adolescent, or young adult, the doctor should weigh the benefits and risks carefully. During treatment, doctors and caregivers need to monitor people taking amitriptyline for worsening symptoms of depression, suicidal thoughts, and unusual behaviors.

Anyone who has experienced an allergic reaction to amitriptyline should refrain from using this drug.

If a person has a history of cardiac problems, such as arrhythmiaheart failure, or a recent heart attack, a doctor should not prescribe amitriptyline.

Anyone over 50 and anyone with a history of heart trouble will undergo an electrocardiogram before beginning amitriptyline treatment. They will repeat this test during treatment so a doctor can check for new or worsening heart conditions.

Amitriptyline can worsen existing angle-closure glaucoma, urinary retention, and seizures. It is important to discuss any symptoms with a doctor, who can rule out these issues, before beginning treatment.

Doctors should prescribe lower doses of amitriptyline to people with liver or kidney failure.

Suicide prevention

  • If you know someone at immediate risk of self-harm, suicide, or hurting another person:
  • Call 911 or the local emergency number.
  • Stay with the person until professional help arrives.
  • Remove any weapons, medications, or other potentially harmful objects.
  • Listen to the person without judgment.
  • If you or someone you know is having thoughts of suicide, a prevention hotline can help. The National Suicide Prevention Lifeline is available 24 hours a day at 1-800-273-8255.

Interactions

When a person takes amitriptyline and certain other drugs, three critical interactions can occur: monoamine oxidase inhibitor (MAOI) interactions, QT prolongation interactions, and serotonin syndrome interactions.

MAOI interactions

amitriptyline overheating fan

A person may experience an increased body temperature when taking amitriptyline.

MAOIs work by blocking the effect of the enzyme monoamine oxidase. This enzyme is responsible for breaking down monoamines in the body.

Monoamines include epinephrine, norepinephrine, dopamine, serotonin, and tyramine. When levels of these chemicals rise in the body, a person may experience:

  • increased heart rate
  • increased body temperature
  • muscle twitching
  • high blood pressure
  • agitation

MAOI drugs include :

  • isocarboxazid
  • phenelzine
  • tranylcypromine
  • selegiline

QT prolongation

The QT interval on an electrocardiogram is an important measure of the electrical conduction of the heart. When this interval lengthens, a person may experience an abnormal heart rhythm, which can lead to arrhythmia.

Amitriptyline can prolong the QT interval. Combining this drug with others that have the same effect puts a person at risk of developing arrhythmia.

Some examples of other drugs that can prolong the QT interval include:

  • astemizole
  • cisapride
  • disopyramide
  • ibutilide
  • indapamide
  • pentamidine
  • pizomide
  • procainamide
  • quinidine
  • sotalol
  • terfenadine

Serotonin syndrome

Serotonin syndrome occurs when there is too much serotonin in the body. This can cause symptoms that can range in severity from mild-to-life-threatening.

Serotonin syndrome symptoms include:

  • dilated pupils
  • flushed skin
  • dry mucous membranes
  • increased bowel sounds
  • excessive sweating
  • increased body temperature
  • a rapid heartbeat
  • muscle rigidity
  • muscle twitching
  • abnormal reflexes agitation
  • anxiety
  • restlessness
  • nausea
  • vomiting
  • tremor
  • disorientation
  • an altered mental status

Amitriptyline increases the amount of serotonin in the brain. When a person also takes other drugs that have this effect, it puts them at risk of developing serotonin syndrome.

Some other drugs that can increase the amount of serotonin in the brain include:

  • isocarboxazid
  • phenelzine
  • procarbazine
  • safinamide
  • selegiline
  • tranylcypromine

Cost

The manufacturer has discontinued the Elavil brand of amitriptyline, so only generic forms are available.

The following list shows the prices for 30 tablets of amitriptyline by dosage.

  • Amitriptyline 10 mg: $4.00
  • Amitriptyline 25 mg: $4.00
  • Amitriptyline 50 mg: $4.00
  • Amitriptyline 75 mg: $4.00
  • Amitriptyline 100 mg: $16.82
  • Amitriptyline 150 mg: $23.50

Summary

Doctors usually prescribe amitriptyline to treat depression. In addition, some off-label uses include treating anxiety, IBS, and chronic pain.

People taking amitriptyline may experience drowsiness, headaches, and dizziness, among other side effects, some of which are more severe.

Anyone taking any antidepressant should remain watchful for worsening of symptoms. Some people have experienced suicidal thoughts and behaviors while taking amitriptyline, and this requires immediate medical attention.

Also, some drugs can interact with amitriptyline. It is crucial that doctors and pharmacists carefully weigh the benefits and risks of adding amitriptyline to a person’s care plan.

 

via Amitriptyline: Uses, side effects, warnings, and interactions

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[BLOG POST] Antidepressants help us understand why we get fatigued during exercise

In general, the term ‘fatigue’ is used to describe any exercise-induced decline in the ability of a muscle to generate force. To identify the causes of fatigue, it is common to examine two divisions of the body that might be affected during exercise. The central component of fatigue includes the many nerves that travel throughout the brain to the spinal cord. The peripheral component predominantly reflects elements in the muscle itself. If there is a problem with either of these components, the ability to contract a muscle might be compromised. For many years, there has been suggestion that central fatigue is heavily influenced by neurotransmitters that get released in the central nervous system (such as dopamine and serotonin). However, little research has been performed in this area.

Serotonin is a chemical that can improve mood, and increasing the amount of serotonin that circulates in the brain is a common therapy for depression. However, serotonin also plays a vital role in activating neurons in the spinal cord which tell the muscle to contract. With the correct amount of serotonin release, a muscle will activate efficiently. However, if too much serotonin is released, there is a possibility that the muscle will rapidly fatigue. Recent animal studies indicate that moderate amounts of serotonin release, which are common during exercise, can promote muscle contractions (Cotel et al. 2013). However, massive serotonin release, which may occur with very large bouts of exercise, could further exacerbate the already fatigued muscle (Perrier et al. 2018).

Selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressants. These medications keep serotonin levels high in the central nervous system by stopping the chemical from being reabsorbed by nerves (reuptake inhibition). Instead of using SSRIs to relieve symptoms of depression, we used them in our recent study (Kavanagh et al. 2019) to elevate serotonin in the central nervous system, and then determine if characteristics of fatigue are enhanced when serotonin is elevated. We performed three experiments that used maximal voluntary contractions of the biceps muscle to cause fatigue in healthy young individuals. Our main goal was to determine if excessive serotonin limits the amount of exercise that can be performed, and then determine which central or peripheral component was compromised by excessive serotonin.

WHAT DID WE FIND?

Given that SSRIs influence neurotransmitters in the central nervous system, it was not surprising that peripheral fatigue was unaltered by the medication. However, central fatigue was influenced with enhanced serotonin. The time that a maximum voluntary contraction could be held was reduced with enhanced serotonin, whereby the ability of the central nervous system to drive the muscle was compromised by 2-5%. We further explored the location of dysfunction and found that the neurons in the spinal cord that activate the muscle were 4-18% less excitable when fatiguing contractions were performed in the presence of enhanced serotonin.

SIGNIFICANCE AND IMPLICATIONS

The central nervous system is diverse, and the fatigue that is experienced during exercise is not just restricted to the brain. Instead, the spinal cord plays an integral role in activating muscles, and mechanisms of fatigue also occur in these lower, often overlooked, neural circuits. This is the first study to provide evidence that serotonin released onto the motoneurones contributes to central fatigue in humans.

PUBLICATION REFERENCE

Kavanagh JJ, McFarland AJ, Taylor JL. Enhanced availability of serotonin increases activation of unfatigued muscle but exacerbates central fatigue during prolonged sustained contractions. J Physiol. 597:319-332, 2019.

If you cannot access the paper, please click here to request a copy.

KEY REFERENCES

Cotel F, Exley R, Cragg SJ, Perrier JF. Serotonin spillover onto the axon initial segment of motoneurons induces central fatigue by inhibiting action potential initiation. Proc Natl Acad Sci U S A. 110:4774-4779, 2013.

Perrier JF, Rasmussen HB, Jørgensen LK, Berg RW. Intense activity of the raphe spinal pathway depresses motor activity via a serotonin dependent mechanism. Front Neural Circuits. 11:111, 2018.

AUTHOR BIO

Associate Professor Justin Kavanagh is a researcher and lecturer at Griffith University. His team explores how the central nervous system controls voluntary and involuntary movement, and he has particular interests in understanding how medications can be used to study mechanisms of human movement.

via Antidepressants help us understand why we get fatigued during exercise – Motor Impairment

 

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[WEB SITE] Dopamine deficiency: Symptoms, causes, and treatment

    1. Symptoms
    2. Causes
    3. Diagnosis
    4. Treatment
    5. Dopamine vs. serotonin
    6. Outlook

 

 

Dopamine is a chemical found naturally in the human body. It is a neurotransmitter, meaning it sends signals from the body to the brain.

Dopamine plays a part in controlling the movements a person makes, as well as their emotional responses. The right balance of dopamine is vital for both physical and mental wellbeing.

Vital brain functions that affect mood, sleep, memory, learning, concentration, and motor control are influenced by the levels of dopamine in a person’s body. A dopamine deficiency may be related to certain medical conditions, including depression and Parkinson’s disease.

A dopamine deficiency can be due to a drop in the amount of dopamine made by the body or a problem with the receptors in the brain.

Symptoms

 

Sad and depressed woman with low dopamine levels. alone in thought.

A dopamine deficiency is associated with depression, but researchers are still investigating this complex link.

 

The symptoms of a dopamine deficiency depend on the underlying cause. For example, a person with Parkinson’s disease will experience very different symptoms from someone with low dopamine levels due to drug use.

Some signs and symptoms of conditions related to a dopamine deficiency include:

  • muscle cramps, spasms, or tremors
  • aches and pains
  • stiffness in the muscles
  • loss of balance
  • constipation
  • difficulty eating and swallowing
  • weight loss or weight gain
  • gastroesophageal reflux disease (GERD)
  • frequent pneumonia
  • trouble sleeping or disturbed sleep
  • low energy
  • an inability to focus
  • moving or speaking more slowly than usual
  • feeling fatigued
  • feeling demotivated
  • feeling inexplicably sad or tearful
  • mood swings
  • feeling hopeless
  • having low self-esteem
  • feeling guilt-ridden
  • feeling anxious
  • suicidal thoughts or thoughts of self-harm
  • low sex drive
  • hallucinations
  • delusions
  • lack of insight or self-awareness

Causes

 

Dopamine model 3D render.

 Dopamine deficiency may be influenced by a number of factors. Existing conditions, drug abuse, and an unhealthy diet may all be factors.

 

Low dopamine is linked to numerous mental health disorders but does not directly cause these conditions.

The most common conditions linked to a dopamine deficiency include:

In Parkinson’s disease, there is a loss of the nerve cells in a specific part of the brain and loss of dopamine in the same area.

It is also thought that drug abuse can affect dopamine levels. Studies have shown that repeated drug use could alter the thresholds required for dopamine cell activation and signaling.

Damage caused by drug abuse means these thresholds are higher and therefore it is more difficult for a person to experience the positive effects of dopamine. Drug abusers have also been shown to have significant decreases in dopamine D2 receptors and dopamine release.

Diets high in sugar and saturated fats can suppress dopamine, and a lack of protein in a person’s diet could mean they do not have enough l-tyrosine, which is an amino acid that helps to build dopamine in the body.

Some studies have found that people who are obese are more likely to be dopamine deficient too.

Diagnosis

There is no reliable way to measure levels of dopamine in a person. However, a doctor may look at a person’s symptoms, lifestyle factors, and medical history to determine if they have a condition related to low levels of dopamine.

Treatment

 

Omega-3 fatty acid supplements.

Omega-3 fatty acid supplements may help to boost dopamine levels naturally.

 

 Treatment of dopamine deficiency depends on whether an underlying cause can be found.

If a person is diagnosed with a mental health condition, such as depression or schizophrenia, a doctor may prescribe medications to help with the symptoms. These drugs may include anti-depressants and mood stabilizers.

Ropinirole and pramipexole can boost dopamine levels and are often prescribed to treat Parkinson’s disease. Levodopa is usually prescribed when Parkinson’s is first diagnosed.

Other treatments for a dopamine deficiency may include:

  • counseling
  • changes in diet and lifestyle
  • physical therapy for muscle stiffness and movement problems

Supplements to boost levels of vitamin Dmagnesium, and omega-3 essential fatty acids may also help to raise dopamine levels, but there needs to be more research into whether this is effective.

Activities that make a person feel happy and relaxed are also thought to increase dopamine levels. These may include exercise, therapeutic massage, and meditation.

Dopamine vs. serotonin

Dopamine and serotonin are both naturally occurring chemicals in the body that have roles in a person’s mood and wellbeing.

Serotonin influences a person’s mood and emotions, as well as sleep patterns, appetite, body temperature, and hormonal activity, such as the menstrual cycle.

Some researchers believe that low levels of serotonin contribute to depression. The relationship between serotonin and depression and other mood disorders is complex and unlikely to be caused by a serotonin imbalance alone.

Additionally, dopamine affects how a person’s moves, but there is no clear link to the role of serotonin in movement.

Outlook

Dopamine deficiency can have a significant impact on a person’s quality of life, affecting them both physically and mentally. Many mental health disorders are linked to low levels of dopamine. Other medical conditions, including Parkinson’s disease, have also been linked to low dopamine.

There is limited evidence that diet and lifestyle can affect the levels of dopamine a person creates and transmits in their body. Certain medications and some therapies may help relieve symptoms, but a person should always speak to a doctor first if they are concerned about their dopamine levels.

 

via Dopamine deficiency: Symptoms, causes, and treatment

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[BLOG POST] Tryptophan in Mood, Anxiety, and Depression

 

Deficiency of monoamines, such as dopamine, epinephrine, and serotonin, is the most widely accepted theory explaining mood disorders. Among these neuromediators, serotonin deficiency is considered as most significant in relation to anxiety and depression. This theory has been proven by the effectiveness of drugs that help to increase monoamines levels in the brain, although research in this direction has been hampered by the limitations of present-day technology in measuring the levels of specific monoamines and their properties. However, studies do indicate that their deficiency plays a role in individuals prone to mood swings.

Tryptophan as precursor for serotonin

Tryptophan is one of the essential amino acids. It can’t be produced by our body and has to come through food products rich in proteins. It is required for both anabolic processes and production of various hormones. Tryptophan is a chemical precursor for the synthesis of the neurotransmitter serotonin. This means that the amount of serotonin produced in our body is dependent on the dietary intake of tryptophan. Since serotonin is related to mood regulation, it is entirely possible that tryptophan deficits may have a negative effect on our mood state. On the other hand, its supplementation may be helpful in disorders like anxiety or depression. Multiple investigations seem to support the idea that decreased levels of tryptophan lead to a reduction in serotonin and changes in mood. Some studies have indicated that higher intake of tryptophan may improve social interactions by improving mood and decreasing aggression and dominant behavior.

Serotonin in mood and cognition

Serotonin is important for both mood regulation and regulation of cognitive functions like learning and memory. The effect of monoamine inhibitors called serotonin reuptake inhibitors in various disorders of mood supports this theory. However, it is important to keep in mind that antidepressants are only partially effective in treating mood disorders since monoamine deficits are just one of the factors influencing mood. Most of the serotonin in our body is produced outside the brain, indicating that this compound has a much broader role in our normal physiology. It is possible that many functions of serotonin are still not understood.

Tryptophan depletion and mood regulation

To understand the role of serotonin, and more specifically tryptophan, many tryptophan-depletion studies have been done in recent times. In one simple crossover study, 25 healthy adults were studied for mood changes like anxiety and depression after consuming either a high tryptophan diet or a low tryptophan diet for four days. Tryptophan consumption seems to affect mood even in such a short interval. The study showed that those on a high tryptophan diet had much better mood as compared to those on a low tryptophan diet, although the negative effects of a low tryptophan diet were less pronounced. If such a quick and straightforward analysis can show the difference, it is entirely possible that long-term low tryptophan consumption or depletion may have much graver consequences for mental health.

Tryptophan and gut-brain axis

When we talk about the gut-brain axis we are not just discussing the digestive role of the gut and its effect on overall health, something that has been well known for many years. Our digestive system is also involved in neuro-hormonal signaling, through which it can have an impact on brain functioning. Recently, the influence of gut health on the brain has been the subject of many studies and for good reason. Our gut has more nerve cells than our spine, and it produces many hormones that have various implications for health. Further, it is now well understood that the neural relationship between the gut and brain is dual-sided, and there are more nerve fibers sending information from the gut to the brain rather than from the brain to the gut. Thus, due to the effect of nerves, hormones, and other neurologically active compounds, the gut plays a prominent role in mental wellbeing. Even small changes in the gut could directly affect our behavior. Gut microbiota and their relationship to mood have also recently received lots of attention.

When it comes to tryptophan, the digestive system is not solely involved in its absorption or metabolism. Now it is well-established that serotonin is mostly produced in the gut rather than in the brain, further strengthening the theory of gut-brain interrelation. This theory explains the mood alterations in irritable bowel syndrome (IBS). Further, the development of IBS has been shown to be connected to tryptophan depletion.

The studies show that tryptophan depletion, due to its relationship with serotonin, is undoubtedly one of the most essential elements to consider when analyzing altered mood and cognition. Low serotonin could generally cause a state of lowered mood, impaired cognition, poor working memory, and lower reasoning. Conversely, high tryptophan supplementation could have a positive effect on mood, memory, energy level, and emotional processing.

Low dietary consumption of tryptophan could be one of the elements leading to chronic conditions like depression and anxiety. Bowel conditions like IBS that disturb tryptophan metabolism and alter serotonin levels may also modify our behavior and feelings.

The search for effective therapeutic approaches to the treatment of mood disorders, anxiety, and depression has gained lots of attention in the last few decades. Understanding the role of tryptophan may open up new possibilities for managing mood and cognition problems. It is quite possible that a high tryptophan diet may not only help to prevent mood disorders but also increase the effectiveness of existing drug therapies.

References

Delgado, P. L. (2000) Depression: the case for a monoamine deficiency. The Journal of Clinical Psychiatry61 Suppl 6, 7–11. PMID: 10775018

Jenkins, T. A., Nguyen, J. C. D., Polglaze, K. E., & Bertrand, P. P. (2016) Influence of Tryptophan and Serotonin on Mood and Cognition with a Possible Role of the Gut-Brain Axis. Nutrients8(1). doi: 10.3390/nu8010056

Lindseth, G., Helland, B., & Caspers, J. (2015). The Effects of Dietary Tryptophan on Affective Disorders. Archives of Psychiatric Nursing29(2), 102–107. doi: 10.1016/j.apnu.2014.11.008

Young, S. N., & Leyton, M. (2002) The role of serotonin in human mood and social interaction. Insight from altered tryptophan levels. Pharmacology, Biochemistry, and Behavior71(4), 857–865. PMID: 11888576

Young, S. N., Smith, S. E., Pihl, R. O., & Ervin, F. R. (1985) Tryptophan depletion causes a rapid lowering of mood in normal males. Psychopharmacology87(2), 173–177. doi: 10.1007/BF00431803

Image via freeGraphicToday/Pixabay.

via Tryptophan in Mood, Anxiety, and Depression | Brain Blogger

 

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[WEB PAGE] Faster-acting antidepressants may soon be a reality

Understanding where antidepressants act is the key to improving their function.

 

Using cutting-edge techniques, researchers have investigated the mechanism by which common antidepressants work, finally pinning down the specific receptors responsible for their action. The findings might pave the way to designing improved, faster-acting antidepressants.

Depression is characterized by persistent low mood and feelings of hopelessness, and it is one of the most common mental disorders in the United States. In 2014, there were an estimated 15.7 million U.S. adults who experienced at least one major depressive episode, representing around 6.7 percent of the country’s adults.

Treatments for depression generally include talking therapies in conjunction with medication. The class of drugs most commonly prescribed is selective serotonin reuptake inhibitors (SSRIs), and these include brands such as Prozac and Zoloft.

SSRIs can help some people with depression, but they are not perfect; not everyone responds well to them, and side effects including nausea, insomnia, agitation, and erectile dysfunction can be unpleasant.

Also, SSRIs can take some time to kick in; although some people might feel some benefit within hours or even minutes, most people do not feel the full antidepressant effect until they have been taking the drugs for weeks or even months.

How do SSRIs work?

In the brain, messages are sent between neurons by releasing neurotransmitters into a gap between the cells, or the synapse. Serotonin is one such neurotransmitter. It is released from the first neuron and binds to receptors on the second neuron.

Normally, once serotonin has been released into the synapse and relayed its message, the majority is reabsorbed into the first nerve cell for reuse at a later date. SSRIs prevent serotonin from being reabsorbed. In this way, they ensure that serotonin hangs around in the synapse for a longer time, exerting more of an effect.

Although SSRIs have been known to medical science since the 1950s, their exact mechanism is not understood. This is because there are at least 1,000 types of neuron that can be influenced by a surge in serotonin, and some of these neurons may be excited, while others might be inhibited.

The mixed response is because there are 14 subtypes of serotonin receptor throughout the body and any single nerve could have a cocktail of receptor types. Teasing out which receptor subtype is playing the most significant role has proven challenging.

The role of the dentate gyrus

A group of scientists from Rockefeller University in New York City, NY, recently set out to take a closer look at the action of SSRIs on a particular type of nerve cell. The team was headed up by Lucian Medrihan and Yotam Sagi, both research associates in the Laboratory of Molecular and Cellular Neuroscience, and Paul Greengard, Nobel laureate.

Their findings were recently published in the journal Neuron.

Many different types of synapses throughout the brain use serotonin as their neurotransmitter. An issue of major importance has been to identify where in the myriad of neurons the antidepressants initiate their pharmacological action.”

Paul Greengard

The team concentrated on a group of cells in the dentate gyrus (DG). According to the authors, they chose the DG because previous work has established that “SSRI treatment promotes a variety of synaptic, cellular, and network adaptations in the DG.”

Specifically, the team investigated cholecystokinin (CCK)-expressing neurons within the DG. These neurons were of interest because they are heavily influenced by neurotransmitter systems that are associated with mood disorders, such as depression.

Finding the right receptor

Using a technique called translating ribosome affinity purification, the team were able to identify the serotonin receptors on CCK cells. Sage explains, “We were able to show that one type of receptor, called 5-HT2A, is important for SSRIs’ long-term effect, while the other, 5-HT1B, mediates the initiation of their effect.

The next step in the study involved efforts to mimic SSRIs’ effects by manipulating CCK neurons in mice. They used chemogenetics to switch nerve cells on or off and implanted tiny electrodes inside the mouse brains.

The findings were clear. When the CCK neurons were inhibited, the pathways important for the mediation of SSRI responses lit up. In other words, the scientists had recreated a Prozac-like effect without using the drug.

To back up these findings, the team used behavioral experiments in a pool and observed swimming patterns. Again, silencing the CCK neurons created behavior that was similar to that displayed by the mice that had been given SSRIs: they swam for longer with increased vigor.

According to the researchers, understanding the importance of the DG and the specific cells important for treating depression will help to design faster-acting, more effective antidepressants with fewer side effects.

The work was carried out using techniques that would have been impossible just 5 years ago, and the studies that follow are likely to improve our understanding even further.

Source: Faster-acting antidepressants may soon be a reality

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[ARTICLE] Selective serotonin reuptake inhibitors to improve outcome in acute ischemic stroke: possible mechanisms and clinical evidence – Full Text HTML

Abstract

Background: Several clinical studies have indicated that selective serotonin reuptake inhibitors (SSRIs) administered in patients after acute ischemic stroke can improve clinical recovery independently of depression. Due to small sample sizes and heterogeneous study designs interpretability was limited in these studies. The mechanisms of action whereby SSRI might improve recovery from acute ischemic stroke are not fully elucidated.

Methods: We searched MEDLINE using the PubMed interface to identify evidence of SSRI mediated improvement of recovery from acute ischemic stroke and reviewed the literature on the potential underlying mechanisms of action.

Results: Among identified clinical studies, a well-designed randomized, double-blind, and placebo-controlled study (FLAME – fluoxetine for motor recovery after acute ischemic stroke) demonstrated improved recovery of motor function in stroke patients receiving fluoxetine. The positive effects of SSRIs on stroke recovery were further supported by a meta-analysis of 52 trials in a total of 4060 participants published by the Cochrane collaboration. Based on animal models, the mechanisms whereby SSRIs might ameliorate functional and structural ischemic-brain damage were suggested to include stimulation of neurogenesis with migration of newly generated cells toward ischemic-brain regions, anti-inflammatory neuroprotection, improved regulation of cerebral blood flow, and modulation of the adrenergic neurohormonal system. However, to date, it remains speculative if and to what degree these mechanisms convert into humans and randomized controlled trials in large populations of stroke patients comparing different SSRIs are still lacking.

Conclusion: In addition to the need of comprehensive-clinical evidence, further elucidation of the beneficial mechanisms whereby SSRIs may improve structural and functional recovery from ischemic-brain damage is needed to form a basis for translation into clinical practice.

Continue —> Selective serotonin reuptake inhibitors to improve outcome in acute ischemic stroke: possible mechanisms and clinical evidence – Siepmann – 2015 – Brain and Behavior – Wiley Online Library

 

Possible mechanisms of action. The figure illustrates three possible mechanisms whereby SSRIs might improve structural-brain tissue recovery from ischemia: stimulation of neurogenesis in the subependymal zone and hippocampal dentate gyrus, inhibition of microglia- and neutrophile-induced inflammation mediated by cytotoxic inflammatory molecules, and improvement of cerebral vascular autoregulation (HO-1, heme oxygenase-1; VEGF, vascular endothelial growth factor).

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[WEB SITE] The New Compounds That Could Treat Depression in 24-Hours

Post image for The New Compounds That Could Treat Depression in 24-HoursCurrent antidepressants take around 3 to 8 weeks to kick in and only help around 50% of people who are depressed.

A new type of antidepressant holds the promise of treating depression quickly, without too many side-effects. Professor Scott Thompson, of the University of Maryland School of Medicine who led the research, said:

“Our results open up a whole new class of potential antidepressant medications.

We have evidence that these compounds can relieve the devastating symptoms of depression in less than one day, and can do so in a way that limits some of the key disadvantages of current approaches.”

Currently used antidepressants, such as Prozac and Lexapro, target levels of the neurotransmitter serotonin.

Unfortunately they are only effective in around half of people with depression. Even amongst people they do help, it can take three to eight weeks for the effects can be felt. For patients who are suicidal, this period can be excruciating.

Also, many now believe that targeting serotonin is not effective (see: Long-Held Belief About Depression Challenged by New Study).

The new compounds focus on another neurotransmitter with the acronym GABA (gamma-aminobutyric acid), instead of serotonin. GABA mainly reduces brain activity in certain key areas related to mood.

The new class of compounds dampen down these inhibitory signals. Theoretically, the result should be to lift mood.

Professor Thompson explained that preliminary tests on animals have been encouraging:

“These compounds produced the most dramatic effects in animal studies that we could have hoped for.

It will now be tremendously exciting to find out whether they produce similar effects in depressed patients.

If these compounds can quickly provide relief of the symptoms of human depression, such as suicidal thinking, it could revolutionize the way patients are treated.”

The study found that the compounds only affected the brains of stressed rats and left unstressed rats unchanged. This may mean that the side-effects of the treatment will be less severe than those seen for current antidepressants.

The study was published in the journal Neuropsychopharmacology (Fischell et al., 2015).

via The New Compounds That Could Treat Depression in 24-Hours.

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