Posts Tagged SSRI
By Jamie Eske, Reviewed by Heidi Moawad, MD
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.
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?
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:
- 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
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:
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
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
- 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:
- fluoxetine (Prozac)
- sertraline (Zoloft)
- escitalopram (Lexapro)
- paroxetine (Paxil)
- citalopram (Celexa)
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.
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.
[ARTICLE] Selective serotonin reuptake inhibitors to improve outcome in acute ischemic stroke: possible mechanisms and clinical evidence – Full Text HTML
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
[REVIEW] Post-Stroke Depression | EBRSR – Evidence-Based Review of Stroke Rehabilitation – Full Text PDF
Depression is a common complication post-stroke affecting approximately one-third of patients. The presence of post-stroke depression has been associated with decreases in functional recovery, social activity and cognition. In addition, the presence of mental health disorders following stroke may be associated with increased mortality. The present review discusses the prevalence, natural history and risk factors for post-stroke depression as well as issues around its assessment and impact on rehabilitation outcomes. Strategies for the prevention and management of post-stroke depression are reviewed. Recommendations for assessment and treatment are provided based on current guidelines. A discussion of post-stroke emotionalism, its impact and treatment is also included.