Serotonin (5-hydroxytryptamine, 5-HT) is a chemical found in the human body.It carries signals along and between nerves - a neurotransmitter. It is mainly found in the brain, bowels and blood platelets.Serotonin is thought to be especially active in constricting smooth muscles, transmitting impulses between nerve cells, regulating cyclic body processes and contributing to wellbeing and happiness.Serotonin is regarded by some researchers as a chemical that is responsible for maintaining mood balance, and that a deficit of serotonin leads to depression.
While overly simplistic, it is thought that low levels of serotonin leads to an increase in anxiety, both generalized anxiety disorder and panic disorder, while hight levels of serotonin can lead to detachment, possibly by inducing hypofrontality.
In OCD, there is hyperfrontality, and SSRIs are the treatment of choice for OCD.
So, as regards induction of anxiety in situations where there is a decrease in serotonin, I would hypothesize that the frontal lobes are involved with generalized anxiety while the locus ceroleus is involved in panic disorder.
Thank you dr.Lewis for yr scientific answer, but why serotonin antagonist (Ondansetron) used in treatment of multiple types of anxiety ?
"Getting to the roots of anxiety"by Marie Suszynski/Linsey Marcellin."Researchers now think that PTSD is due to an interplay between stress and genetic functions.I'm sure,that "some anxiety is a natural response to stress" We are not robots..http://www.everydayhealth.com/emotional-health/anxiety/getting-to-the-roots-of-anxiety.aspx
Several lines of evidence implicate decreased serotonergic activity in anxiety and major depression, but its importance in the etiology and severity of these disorders remains unclear. Acute tryptophan depletion studies support a role for decreased serotonin in depression, or at least in relapse of recovered depressed patients. Imaging and post-mortem studies indicate altered activity of discrete regions within the prefrontal cortex (PFC) and their atrophy are associated with depression. Genetic polymorphisms in serotonin genes [e.g., 5-HT transporter (5-HTT), 5-HT1A receptor] have been associated with depression, but these associations are weak and not always reproducible, suggesting that serotonin may be a predisposing factor rather than a cause of depression or anxiety. Pl. refer following thread for further details:-
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047678/
Once one adds receptor subtypes, the "plot thickens"
For example: ondansetron is a 5HT3 antagonist; buspirone is a 5HT1a agonist
To Irvin Yalom,"School of existential therapy"Our existence begins from the cry of the lone soul in the anxious waiting for reply.There is no medicine from despair.There are no doctors for the soul...One of the greatest life paradoxes is that self-consciousness aggravates anxiety.A human being is becoming free from the anxiety through loosing himself-falling in love ("Ego"(I) is dissolved in "we").I think,anti-depressants are not panacea from depression(side-effects are terrible,we are unique-every individual has own peculiarities).The level of stress hormones(cortisol) is raised,but people should replaice it to "the love hormones".Self-regulation(positive thinking),dancing,swimming,sauna,arts,travelling, nature,communication with children and friends,church,massage,dream...
http://cpsy.ru/cit1199.htm
I believe dr stahl recently published a paper re: when there is TOO MUCH serotonin
which is not even one year old
Dear Ali,
Excellent question. However I think most of the answers here about involvement of serotonin in anxiety. Yes sure it is involved but is serotonin involved in induction or in maintenance of anxiety or both. Is it possible that actual anxiety is started (induced) by another fast transmitter, then once induced maintained (prolonged by too much or insufficient serotonin)? Or different types of serotonin receptors (fast vs slow) involved seperately in induction and maintanence of anxiety?
best wishes,
Refik
I suggest you read my review on anxiety disorders as you may find the information in this helpful.
http://www.ncbi.nlm.nih.gov/pubmed/25237115
Please see the paper 'Acute tryptophan depletion increases translational indices of anxiety but not fear: serotonergic modulation of the bed nucleus of the stria terminalis?'
(http://www.ncbi.nlm.nih.gov/pubmed/22491355)
It supports that serotonin exerts its influence over anxiety responding by mediating CRH in the BNST.
Anxiety as a symptom-complex entails a number of neurotransmitter e.g. serotonin (5HT), NE, and, GABA within neurocircuity of firing amygdala and related structure.
5HT1A receptors has long been shown to be tied to anxiety- so agents that are agonists to these receptors either partially (e.g. buspirone) or fully by boosting synaptic serotonin to stimulate post-synaptic receptors by SSRIs antidepressants
All SSRIs as such are anti-anxiety agents too- but SNRIs look superior when tackling NE too. Sertraline and paroxetine are FDA-approved for almost all anxiety disorders.
GABAergic agents e.g. BDZs (alprazolam, etc.) are also helpful especially acutely, short-term or as PRN use.
Of note, boosting serotonin initially would also stimulate post-synaptic 5HT2 with resultant anxiety and/or akathisia. So, early-on in treatment, BDZs coverage, or low-dose mirtazapine (to block 5-HT receptors) or starting low and going slow strategies might help overcome this detracting side-effects. Patients need psycho-education about this issue that usually jeopardizes treatment-adherence.
Trust this might help.
All said and done, including the use of SSRIs, Serotonin "only appears" to be one of the major players in mood and a variety of other disorders. But exactly how remains an open question!! Still
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