Dopamine hypothesis of schizophrenia - Wikipedia

Figure 2. Neurotrophic hypothesis for antidepressant action. Panel A: Timeline of events involved in mediating a therapeutic response to antidepressant therapy. Antidepressants rapidly elevate synaptic levels of monoamines. Over several weeks, an upregulation in the expression of BDNF produces an increased growth of neurons and upregulation of biochemical pathways involved synaptic transmission, resulting in a reversal of depressive symptoms. Panel B: Antidepressants produce a rapid increase in synaptic levels of serotonin & norepinephrine, which stimulate cAMP response element-binding protein (CREB) through different converging signal transduction pathways. CREB stimulation upregulates the expression of BDNF which causes increased neuronal growth and plasticity (as illustrated in Panels C & D). Psychotherapy may produce similar &/or complementary effects by stress reduction, which can reduce cortisol levels.

Depression: Death to the serotonin hypothesis ..

According to the (WHO), depression is now recognized as the leading cause ofdisability.

and heard that the serotonin hypothesis of depression …

Historically, antidepressants alone have been used more often than either psychotherapy alone, or combination treatment for numerous reasons (Simon & Cienchanowski, 2015) including:

The Neurotransmitter Hypothesis of Schizophrenia - …

People not suffering from depression have a balance in degradation and regeneration processes in the brain. The degradation process refers to the breaking down of nerve cells, while regeneration refers to the formation of nerve cells (1). Depressed patients show greater activity in the degradation system, which explains Videbech’s findings that brain structures are reduced in patients with depression. The location of reduction cited by Videbech is the hippocampus, the structure of the brain responsible for the storage and retrieval of memories. Hippocampal reduction explains the common symptom of memory problems in patients with depression. With antidepressant use, and hence a return of neurogenesis, memory problems and depressive symptoms are reduced. Meaning, boosting neurogenesis results in a returned balance between the degradation and regeneration processes. (2)

postulated a "catecholaminehypothesis of depression" that is still often referenced.

of how the ‘low serotonin hypothesis’ came to be ..

Compared to 1st generation antidepressants (TCAa & MAOIs), SSRIs have “relatively benign” side effects due to their selectivity in affecting serotonin. For most patients, the most bothersome side effects include (Hu et al, 2004; Hirsch & Birnbaum, 2016). In order of incidence, the most commonly reported side effects include:

that increases the risk of depression

Metabolism and elimination of SSRIs is primarily due to hepatic (P450) metabolism. The elimination half-life for most SSRIs is 20-30 hrs. Fluoxetine metabolism yields an active metabolite (norfluoxetine) that has a half-life of 4-16 days. When switching from fluoxetine to another antidepressant, doses of the new agent should typically be initially reduced to account for the long half-life of norfluoxetine when cross-tapering from one agent to another (Hirsch & Birnbaum, 2016b).

Selective NRIs on the market for the treatment of depression islimited to and .

biogenic amine” theory of depression

Antidepressant medications, also called antidepressive agents, are "mood-stimulating drugs used primarily in the treatment of affective disorders and related conditions. Several are useful as antidepressants apparently as a long-term consequence of their modulation of catecholamine levels. The tricyclic compounds useful as antidepressive agents () also appear to act through brain catecholamine systems. A third group ( agents) is a diverse group of drugs including some that act specifically on serotonergic systems."

A shortage of mesolimbic dopamine is actually one of thecardinal cues for triggering depression.

09/04/2014 · Depression: Dopamine vs

There are several lines of evidence linking the role ofmonoamines (ie 5HT/NE/DA) to depression. Firstly, when was firstimported to the westernized continent from , it was shown that this agent precipitateda depressive syndrome. Itwas further shown that reserpine causes a depletion of monoamineconcentrations in the brain.

Following on from the discovery of the

Trazodone inhibits the reuptake of serotonin, ..

The first antidepressant agents (the MAOIs and the TCAs) werediscovered entirely by serendipity.Amphetamines and opioids had in fact been used before these,although they were phased-out with the advent of newer, lessaddictive, medications.