TITLE:- Explain the biological mechanism of Selective Serotonin Reuptake
Inhibitors (SSRI) and critically evaluate the efficiency of SSRI in treating
depression. Support your argument using empirical evidence.
MODULE: PSYC2091
P NUMBER: P2825456
, 2
Selective serotonin reuptake inhibitors (SSRIs) are among the most widely
prescribed drugs in psychiatry. Besides serving as antidepressants, they are also used in the
treatment of anxiety-related disorders (obsessive compulsive disorder, social anxiety, panic
disorders) (Bespalov et al., 2010), autism (Williams et al., 2010), eating disorders (Flament et al.,
2012), and occasionally posttraumatic stress disorder (Stein et al., 2009). Serotonin reuptake
inhibitors (SSRIs) have emerged as a significant therapeutic development in
psychopharmacology.
SSRIs enhance extracellular serotonin (5-hydroxytryptamine; 5-HT) levels in the
synaptic cleft by inhibiting the serotonin transporter (5-HTT), a Na+/Cl inward rectifying
transporter found on presynaptic nerve terminals (Tavoulari et al., 2009). Microanalysis followed
by high-performance liquid chromatography consistently shows an increase in extracellular
levels of 5-HT in several brain regions (Bel and Artigas, 1993, Invernizzi et al., 1995, Kreiss and
Lucki, 1995, Wong et al., 1995, Gundlah et al., 1997, Ceglia et al., 2004). The magnitude of
increase varies between research, which could be due to changes in SSRI therapy, brain area, or
measuring time point. In one study, it has been demonstrated that acute SSRI treatment resulted
in a temporary increase in 5-HT levels, whereas persistent treatment raises baseline 5-HT levels
(Kreiss & Lucki, 1995). There is no indication that SSRIs create a rise in extracellular serotonin
via inhibiting serotonin breakdown or enhancing serotonin synthesis.
Serotonin (5-HT) is a vital neurotransmitter in the central nervous system as well as a
regulatory hormone that regulates a wide variety of physiological functions. Perhaps the most
classically defined roles of 5-HT are central to mood, sleep, and anxiety management, and
peripheral to gastrointestinal motility modulation. The "serotonin hypothesis" of clinical
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