Part Of The Neurons Affected By Ssri Inhibitor/Prozac

2000 words - 8 pages

Part of the Neurons affected by SSRI Inhibitor/Prozac

Pharmacological Effects

SSRI selectively blocked the reuptake of 5HT through their
inhibiting effects on the Na+/K+ adenosine triphosphatase
(ATPase) dependant carrier in presynaptic neurons.
A standard TCA such as amitriptyline, which has about an
equal tendency to block neuronal reuptake of 5HT and
norepinephrine, Fluoxetine in 200 times more selective in
blocking the reuptake of 5HT than of norepinephrine. Florentine
is approximately 4 times as potent as 5-HT reuptake inhibitor in
vito as is amitriptyline and paroxetine is approximately 80
times as potent an inhibitor as amitriplyline.

Of the five available SSRI's, paroxetine and citalopram
appear to be the most potent 5HT uptake blockers. The reuptake
blocking properties of the SSRI's enhance general serotonergic
tone in at least two distinct steps. Initially the SSRI's
contribute to a significant increase in the availability of 5HT
in the synaptic cleft.

Serotonin (5HT) interacts with multiple brain receptors.
Three receptors subtype to influences a wide range of behaviors.
There main families of 5HT receptors (5HT, 5HT2, 5HT3) have been
described which differ in their binding affinity for selective
ligands their receptor effectors coupling mechanism and the
behavioral processes they regulate. Manipulation of several
different %HT receptor subtypes (5HT1A, 5HTIC, 5HT2 and may
produce anxiolytic effects; 5HTIA and 5HT2 receptors maybe
involved in the etiology of major depression and the therapeutic
effects of antidepressants treatment. 5HT3 receptors have been
linked to reward mechanisms and cognitive processes. These
advances offer therapeutic possibilities, the value of which can
only be satisfactorily assessed by controlled clinical trails.
SSRI class antidepressant drugs are believed to have a
similar mechanism of action, we wanted to explore whether the
prototype SSRI drug Fluoxetine, share the effects of catalpa on
subcortical dopamine neurotransmission. Eight healthy male
volunteers were studied design. Striatal and thalamic D2-
receptor binding with measured at baseline,
after a single oral dose (20mg ld). The D2 receptor binding
potential (BP) was assessed using [1 raclopide and 3D position
emission topography. Repeated dosing of Fluoxetine decreased BP
in the right medial thalamus (p=0.022). Fluoxetine did not
decrease Striatal BP, but there was a trend (P=0.090) towards
increased BP in the left putamen after repeated dosing. A single
dose of Fluoxetine did not affect BP, in the thalamus or
striatum. Fluoxetine appears to have a regionally selective
effect on the dopaminergic neurotransmission in various areas of
the brain. The current results after Fluoxetine together with
our previous data on citalopram suggest that the modulatory
effects of these drugs on Striatal dopaminergic
neurotransmission are different upon repeated dosing...

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