Part of the Neurons affected by SSRI Inhibitor/Prozac
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
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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 and further substantiates pharmacological differences between SSRI class drugs. Dopaminergic and glutamatergic neurotransmissions in the stratum play an essential role in motor-reward related behavior.
Dysfunction of these neurotransmitter systems has been found in
Parkinson's disease, schizophrenia disease, and drug addiction.