Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1519176 (PSA)
 5,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of 5-HT3-receptor-related agents on long-term potentiation (LTP) in the mossy fiber-CA3 system were studied in guinea pig hippocampal slices. 5-HT3 receptor agonists, 1-(m-chlorophenyl)-biguanide (mCPBG) and 2-methyl serotonin (2-Me-5-HT) significantly attenuated the magnitude of LTP of the population spike at 0.3-1 microM and at 10 microM respectively. At these doses neither of these drugs did affect the amplitude of the population spike (PSA) evoked by test stimuli in the absence of tetanic stimulation. The attenuating effect of mCPBG on LTP was reversed by the GABAA receptor antagonist bicuculline. On the other hand, 5-HT3 receptor antagonists ondansetron and granisetron significantly augmented the magnitude of LTP at 1-3 microM and at 0.1-0.3 microM, respectively, without changes in PSA before tetanus. The augmenting effect of granisetron on LTP was partially but significantly reversed by the muscarinic receptor antagonist atropine. These findings suggest that the induction of the LTP in the mossy fiber-CA3 system is inhibited by an activation of 5-HT3 receptors through the facilitation of GABAergic neurons (GABAA receptors) and the inhibition of cholinergic neurons (muscarinic receptors).
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PMID:Inhibitory influence via 5-HT3 receptors on the induction of LTP in mossy fiber-CA3 system of guinea-pig hippocampal slices. 819 Mar 70

Recent hypotheses suggest that changes in neuronal structure and connectivity may underlie the etiology of depression. The medial prefrontal cortex (mPFC) is affected by depression and shows neuronal remodeling during adulthood. This plasticity may be mediated by the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), which is intensely expressed in the adult mPFC. As the expression of PSA-NCAM is increased by serotonin in other cerebral regions, antidepressants acting on serotonin reuptake may influence PSA-NCAM expression and thus counteract the effects of depression by modulating neuronal structural plasticity. Using immunohistochemistry, we have studied the relationship between serotoninergic fibers and PSA-NCAM expressing neurons in the adult rat mPFC and the expression of serotonin receptors in these cells. The effects of fluoxetine treatment for 14 days on mPFC PSA-NCAM expression have also been analyzed. Although serotoninergic fibers usually do not contact PSA-NCAM immunoreactive neurons, most of these cells express 5-HT3 receptors. In general, chronic fluoxetine treatment induces significant increases in the number of PSA-NCAM immunoreactive neurons and in neuropil immunostaining and coadministration of the 5-HT3 antagonist ondansetron blocks the effects of fluoxetine on PSA-NCAM expression. These results indicate that fluoxetine, acting through 5-HT3 receptors, can modulate PSA-NCAM expression in the mPFC. This modulation may mediate the structural plasticity of this cortical region and opens new perspectives on the study of the molecular bases of depression.
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PMID:Chronic fluoxetine treatment increases the expression of PSA-NCAM in the medial prefrontal cortex. 1690 Jan 4