Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P46098 (5-HT3 receptor)
 2,290 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Three ipsilateral (MSR, PSR, IPSI SLOW) and two contralateral segmental reflexes (CON FAST, CON SLOW) were recorded from L4 or L5 ventral roots of the neonate rat spinal cord in vitro. MSR, PSR and CON FAST were evoked from lower threshold afferents; more intense stimulation evoked IPSI SLOW and CON SLOW. 2. Kainate/AMPA receptors were involved in mediation of MSR, PSR, CON FAST, IPSI SLOW and CON SLOW and NMDA receptors in mediation of CON FAST, IPSI SLOW and CON SLOW. 3. All five reflexes were depressed by 5-HT (IC50 1.2-7.9 microM; order of sensitivity, CON SLOW > CON FAST = IPSI SLOW > MSR = PSR); and by 5-CT (IC50 1.9-8.8 nM; order of sensitivity, MSR > IPSI SLOW = CON FAST = CON SLOW > PSR). alpha-Me-5-HT also depressed all five reflexes. 4. Dipropyl-5-CT selectively depressed MSR and CON SLOW (IC50 90-170 nM) but was less potent than 5-CT. 8-OH-DPAT selectively depressed MSR (IC50 1.1 microM), IPSI SLOW and CON SLOW (IC50 5.7-7.6 microM), while methylsergide depressed only MSR (IC50 26 nM). 5. Phenyl biguanide and m-chlorophenyl biguanide (5-HT3 receptor agonists) had no significant effects on any reflex. 6. It is concluded that a 5-HT1-like receptor mediates depression of the MSR. A different receptor or a mixed population of receptors, but not 5-HT3 receptors, mediate inhibition of PSR, CON FAST, IPSI SLOW and CON SLOW.
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PMID:FAST and SLOW ipsilateral and contralateral spinal reflexes in the neonate rat are modulated by 5-HT. 148 13

The involvement of 5-hydroxytryptaminergic (5-HTergic) system for the 3-nitropropionic acid (3-NPA)-induced depression of spinal reflexes was evaluated and compared with other energy deficiency condition (ischemia; glucose-free and O2-free). The monosynaptic (MSR) and polysynaptic reflex (PSR) potentials were recorded at ventral root by stimulating the corresponding dorsal root in neonatal rat spinal cord in vitro. Superfusion of 3-NPA (3.4 mM) or ischemic solution depressed the reflexes in a time-dependent manner abolishing them by 35 min. Pretreatment with pindolol (1 microM), ketanserin (10 microM) or ondansetron (0.1 microM); 5-HT1, 5-HT2, or 5-HT3 receptor antagonist, respectively, did not block the 3-NPA-induced depression of reflexes whereas, ischemia-induced depression was blocked by ondansetron. 5-HT content of the spinal cords incubated with 3-NPA (3.4 mM) for 30 min was decreased significantly (33 ng/g tissue) while increased (286 ng/g) in cords exposed to ischemic solution as compared to saline-treated cords (161 ng/g). Thus, 3-NPA-induced depression of spinal reflexes does not involve 5-HTergic pathway unlike ischemia-induced depression.
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PMID:3-Nitropropionic acid-induced depression of spinal reflexes does not involve 5-hydroxytryptaminergic system in contrast to ischemia-induced depression in neonatal rat spinal cord in vitro. 1881 48