Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neuroprotective activity of riluzole has been studied on N-methyl-D-aspartate (NMDA)- or veratridine-induced toxicity in immature rat hippocampal slices. Neurodegeneration was assessed by the measurement of LDH release and histology. Veratridine-induced LDH release can be inhibited by 100 microM riluzole (-90% and by tetrodotoxin (1 microM). Riluzole markedly reduced (-59%) the NMDA-induced LDH release and this protective effect was confirmed by histology. Riluzole inhibited the NMDA-induced LDH release in the presence of tetrodotoxin. Moreover, a pretreatment with pertussis toxin (1 microgram/ml) abolished the effect of riluzole against NMDA-induced neurotoxicity. These results support the view that the neuroprotective properties of riluzole could be exerted via two distinct mechanisms of action.
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PMID:Neuroprotective effects of riluzole on N-methyl-D-aspartate- or veratridine-induced neurotoxicity in rat hippocampal slices. 782 90

Opiates are known to influence intestinal motility via modulation of cholinergic transmission. The aims of this study are to characterize the opioid receptor subtype that modulates cholinergic transmission and to investigate the intracellular mechanism responsible for inhibition of acetylcholine (ACh) release by opiates using longitudinal muscle-myenteric plexus preparations of the guinea pig ileum. The kappa-receptor agonist U50488H and the mu-receptors agonist [D-Ala2,N-Me-Phe4, Gly5-ol]enkephalin, inhibited the release of ACh evoked by electrical stimulation (0.2 and 2 Hz) in a dose-dependent fashion, whereas the delta-receptor agonist DPDPE, had no effect. ACh release evoked by depolarization with veratridine, which was more analogous to high frequency stimulation, was inhibited only by U50488H. Pertussis toxin abolished the inhibitory effect of U50488H on veratridine-induced ACh release suggesting that the principal mechanism by which opiates inhibit cholinergic transmission is via activation of an inhibitory regulatory G protein. Veratridine-stimulated release of ACh was antagonized by omega-Conotoxin GVIA (a preferential N channel blocker) but was not affected by nifedipine (an L channel blocker) or nickel (a T channel blocker). U50488H did not produce further inhibition of veratridine-evoked ACh release in the presence of omega-Conotoxin GVIA. These results suggest that both kappa- and mu-agonists can modulate cholinergic transmission, although the kappa-agonist appears to be more potent. The kappa receptors modulate ACh release by inhibition of N-type voltage-sensitive Ca++ channels via a pertussis toxin-sensitive G protein in guinea pig ileum.
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PMID:Inhibition of cholinergic transmission by opiates in ileal myenteric plexus is mediated by kappa receptor. Involvement of regulatory inhibitory G protein and calcium N-channels. 811 12