Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subcutaneous administration of caerulein (100-500 micrograms/kg) significantly reduced the development of picrotoxin (8 mg/kg) seizures in male mice. The same doses of caerulein inhibited 3H-flunitrazepam binding in in vivo experiments. Proglumide, an antagonist of cholecystokinin receptors, in low dose (5 mg/kg) potentiated the effects of caerulein (100 micrograms/kg), whereas the administration of proglumide in high dose (25 mg/kg) reduced the action of caerulein on 3H-flunitrazepam binding and picrotoxin seizures. Caerulein (5-1000 nM) decreased 3H-flunitrazepam binding in in vitro experiments only after supplementation of the binding medium with 120 mM NaCl and 5mM KCl. The results suggest the possible interaction of caerulein with chloride ionophor. It seems probable that the direct interaction of caerulein with chloride ionophor in involved in the inhibitory effect of caerulein on picrotoxin seizures and 3H-flunitrazepam binding.
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PMID:[Modulating effect of cerulein on benzodiazepine receptors]. 300 Apr 72

Recent evidence suggest that endogenous cholecystokinin (CCK) has important roles in central responses to stress. CCK receptors are known as functional modulators of opioidergic system with a tonic antiopioid effect in nociceptive pathways. In contrast, CCK receptor ligands are known to induce anticonvulsant effects similar to endogenous opioids. It is not clear whether endogenous CCK may play a role in the anticonvulsant effects of stress, especially in those stressful paradigms that are associated with strong activation of opioid pathways. The present study examined the role of endogenous CCK receptors in acute stress-induced modulation of seizure (clonic seizures induced by pentylenetetrazole) and nociception (tail-flick) thresholds. Acute restraint stress (for 2 h) and prolonged intermittent footshock stress (30 min) both induced opioid-dependent anticonvulsant and antinociceptive effects. While CCK receptor antagonist proglumide (10, 20, or 40 mg/kg) had no effect on seizure or nociception threshold by itself, it inhibited the anticonvulsant effects of both these types of stress while potentiating their antinociceptive effects. Moreover, proglumide exerted a similar inhibition of the anticonvulsant effect and potentiation of the antinociceptive effect of acute morphine at 1 mg/kg. In contrast, brief and continuous footshock stress (3 min) that induced a nonopioid type of antinociception did not increase the seizure threshold. Proglumide pretreatment did not alter any of these effects of brief footshock stress paradigm. The present data suggest that CCK receptors specifically and differentially modulate the opioid-mediated anticonvulsant and antinociceptive effects of acute stress.
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PMID:Differential contribution of cholecystokinin receptors to stress-induced modulation of seizure and nociception thresholds in mice. 1521 60