An increase in cerebral benzodiazepine receptors induced by a subacute administration of ammonia, mercaptans and short-chain fatty acids in rats.
1. In the search to identify peripheral toxins which could be responsible for the supersensitivity of brain benzodiazepine receptors in experimental models of hepatic encephalopathy, [3H]diazepam-binding studies have been performed on brain tissues of normal rats treated with ammonium chloride, dimethyldisulphide and octanoic acid administered alone or in combination. 2. The subacute administration of the three toxins in combination induced a 30% increase in the number of benzodiazepine recognition sites. The administration of these toxins alone or in combination showed that this increase was mainly linked to the synergistic action of dimethyldisulphide or octanoic acid with ammonia, since dimethyldisulphide plus octanoic acid was ineffective. 3. These observations seem to reinforce the suggestion that these three toxins are able to induce neurochemical derangements similar to those described in experimental hepatic encephalopathy.
Baraldi
M
M
Department of Pharmaceutical Sciences, Modena University, Italy.
Zeneroli
M L
ML
Ventura
E
E
Vezzelli
C
C
D000643:Ammonium Chloride / Q000494:pharmacology*; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002210:Caprylates / Q000494:pharmacology*; D004220:Disulfides / Q000494:pharmacology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011963:Receptors, GABA-A / Q000187:drug effects* / Q000378:metabolism
D002210:Caprylates; D004220:Disulfides; D011963:Receptors, GABA-A; D000643:Ammonium Chloride; C021181:dimethyl disulfide; C031492:octanoic acid