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715447 [2018/11/20 14:26] (current)
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 +====== Benzodiazepine/​gamma-aminobutyric acid receptor deficit in the midbrain of the seizure-susceptible gerbil.======
 +
 +** Article date:** 1985/10/1
 +~~META:date created = 1985-10-01~~
 +
 +** PubMed ID: 715447 **
 +
 +** Journal name: Proceedings of the National Academy of Sciences of the United States of America (ISSN: 0027-8424) **
 +
 +** ABSTRACT **
 +
 +The density of benzodiazepine/​gamma-aminobutyric acid receptor binding sites was lower in the midbrain of seizure-susceptible gerbils compared to control seizure-resistant gerbils. Binding of [3H]diazepam to high-affinity brain-specific sites in membrane homogenates of gerbil brain showed a 20-30% lower binding in midbrain (but not other regions) in adult seizure-susceptible gerbils than in controls. This binding deficit was localized by tissue slice autoradiography with [3H]flunitrazepam to the substantia nigra and mesencephalic periaqueductal gray regions, while higher binding was observed in the interpeduncular nucleus. These differences were also seen in animals sacrificed immediately after a seizure. A parallel deficit of [3H]bicuculline methochloride binding to low-affinity gamma-aminobutyric acid receptors also was seen in the same midbrain regions. Scatchard plot analysis showed that the benzodiazepine binding deficit in the nigra was due to a lower number of binding sites with not significant difference in affinity. Lower [3H]flunitrazepam binding was likewise seen in younger animals (29% lower at 30 days of age, 38% at 60 days, and 21% at 90 days), indicating that the midbrain receptor deficit is present in the seizure-susceptible gerbil prior to the age of onset of seizures at 50-100 days. Therefore, these changes are not likely to result from seizures but reflect genetically determined biochemical differences that could play a role in the expression of seizure susceptibility. The deficit in midbrain benzodiazepine/​gamma-aminobutyric acid receptors in the seizure-susceptible gerbil would be consistent with the hypothesis that a deficit of gamma-aminobutyric acid-mediated inhibition might contribute to some kinds of epilepsy.
 +
 +===== ===== 
 +
 +Author List: Olsen R W, Wamsley J K, McCabe R T, Lee R J, Lomax P
 +
 +Publication Types: Journal Article; Research Support, U.S. Gov't, P.H.S.
 +
 +Substances mentioned in the article: Receptors, GABA-A; Muscimol; Flunitrazepam;​ bicuculline methochloride;​ Pentobarbital;​ Diazepam; Bicuculline; ​
 +
 +Mesh terms: Animals; Bicuculline/​analogs & derivatives;​ Diazepam/​metabolism;​ Disease Models, Animal/​genetics;​ Flunitrazepam/​metabolism;​ Gerbillinae/​metabolism;​ Mesencephalon/​analysis;​ Muscimol/​metabolism;​ Pentobarbital/​pharmacology;​ Receptors, GABA-A/​deficiency;​ Seizures/​genetics; ​
 +
 +Citations: ​  - //​[[4523020]]//​
 +  - //​[[6099474]]//​
 +  - //​[[109922]]//​
 +  - //​[[501361]]//​
 +  - //​[[6930682]]//​
 +  - //​[[6261261]]//​
 +  - //​[[7256289]]//​
 +  - //​[[6267249]]//​
 +  - //​[[6269695]]//​
 +  - //​[[6272394]]//​
 +  - //​[[7308174]]//​
 +  - //​[[6275045]]//​
 +  - //​[[6282187]]//​
 +  - //​[[6284878]]//​
 +  - //​[[6815309]]//​
 +  - //​[[6292381]]//​
 +  - //​[[7146907]]//​
 +  - //​[[6308374]]//​
 +  - //​[[6411901]]//​
 +  - //​[[6315877]]//​
 +  - //​[[6329784]]//​
 +  - //​[[6090223]]//​
 +  - //​[[6481454]]//​
 +  - //​[[715447]]//​
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 +{{tag> Flunitrazepam bicuculline_methochloride Pentobarbital Bicuculline Receptors,​_GABA-A Diazepam Muscimol }}
 +
 +{{keywords>​ Flunitrazepam,​ bicuculline methochloride,​ Pentobarbital,​ Bicuculline,​ Receptors, GABA-A, Diazepam, Muscimol}}
 +
  
715447.txt ยท Last modified: 2018/11/20 14:26 (external edit)