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Adenosine inhibits epileptiform activity arising in hippocampal area CA3
Author(s) -
Ault Brian,
Wang Ching M.
Publication year - 1986
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1986.tb14587.x
Subject(s) - adenosine , bicuculline , bursting , adenosine deaminase , chemistry , theophylline , hippocampal formation , adenosinergic , pharmacology , anticonvulsant , medicine , adenosine receptor , endocrinology , neuroscience , antagonist , biology , biochemistry , epilepsy , agonist , receptor
1 The ability of adenosine and structurally‐related compounds to inhibit epileptiform activity induced by bicuculline in the CA3 region of the hippocampal slice of the rat was examined. 2 Bath application of all purinoceptor agonists tested reduced the frequency of generation of burst potentials. Analysis of dose‐response curves yielded the following IC 50 values: adenosine, 1.5 μ m ; 2‐chloroadenosine, 0.144 μ m ; 5′‐(N‐ethyl)carboxamidoadenosine, 30.2 n m ; L‐phenylisopropyladenosine, 12.1 n m ; cyclohexyladenosine, 7.9 n m . 3 Theophylline (30 μ m ) increased the rate of bursting and antagonized the effect of exogenous adenosine. 4 Dipyridamole (0.03–1 μ m ) reduced the occurrence of burst firing. 5 In slices untreated with bicuculline, theophylline (30 μ m ) and adenosine deaminase (10 μg ml −1 ) induced bursting activity. 6 These results demonstrate that purinoceptor agonists can suppress epileptiform activity in the hippocampus and suggest that adenosine may act as an endogenous anticonvulsant.