Possible involvement of low and high affinity GABA receptors in the chloride influx into synaptosomes.
Experiments carried out in the absence or presence of GABA using a synaptosomal fraction from which endogenous GABA was as far as possibly eliminated, seem to indicate that both GABA receptors are involved in the chloride channel opening. This hypothesis is supported by results obtained in the presence of GABA agonist (muscimol) or drugs which are related to the complex GABA receptor-ionophore (diazepam and phenobarbital).
D000612:4-Aminobutyrate Transaminase / Q000378:metabolism; D000445:Aldehyde Oxidoreductases / Q000378:metabolism; D000818:Animals; D002712:Chlorides / Q000378:metabolism*; D003975:Diazepam / Q000494:pharmacology; D007473:Ion Channels / Q000378:metabolism*; D009118:Muscimol / Q000494:pharmacology; D010634:Phenobarbital / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011963:Receptors, GABA-A / Q000145:classification / Q000187:drug effects / Q000378:metabolism*; D013574:Synaptosomes / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D002712:Chlorides; D007473:Ion Channels; D011963:Receptors, GABA-A; C046738:gabase; D009118:Muscimol; D005680:gamma-Aminobutyric Acid; D000445:Aldehyde Oxidoreductases; D000612:4-Aminobutyrate Transaminase; D003975:Diazepam; D010634:Phenobarbital