Picrotoxin increased acetylcholine release from rat cultured embryonic septal neurons.
GABA is a major inhibitory neurotransmitter in the mature mammalian brain. In the early stages of brain development, it has been reported that GABA(A) receptor stimulation and the associated increase in Cl(-) conductance lead to membrane depolarization. In this study, we tested the effects of picrotoxin, a GABA(A) receptor Cl(-) channel blocker, on spontaneously released acetylcholine (ACh) from cultured rat embryonic septal cells. Picrotoxin increased spontaneously released ACh. These results indicate that blockade of GABA-activated Cl(-) channel increases neuronal excitability even in an early stage of the development.
Suzuki
Takeshi
T
Department of Pharmacology, Kyoritsu College of Pharmacy, 1-5-30 Shibakoen, Minato-ku, Tokyo 105-8512, Japan. suzuki-tk@kyoritsu-ph.ac.jp
Takagi
Ryoichi
R
Kawashima
Koichiro
K
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002478:Cells, Cultured; D018920:Coculture Techniques / Q000379:methods; D004622:Embryo, Mammalian; D005260:Female; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism*; D010852:Picrotoxin / Q000494:pharmacology*; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D020665:Septum of Brain / Q000187:drug effects* / Q000378:metabolism
D000109:Acetylcholine; D010852:Picrotoxin