Ammonia potentiates GABAA response in dissociated rat cortical neurons.
The ammonium ion (NH4+) evoked no response itself but facilitated the GABA-induced Cl- current (ICl) in dissociated rat cortical neurons. The GABA concentration-response curve shifted parallely to the left without changing the maximum response. Reversal potential of GABA response did not change in the presence of NH4+ at the concentration range between 0.1 and 1 mM. Ro 15-1788, a selective benzodiazepine receptor antagonist, did not affect the facilitatory action of NH4+ on GABAA receptor. The results suggest that NH4+ modifies the affinity of GABAA receptor for GABA, without the involvement of benzodiazepine receptors.
Takahashi
K
K
Research Laboratory Roussel Morishita Co., Ltd., Shiga, Japan.
Kameda
H
H
Kataoka
M
M
Sanjou
K
K
Harata
N
N
Akaike
N
N
D000641:Ammonia / Q000494:pharmacology*; D000818:Animals; D001463:Barbiturates / Q000494:pharmacology; D002540:Cerebral Cortex / Q000166:cytology* / Q000187:drug effects; D018118:Chloride Channels; D004357:Drug Synergism; D005442:Flumazenil / Q000494:pharmacology; D066298:In Vitro Techniques; D008565:Membrane Proteins / Q000187:drug effects; D009474:Neurons / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D001463:Barbiturates; D018118:Chloride Channels; D008565:Membrane Proteins; D011963:Receptors, GABA-A; D005442:Flumazenil; D005680:gamma-Aminobutyric Acid; D000641:Ammonia