Activation and modulation of neuronal K+ channels by GABA.
Although the concept of GABAB receptors was introduced only ten years ago, several actions of GABAB agonists are already well established. They cause depression of transmitter release, a decrease in voltage-dependent Ca2+ conductance and an increase in K+ conductance. It has recently been reported that GABA also changes the voltage dependence of the transient ('A' type) K+ channel. Depression of transmitter release by GABAB agonists may be caused by a decrease in Ca2+ conductance, an increase in K+ conductance or a modulation of A channels in presynaptic nerve terminals. Slow IPSPs in some neurons are generated by an increase in K+ conductance that can be blocked by GABAB antagonists and pertussis toxin. K+ channels of variable amplitude that are blocked by pertussis toxin are activated by GABAB agonists in cultured hippocampal neurons. Since arachidonic acid activates similar channels in excised patches of membrane, it may form part of a normal second messenger system linking GABAB receptors to K+ channels.
Gage
P W
PW
John Curtin School of Medical Research, Australian National University, Canberra.
D000818:Animals; D006801:Humans; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects*; D011963:Receptors, GABA-A / Q000187:drug effects / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D015221:Potassium Channels; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid