Use-dependent facilitation of L-like Ca2+ channels counteracts GABAB-mediated inhibition of N-like Ca2+ channels in rat sensory neurons.
Baclofen selectively blocked the inactivating N-like component of the high voltage-activated Ca2+ current (HVA-ICa) without affecting the sustained L-like component of the HVA-ICa in rat sensory neurons. The inhibition of the N-like component by baclofen was reversed by a large depolarizing prepulse to +50 mV as a result of facilitation of the L-like component. These results might indicate that a decrease in influx of Ca2+ through N-like Ca2+ channels due to the baclofen-induced block or due to the voltage-dependent inactivation induced by the depolarizing prepulse can be partially compensated by a rapid Ca2+ influx through extra L-like component facilitated by the depolarizing prepulse. Such a compensation of the Ca2+ influx by the use-dependent facilitation of L-like component may be a significant mechanism for adaptive regulation of Ca2+ channels in response to stimulation with a wide range of amplitude and frequency.
Tatebayashi
H
H
Department of Pharmacology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Ogata
N
N
D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000502:physiology*; D015640:Ion Channel Gating / Q000187:drug effects; D009475:Neurons, Afferent / Q000502:physiology*; D051381:Rats; D011963:Receptors, GABA-A / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology
D015220:Calcium Channels; D011963:Receptors, GABA-A; D013779:Tetrodotoxin; D001418:Baclofen; D002118:Calcium