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.