USE-DEPENDENT FACILITATION OF L-LIKE CA2-B-MEDIATED INHIBITION OF N-LIKE CA2+ CHANNELS IN RAT SENSORY NEURONS( CHANNELS COUNTERACTS GABA)

Baclofen selectively blocked the inactivating N-like component of the high voltage-activated Ca2+ current (HVA-I(Ca)) without affecting the sustained L-like component of the HVA-I(Ca) in rat sensory neurons. Th e inhibition of the N-like component by baclofen was reversed by a lar ge depolarizing prepulse to +50 mV as a result of facilitation of the L-like component. These results might indicate that a decrease in infl ux of Ca2+ through N-like Ca2+ channels due to the baclofen-induced bl ock or due to the voltage-dependent inactivation induced by the depola rizing prepulse can be partially compensated by a rapid Ca2+ influx th rough extra L-like component facilitated by the depolarizing prepulse. Such a compensation of the Ca2+ influx by the use-dependent facilitat ion of L-like component may be a significant mechanism for adaptive re gulation of Ca2+ channels in response to stimulation with a wide range of amplitude and frequency.