The mechanism of GABAB-mediated slowing of the activation phase of high voltage-activated Ca2+ channels in rat sensory neurons.
The mechanism underlying the slowed activation of the high voltage-activated Ca2+ current (HVA-ICa) in the presence of (-)-baclofen was studied in cultured neurons of rat dorsal root ganglia. The decay phase of the baclofen-sensitive component of HVA-ICa was described by a sum of two exponential functions. Although the inhibited portion in the amplitude of the baclofen-sensitive component of HVA-ICa was increased in a concentration-dependent manner, the two decay time constants remained unaffected regardless of the concentration of baclofen. Furthermore, the baclofen-sensitive component of HVA-ICa was largely inactivated by a depolarizing prepulse (-30 mV for 0.5 s). These results support the notion that the slowed activation of the HVA-ICa in the presence of baclofen is due to a preferential inhibition of the inactivating component of HVA-ICa rather than due to voltage-dependent unblocking of a single population of HVA-ICa.
Tatebayashi
H
H
Department of Pharmacology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Ogata
N
N
D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D004594:Electrophysiology; D005727:Ganglia, Spinal / Q000187:drug effects / Q000378:metabolism; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011963:Receptors, GABA-A / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D015220:Calcium Channels; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D001418:Baclofen