Regulation of Nuscarinic Acetylcholine Receptor Number in Cultured Neuronal Cells by Chronic Membrane Depolarization

摘要

Electrical activity has been shown to play an important role in the regulation of functional properties of neurons and other electrically excitable cells. One mechanism by which neuronal function is regulated is via alterations in the number of neurotransmitter receptors on the neuronal cell surface. Electrical activity has been reported on th neuronal cell surface. Electrical activity has been reported to modulate muscarinic acetylcholine (mAChR) levels in vivo and in vitro. Both increases and decreases in CNS mAChR number have been observed following kindling, an animal model of epilepsy and neuronal plasticity in which the repeated administration of an initally subconvulsive electrical stimulus to the brain induces progressive intensification of stimulus-induced seizure activity. Data demonstrate that chronic membrane depolarization of cultured neuroblastoma cells increases mAChR number by inhibiting mAChR degradation. Our results suggest that inactivation of voltage-sensitive Ca2+ channels may account for the alteration in regulation of mAChR number induced by chronic membrane depolarization of neuroblastoma cells.