Regulation of the rebound depolarization and spontaneous firing patterns of deep nuclear neurons in slices of rat cerebellum

Current-clamp recordings were made from the deep cerebellar nuclei (DCN) of 12- to 15-day-old rats to understand the factors that mediate intrinsic sp ontaneous firing patterns. All of the cells recorded were spontaneously act ive with spiking patterns ranging continuously from regular spiking to spon taneous bursting with the former predominating. A robust rebound depolariza tion (RD) leading to a Na+ spike burst was elicited after the offset of hyp erpolarizing current injection. The voltage and time dependence of the RD w as consistent with mediation by low-threshold voltage-gated Ca2+ channels. Tn addition, induction of a RD also may be affected by activation of a hype rpolarization-activated cation current, I-h. A RD could be evoked efficient ly after brief high-frequency bursts of inhibitory postsynaptic potentials (IPSPs) induced by stimulation of Purkinje cell axons. IPSP-driven RDs were typically much larger and longer than those elicited by direct hyperpolari zing pulses of approximately matched amplitude and duration. Intracellular perfusion of the Ca2+ buffer bis-(o-aminophenoxy)-N,N,N',N'-terraacetic aci d (BAPTA) dramatically enhanced the RD and its associated spiking, sometime s leading to a plateau potential that lasted several hundred milliseconds. The effects of BAPTA could be mimicked partly by application of apamin. a b locker of small conductance Ca2+-gated K+ channels, but not by paxilline, w hich blocks large conductance Ca2+-gated K+ channels. Application of both B APTA and apamin, but not paxilline, caused cells that were regularly spikin g to burst spontaneously. Taken together, our data suggest that there is a strong relationship between the ability of DCN cells to elicit a RD and the ir tendency burst spontaneously. The RD can be triggered by the opening of T-type Ca2+ channels with an additional contribution of hyperpolarization-a ctivated current I-h. RD duration is regulated by small-conductance Ca2+-ga ted K+ channels. The RD also is modulated tonically by inhibitory inputs. A ll of these factors are in turn subject to alteration by extrinsic modulato ry neurotransmitters and are, at least in part, responsible for determining the firing modes of DCN neurons.