The Journal of Neurophysiology Vol. 86 No. 2 August 2001, pp. 771-781
Copyright ©2001 by the American Physiological Society

Ionic Mechanisms Underlying Burst Firing of Layer III Sensorimotor Cortical Neurons of the Cat: An In Vitro Slice Study

Department of Physiology, Faculty of Medicine, Mie University, Mie 514-8507, Japan

Nishimura, Yoshihiro, Masaru Asahi, Koichi Saitoh, Hirofumi Kitagawa, Yuichi Kumazawa, Kunio Itoh, Min Lin, Takanobu Akamine, Hiroshi Shibuya, Toshihiro Asahara, and Tetsuro Yamamoto. Ionic Mechanisms Underlying Burst Firing of Layer III Sensorimotor Cortical Neurons of the Cat: An In Vitro Slice Study. J. Neurophysiol. 86: 771-781, 2001. We examined the ionic mechanisms underlying burst firing in layer III neurons from cat sensorimotor cortex by intracellular recording in a brain slice. Regular spiking was observed in 77.4% of 137 neurons in response to constant intracellular current pulses of 0.5- to 1-s duration. The rest of the neurons showed burst firing. An initial burst followed by regular-spike firing was seen in 71.0% of 31 bursting neurons. The rest of the bursting neurons (n = 9) exhibited repetitive bursting. In the bursting neurons, spikes comprising the burst were triggered from the afterdepolarization (ADP) of the first spike of the burst. We examined the ionic mechanisms underlying the ADP by applying channel-blocking agents. The ADP was enhanced (rather than blocked) by Ca²⁺ channel blockade. This enhancement of the ADP by Ca²⁺ channel blockade was apparent even after blockade of the afterhyperpolarization by apamin or intracellular Ca²⁺ chelation by EGTA. The firing rate of the regular-spiking cells was increased by apamin, intracellular EGTA or Ca²⁺ channel blockers. In 17.9% of the neurons examined (n = 56), these agents switched the regular-spiking pattern into a bursting one. Burst firing could not be changed to regular spiking by these agents. Four neurons that responded with a single initial burst in control solution responded with repetitive bursting after application of these agents. We conclude that the main function of Ca²⁺ influx in layer III neurons is to activate Ca²⁺-dependent K⁺ conductance, which prevents or limits burst firing. At a time when spike amplitude was unchanged, the ADP was blocked and the burst firing changed to regular spiking by extracellularly applied tetrodotoxin (TTX) or intracellularly applied N-(2,6-dimethylphenylcarbamoylmethyl) triethyl ammonium bromide (QX314). We concluded that a TTX- and QX314-sensitive Na⁺ current underlies the ADP and therefore contributes to the burst firing of layer III neurons from the cat cortex.