Mechanisms and consequences of action potential burst firing in rat neocortical pyramidal neurons.

摘要: 1. Electrophysiological recordings and pharmacological manipulations were used to investigate the mechanisms underlying generation of action potential burst firing its postsynaptic consequences in visually identified rat layer 5 pyramidal neurons vitro. 2. Based upon repetitive properties subthreshold membrane characteristics, separated into three classes: regular weak strong intrinsically firing. 3. High frequency (330 +/- 10 Hz) was abolished or greatly weakened by removal Ca2+ (n = 5) from, addition channel antagonist Ni2+ (250-500 microm; n 8) to, perfusion medium. 4. The blockade apical dendritic sodium channels local application TTX (100 nM; firing, as did (1 mM; 5). 5. Apical depolarisation resulted low (157 26 Hz; 6) neurons, classified somatic current injection. intensity discharges facilitated 11). 6. Action amplitude decreased throughout a when recorded somatically, suggesting that later potentials may fail propagate axonally. Axonal demonstrated each is axonally initiated no decrement apparent axon > 30 microm from soma. 7. Paired 16) synaptically coupled indicated could cause transmitter release. EPSPs EPSCs evoked presynaptic showed use-dependent synaptic depression. 8. A postsynaptic, TTX-sensitive voltage-dependent amplification process ensured amplified generated positive -60 mV, providing mechanism counteracts depression at synapses between neurons.