J Neurophysiol (April 1, 2003). 10.1152/jn.00695.2002
Submitted on Submitted 19 August 2002; accepted in final form 6 December 2002

Na⁺-Activated K⁺ Current Contributes to Postexcitatory Hyperpolarization in Neocortical Intrinsically Bursting Neurons

 ¹National Neurological Institute "C. Besta", 20133 Milan; and  ²Department of Physiological and Pharmacological Sciences, University of Pavia, 27100 Pavia, Italy

Franceschetti, Silvana, Tatiana Lavazza, Giulia Curia, Patrizia Aracri, Ferruccio Panzica, Giulio Sancini, Giuliano Avanzini, and Jacopo Magistretti. Na⁺-Activated K⁺ Current Contributes to Postexcitatory Hyperpolarization in Neocortical Intrinsically Bursting Neurons. J. Neurophysiol. 89: 2101-2111, 2003. The ionic mechanisms underlying the termination of action-potential (AP) bursts and postburst afterhyperpolarization (AHP) in intrinsically bursting (IB) neocortical neurons were investigated by performing intracellular recordings in thin slices of rat sensorimotor cortex. The blockade of Ca²⁺-activated K⁺ currents enhanced postburst depolarizing afterpotentials, but had inconsistent and minor effects on the amplitude and duration of AHPs. On the contrary, experimental conditions resulting in reduction of voltage-dependent Na⁺ entry into the cells caused a significant decrease of AHP amplitude. Slice perfusion with a modified artificial cerebrospinal fluid in which LiCl (40 mM) partially replaced NaCl had negligible effects on the properties of individual APs, whereas it consistently increased burst length and led to an approximately 30% reduction in the amplitude of AHPs following individual bursts or short trains of stimulus-induced APs. Experiments performed by partially replacing Na⁺ ions with choline revealed a comparable reduction in AHP amplitude associated with an inhibition of bursting activity. Moreover, in voltage-clamp experiments carried out in both in situ and acutely isolated neurons, partial substitution of extracellular NaCl with LiCl significantly and reversibly reduced the amplitude of K⁺ currents evoked by depolarizing stimuli above-threshold for Na⁺-current activation. The above effect of Na⁺-to-Li⁺ substitution was not seen when voltage-gated Na⁺ currents were blocked with TTX, indicating the presence of a specific K⁺-current component activated by voltage-dependent Na⁺ (but not Li⁺) influx. The above findings suggest that a Na⁺-activated K⁺ current recruited by the Na⁺ entry secondary to burst discharge significantly contributes to AHP generation and the maintenance of rhythmic burst recurrence during sustained depolarizations in neocortical IB neurons.