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1Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada; and 2Dipartimento di Scienze Fisiologiche-Farmacologiche Cellulari-Molecolari, Sezione di Fisiologia Generale e Biofisica Cellulare, Università degli Studi di Pavia, 27100 Pavia, Italy
Submitted 12 January 2004; accepted in final form 14 May 2004
In entorhinal cortex layer II neurons, muscarinic receptor activation promotes depolarization via activation of a nonspecific cation current (INCM). Under muscarinic influence, these neurons also develop changes in excitability that result in activity-dependent induction of delayed firing and bursting activity. To identify the membrane processes underlying these phenomena, we examined whether INCM may undergo activity-dependent regulation. Our voltage-clamp experiments revealed that appropriate depolarizing protocols increased the basal level of inward current activated during muscarinic stimulation and suggested that this effect was due to INCM upregulation. In the presence of low buffering for intracellular Ca2+, this upregulation was transient, and its decay could be followed by a phase of INCM downregulation. Both up- and downregulation were elicited by depolarizing stimuli able to activate voltage-gated Ca2+ channels (VGCC); both were sensitive to increasing concentrations of intracellular Ca2+-chelating agents with downregulation being abolished at lower Ca2+-buffering capacities; both were reduced or suppressed by VGCC block or in the absence of extracellular Ca2+. These data indicate that relatively small increases in [Ca2+]i driven by firing activity can induce upregulation of a basal muscarinic depolarizing-current level, whereas more pronounced [Ca2+]i elevations can result in INCM downregulation. We propose that the interaction of activity-dependent positive and negative feedback mechanisms on INCM allows entorhinal cortex layer II neurons to exhibit emergent properties, such as delayed firing and enhanced or suppressed responses to repeated stimuli, that may be of importance in the memory functions of the temporal lobe and in the pathophysiology of epilepsy.
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