Capacitative calcium entry supports calcium oscillations in human embryonic kidney cells
Open Access
- 20 January 2005
- journal article
- research article
- Published by Wiley in The Journal of Physiology
- Vol. 562 (3) , 697-706
- https://doi.org/10.1113/jphysiol.2004.077289
Abstract
The slow oscillation (SO) generated within the corticothalamic system is composed of active and silent states. The studies of response variability during active versus silent network states within thalamocortical system of human and animals provided inconsistent results. To investigate this inconsistency, we used electrophysiological recordings from the main structures of the somatosensory system in anaesthetized cats. Stimulation of the median nerve (MN) elicited cortical responses during all phases of SO. Cortical responses to stimulation of the medial lemniscus (ML) were virtually absent during silent periods. At the ventral-posterior lateral (VPL) level, ML stimuli elicited either EPSPs in isolation or EPSPs crowned by spikes, as a function of membrane potential. Response to MN stimuli elicited compound synaptic responses and spiked at any physiological level of membrane potential. The responses of dorsal column nuclei neurones to MN stimuli were of similar latency, but the latencies of antidromic responses to ML stimuli were variable. Thus, the variable conductance velocity of ascending prethalamic axons was the most likely cause of the barrages of synaptic events in VPL neurones mediating their firing at different level of the membrane potential. We conclude that the preserved ability of the somatosensory system to transmit the peripheral stimuli to the cerebral cortex during all the phases of sleep slow oscillation is based on the functional properties of the medial lemniscus and on the intrinsic properties of the thalamocortical cells. However the reduced firing ability of the cortical neurones during the silent state may contribute to impair sensory processing during sleep.Keywords
This publication has 33 references indexed in Scilit:
- Calcium entry and the control of calcium oscillationsBiochemical Society Transactions, 2003
- Signaling Mechanism for Receptor-activated Canonical Transient Receptor Potential 3 (TRPC3) ChannelsJournal of Biological Chemistry, 2003
- Comparison of Human TRPC3 Channels in Receptor-activated and Store-operated ModesJournal of Biological Chemistry, 2002
- Signaling Pathways Underlying Muscarinic Receptor-induced [Ca2+] Oscillations in HEK293 CellsJournal of Biological Chemistry, 2001
- Effects of elevated cytoplasmic calcium and protein kinase C on endoplasmic reticulum structure and function in HEK293 cellsCell Calcium, 2000
- What drives calcium entry during [Ca2+]ioscillations? – challenging the capacitative modelCell Calcium, 1999
- The Store-Operated Calcium Current ICRAC: Nonlinear Activation by InsP3 and Dissociation from Calcium ReleaseCell, 1997
- Differential Effects of Protein Kinase C Activation on Calcium Storage and Capacitative Calcium Entry in NIH 3T3 CellsJournal of Biological Chemistry, 1996
- Agonist-induced oscillations in cytoplasmic free calcium concentration in single rat hepatocytesCell Calcium, 1987
- A model for receptor-regulated calcium entryCell Calcium, 1986