Interactive report High-threshold calcium channel activity in rat hippocampal neurones during hypoxia 1

AbstractWhole-cell patch clamp recordings in combination with direct control and measurements of O tension.pO in bath solution were 22 used to determine the sensitivity of Ca 2q channels of cultured hippocampal neurones to hypoxia in glucose free solution. In all testedneurones, a lowering of pOto4 2 %50 mmHg did not induce changes either in magnitude, kinetics or voltage-current relations of totalCa currents, which composed mainly from two types, L-type 64% and N-type 31% components. Hypoxia only induced a delay of2 q . .Ca 2q current run-down about 27.5% and 39% at 50 and 4 mmHg pO respectively that presumably depended on changes in cytoplasmic 2 channel-modulatory metabolites. The obtained results demonstrate that Ca 2q channel molecules in cultured hippocampal neurones arethemselves insensitive to short-lasting 10–20 min oxygen and glucose deprivation, and that they are not a principal target for hypoxic.influences on hippocampal function. q1999 Elsevier Science B.V. All rights reserved.

[1]  D. Richter,et al.  L‐type Ca2+ channels in inspiratory neurones of mice and their modulation by hypoxia , 1998, The Journal of physiology.

[2]  E. Lukyanetz,et al.  Calcineurin involvement in the regulation of high‐threshold Ca2+ channels in NG108–15 (rodent neuroblastoma × glioma hybrid) cells , 1998, The Journal of physiology.

[3]  E. Lukyanetz Diversity and properties of calcium channel types in NG108-15 hybrid cells , 1998, Neuroscience.

[4]  J. López-Barneo,et al.  Oxygen regulation of ion channels and gene expression , 1998 .

[5]  N. Prabhakar,et al.  Ca2+ current in rabbit carotid body glomus cells is conducted by multiple types of high-voltage-activated Ca2+ channels. , 1997, Journal of neurophysiology.

[6]  S. Waxman,et al.  Downregulation of Tetrodotoxin-Resistant Sodium Currents and Upregulation of a Rapidly Repriming Tetrodotoxin-Sensitive Sodium Current in Small Spinal Sensory Neurons after Nerve Injury , 1997, The Journal of Neuroscience.

[7]  A. Buchan,et al.  Identification of calcium channels involved in neuronal injury in rat hippocampal slices subjected to oxygen and glucose deprivation , 1997, Brain Research.

[8]  E. Lukyanetz Evidence for Colocalization of Calcineurin and Calcium Channels in Dorsal Root Ganglion Neurons , 1997, Neuroscience.

[9]  A. Schousboe,et al.  Characterization of a chemical anoxia model in cerebellar granule neurons using sodium azide: Protection by nifedipine and MK‐801 , 1996, Journal of neuroscience research.

[10]  D. Linden,et al.  Reduced nicotinamide adenine dinucleotide-selective stimulation of inositol 1,4,5-trisphosphate receptors mediates hypoxic mobilization of calcium , 1996, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[11]  R. S. Payne,et al.  Synergism between diltiazem and MK-801 but not APV in protecting hippocampal slices against hypoxic damage , 1995, Brain Research.

[12]  G. Erdemli,et al.  Nitric oxide may be a mediator of effects of prolonged but not brief anoxia in CA1 neurons in slices , 1995, Neuropharmacology.

[13]  D. Reis,et al.  Hypoxia‐activated Ca2+ currents in pacemaker neurones of rat rostral ventrolateral medulla in vitro. , 1994, The Journal of physiology.

[14]  P. Kostyuk,et al.  Ionic mechanism of electrical excitability in rat sensory neurons during postnatal ontogenesis , 1991, Neuroscience.

[15]  K. Krnjević,et al.  Hypoxic changes in hippocampal neurons. , 1989, Journal of neurophysiology.

[16]  D. Choi,et al.  Glutamate neurotoxicity and diseases of the nervous system , 1988, Neuron.