Ischemia induces short‐ and long‐term remodeling of synaptic activity in the hippocampus

One of the most vulnerable areas to ischemia or hypoglycemia is CA1 hippocampal region due to pyramidal neurons death. Glutamate receptors are involved together with protein‐kinase C and nitric oxide synthase. Long‐term potentiation (LTP) is generated in anoxic or hypoglycemic conditions via activation of NMDA while inhibition of these receptors atenuates this response. Protein‐kinase C and nitric oxide synthase are involved in anoxic LTP mechanism. Postischemic neurons are hyperexcitable in CA3 area while CA1 pyramidal neurons degenerate and dissapear. Changes of glutamate receptors triggered by ischemia and hypoglycemia are discussed in this review.

[1]  R. Nicoll,et al.  Long-term potentiation--a decade of progress? , 1999, Science.

[2]  Y. Ben‐Ari,et al.  Alterations of the GluR-B AMPA receptor subunit flip/flop expression in kainate-induced epilepsy and ischemia , 1993, Neuroscience.

[3]  K. Hsu,et al.  Characterization of the anoxia‐induced long‐term synaptic potentiation in area CA1 of the rat hippocampus , 1997, British journal of pharmacology.

[4]  J. Connor,et al.  Global Ischemia Induces Downregulation of Glur2 mRNA and Increases AMPA Receptor-Mediated Ca2+ Influx in Hippocampal CA1 Neurons of Gerbil , 1997, The Journal of Neuroscience.

[5]  J. Gaiarsa,et al.  Permanent reduction of seizure threshold in post-ischemic CA3 pyramidal neurons. , 2000, Journal of neurophysiology.

[6]  Daniel Johnston,et al.  Endogenous nature of spontaneous bursting in hippocampal pyramidal neurons , 1981, Cellular and Molecular Neurobiology.

[7]  Stephen J. Smith,et al.  NMDA-receptor activation increases cytoplasmic calcium concentration in cultured spinal cord neurones , 1986, Nature.

[8]  D. Carpenter,et al.  Transient ischemia causes a reduction of Mg2+ blockade of NMDA receptors , 1994, Neuroscience Letters.

[9]  M. Moskowitz,et al.  Pathobiology of ischaemic stroke: an integrated view , 1999, Trends in Neurosciences.

[10]  L. Squire,et al.  Human amnesia and the medial temporal region: enduring memory impairment following a bilateral lesion limited to field CA1 of the hippocampus , 1986, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[11]  K. Zilles,et al.  Long-term cellular dysfunction after focal cerebral ischemia: in vitro analyses , 1998, Neuroscience.

[12]  R. Schmidt-Kastner,et al.  Selective vulnerability of the hippocampus in brain ischemia , 1991, Neuroscience.

[13]  P. Andiné,et al.  Calcium Uptake Evoked by Electrical Stimulation is Enhanced Postischemically and Precedes Delayed Neuronal Death in CA1 of Rat Hippocampus: Involvement of N-Methyl-D-Aspartate Receptors , 1988, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[14]  C. Hammond,et al.  Anoxic LTP sheds light on the multiple facets of NMDA receptors , 1994, Trends in Neurosciences.

[15]  R. P. McIntyre,et al.  Empirical Relationships between Need for Cognition and Cognitive Style: Implications for Consumer Psychology , 1994 .

[16]  A. Buchan,et al.  Blockade of the AMPA receptor prevents CA1 hippocampal injury following severe but transient forebrain ischemia in adult rats , 1991, Neuroscience Letters.

[17]  D. Prince,et al.  Transient enhancement of low-threshold calcium current in thalamic relay neurons after corticectomy. , 1993, Journal of neurophysiology.

[18]  K. Krnjević,et al.  Calcium dependence of LTP induced by 2-deoxyglucose in CA1 neurons. , 1996, Journal of neurophysiology.

[19]  W. Pulsinelli.  Selective neuronal vulnerability: morphological and molecular characteristics. , 1985, Progress in brain research.

[20]  C. Hammond,et al.  A selective LTP of NMDA receptor-mediated currents induced by anoxia in CA1 hippocampal neurons. , 1993, Journal of neurophysiology.

[21]  P. Andiné,et al.  Enhanced Calcium Uptake by CA1 Pyramidal Cell Dendrites in the Postischemic Phase despite Subnormal Evoked Field Potentials: Excitatory Amino Acid Receptor Dependency and Relationship to Neuronal Damage , 1992, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[22]  Paul Antoine Salin,et al.  Axonal sprouting and epileptogenesis. , 1997, Advances in neurology.

[23]  J. McNamara.  Human hypoxia and seizures: effects and interactions. , 1979, Advances in neurology.

[24]  T. Wieloch,et al.  Postischemic Blockade of AMPA but Not NMDA Receptors Mitigates Neuronal Damage in the Rat Brain following Transient Severe Cerebral Ischemia , 1992, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[25]  L Cocito,et al.  Epileptic seizures in cerebral arterial occlusive disease. , 1982, Stroke.

[26]  R. Malinow,et al.  Transient oxygen–glucose deprivation induces rapid morphological changes in rat hippocampal dendrites , 2001, Neuropharmacology.

[27]  A. Foster,et al.  MK-801 is neuroprotective in gerbils when administered during the post-ischaemic period , 1988, Neuroscience.

[28]  N. Diemer,et al.  Ischemia induced delayed neuronal death in the ca 1 hippocampus is dependent on intact glutamatergic innervation , 1987 .

[29]  S M Davis,et al.  Epileptic seizures in acute stroke. , 1990, Archives of neurology.

[30]  Y. Shinoda,et al.  Appearance of NMDA receptors triggered by anoxia independent of voltage in vivo and in vitro , 1991, Experimental Neurology.

[31]  Protein kinase C inhibitors block generation of anoxia‐induced long‐term potentiation , 1998, Neuroreport.

[32]  M. Bennett,et al.  Switch in glutamate receptor subunit gene expression in CA1 subfield of hippocampus following global ischemia in rats. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[33]  H. Robinson,et al.  Single glutamate channels in CA1 pyramidal neurones after transient ischaemia. , 1995, Neuroreport.

[34]  K. Hsu,et al.  Nitric Oxide Signalling is Required for the Generation of Anoxia‐induced Long‐term Potentiation in the Hippocampus , 1997, The European journal of neuroscience.

[35]  T. Mittmann,et al.  Ischaemia‐induced Long‐term Hyperexcitability in Rat Neocortex , 1995, The European journal of neuroscience.

[36]  Y. Ben‐Ari,et al.  Intracellular injection of a Ca2+ chelator prevents generation of anoxic LTP. , 1996, Journal of neurophysiology.

[37]  C. McBain,et al.  N-methyl-D-aspartic acid receptor structure and function. , 1994, Physiological reviews.

[38]  J. Liebman,et al.  The N-methyl-d-aspartate antagonists CGS 19755 and CPP reduce ischemic brain damage in gerbils , 1988, Brain Research.

[39]  D. Muller,et al.  Remodeling of Hippocampal Synaptic Networks by a Brief Anoxia–Hypoglycemia , 2002, The Journal of Neuroscience.

[40]  S N Davies,et al.  Paired‐pulse depression of monosynaptic GABA‐mediated inhibitory postsynaptic responses in rat hippocampus. , 1990, The Journal of physiology.