Degeneration of hippocampal CA1 neurons following transient ischemia due to raised intracranial pressure: evidence for a temperature-dependent excitotoxic process.
Degeneration of hippocampal CA1 neurons occurs following transient complete ischemia produced by raised intracranial pressure. Both systemic injection of MK-801 and profound cerebral hypothermia produced by cisternal infusion of room temperature (22-25 degrees C) fluids protect vulnerable CA1 neurons from degeneration. Hypothermia appears to decrease hippocampal extracellular levels of glutamate during and after ischemia but provides only relative protection from ischemia as CA1 degeneration does occur with prolonged (30 min) periods of ischemia. Elevated intracranial pressure appears to produce ischemic degeneration in the hippocampus via an NMDA receptor mediated excitotoxic process which is highly temperature dependent.
Duhaime
A C
AC
Department of Neurological Surgery, University of Florida, Gainesville 32610.
Ross
D T
DT
D000818:Animals; D001833:Body Temperature Regulation; D003986:Dibenzocycloheptenes / Q000494:pharmacology; D016291:Dizocilpine Maleate; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D007427:Intracranial Pressure; D002546:Ischemic Attack, Transient / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D051381:Rats; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000502:physiology*
D003986:Dibenzocycloheptenes; D005971:Glutamates; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D018698:Glutamic Acid; D016291:Dizocilpine Maleate