Intrinsic Neurons of Fastigial Nucleus Mediate Neurogenic Neuroprotection Against Excitotoxic and Ischemic Neuronal Injury in Rat
The Journal of Neuroscience, May 15, 1999, 19(10):4142–4154 Intrinsic Neurons of Fastigial Nucleus Mediate Neurogenic Neuroprotection against Excitotoxic and Ischemic Neuronal Injury in Rat Sara B. Glickstein, Eugene V. Golanov, and Donald J. Reis Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York 10021 Electrical stimulation of the cerebellar fastigial nucleus (FN) of FN, but not DN, abolished neuroprotection but not the elevates regional cerebral blood flow (rCBF) and arterial pres- elevations of rCBF and AP elicited from FN stimulation. Exci- sure (AP) and provides long-lasting protection against focal and totoxic lesions of FN, but not DN, also abolished the 37% global ischemic infarctions. We investigated which neuronal reduction in focal ischemic infarctions produced by middle element in FN, perikarya or axons, mediates this central neu- cerebral artery occlusion. Excitation of intrinsic FN neurons rogenic neuroprotection and whether it also protects against provides long-lasting, substantial, and reversible protection of excitotoxicity. In anesthetized rats, the FN was stimulated for 1 central neurons from excitotoxicity, as well as focal ischemia, hr, and ibotenic acid (IBO) was microinjected unilaterally into whereas axons in the nucleus, probably collaterals of ramified the striatum. In unstimulated controls, the excitotoxic lesions brainstem neurons, mediate the elevations in rCBF, which do averaged ;40 mm 3. Stimulation of FN, but not dentate nucleus not contribute to neuroprotection. Long-lived protection (DN), significantly reduced lesion volumes up to 80% when IBO against a range of injuries is an unrecognized function of FN was injected 15 min, 72 hr, or 10 d, but not 30 d, thereafter.
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