TY - JOUR
T1 - Central neurogenic neuroprotection
T2 - Protection of brain from focal ischemia by cerebellar stimulation
AU - Reis, D. J.
AU - Feinstein, D.
AU - Galea, E.
AU - Golanov, E. V.
PY - 1997
Y1 - 1997
N2 - Electrical stimulation of the cerebellar fastigial nucleus (FN) elevates regional cerebral blood flow (rCBF) independently of cerebral metabolism (rCGU) throughout the brain. One hour of FN stimulation also reduces, by up to 50%, the volume of the focal ischemic infarction produced by occlusion of the middle cerebral artery in rat. Protected areas correspond to the ischemic penumbra. Neuroprotection, while reversible, persists for weeks after 1 h of stimulation. It cannot be attributed to increasing rCBF and/or reducing rCGU to improve matching of flow and metabolism. Conditional stimulation of FN initiates long-lived inhibition of expression of peri-infarction depolarizing waves, possibly by altering potassium-channel function and suppresses induction of inducible nitric oxide synthase (iNOS) and ICAM in cerebral microvessels. The brain contains intrinsic networks which may protect the brain from ischemic injury, possibly by producing widespread and longterm suppression of electrical excitability and/or expression of proinflammatory molecules.
AB - Electrical stimulation of the cerebellar fastigial nucleus (FN) elevates regional cerebral blood flow (rCBF) independently of cerebral metabolism (rCGU) throughout the brain. One hour of FN stimulation also reduces, by up to 50%, the volume of the focal ischemic infarction produced by occlusion of the middle cerebral artery in rat. Protected areas correspond to the ischemic penumbra. Neuroprotection, while reversible, persists for weeks after 1 h of stimulation. It cannot be attributed to increasing rCBF and/or reducing rCGU to improve matching of flow and metabolism. Conditional stimulation of FN initiates long-lived inhibition of expression of peri-infarction depolarizing waves, possibly by altering potassium-channel function and suppresses induction of inducible nitric oxide synthase (iNOS) and ICAM in cerebral microvessels. The brain contains intrinsic networks which may protect the brain from ischemic injury, possibly by producing widespread and longterm suppression of electrical excitability and/or expression of proinflammatory molecules.
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U2 - 10.1111/j.1472-8206.1997.tb00873.x
DO - 10.1111/j.1472-8206.1997.tb00873.x
M3 - Article
AN - SCOPUS:0030944491
SN - 0767-3981
VL - 11
SP - 39s-43s
JO - Fundamental and Clinical Pharmacology
JF - Fundamental and Clinical Pharmacology
IS - SUPPL. 1
ER -