Stimulation of the subthalamic vasodilator area and fastigial nucleus independently protects the brain against focal ischemia
| Autor: | Eugene V. Golanov, Christopher P Ilch, Sara B. Glickstein, Donald J. Reis |
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| Rok vydání: | 2001 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Central nervous system Neurotoxins Ischemia Stimulation Electric Stimulation Therapy Neuroprotection Brain Ischemia Rats Sprague-Dawley chemistry.chemical_compound medicine.artery Internal medicine Neural Pathways medicine Excitatory Amino Acid Agonists Animals Molecular Biology Ibotenic Acid Fastigial nucleus business.industry General Neuroscience Infarction Middle Cerebral Artery medicine.disease Denervation Rats Inbred F344 Rats Vasodilation Endocrinology medicine.anatomical_structure chemistry Cerebral blood flow Cerebellar Nuclei Anesthesia Cerebrovascular Circulation Subthalamus Middle cerebral artery Nerve Degeneration Neurology (clinical) business Ibotenic acid Developmental Biology |
| Zdroj: | Brain research. 912(1) |
| ISSN: | 0006-8993 |
| Popis: | We investigated whether stimulation of the functionally discrete subthalamic region, subthalamic cerebrovasodilator area (SVA), which increases cerebral blood flow (CBF) when excited, would, like stimulation of cerebellar fastigial nucleus (FN), produce central neurogenic neuroprotection. A 1-h electrical stimulation of SVA or FN reduced infarctions triggered by permanent occlusion of middle cerebral artery (MCA) by 48–55% in Sprague–Dawley rats and by 59% in Fisher rats. The salvaging effect of SVA stimulation, similar to FN, was long lasting and reduced the volume of infarctions placed 72 h or 10 days later by 58 and 26%, respectively, in Fisher rats. Bilateral lesioning of FN neurons by the microinjection of ibotenic acid 5 days before SVA stimulation did not affect SVA-evoked neuroprotection. Bilateral lesions of SVA neurons administered 5 days before FN stimulation had no effect on FN-induced neuroprotection but reversed the stimulus-locked increase in CBF accompanying FN stimulation. This study demonstrates that (1) excitation of neurons and/or fibers projecting through the SVA reduces ischemic infarctions as substantially as excitation of FN neurons; (2) the effects are long-lasting and not attributable to increases in cerebral blood flow, changes in blood gases or brain temperature, or rat strain; (3) the neuroprotective effects of SVA and FN stimulation are mutually independent and (4) FN-evoked cerebrovasodilation is mediated by SVA neurons. The SVA and FN are part of a neuronal system in CNS, which is distributed and, when excited, acts to protect the brain from ischemic injury. |
| Databáze: | OpenAIRE |
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