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Increased brain damage after stroke or excitotoxic seizures in melatonin‐deficient rats
Author(s) -
Manev Hari,
Uz Tolga,
Kharlamov Alexander,
Joo JinYang
Publication year - 1996
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.10.13.8940301
Subject(s) - melatonin , neuroprotection , neurodegeneration , pinealectomy , medicine , melatonin receptor , epilepsy , glutamate receptor , endocrinology , neuroscience , pineal gland , biology , receptor , disease
The pineal hormone melatonin is neuroprotective in vitro, and in vivo it is neuropro‐ tective when given in pharmacological doses. Conse‐quently, it has been hypothesized that with aging, as circulating levels of melatonin in mammals normally decrease, the brain might be at increased risk of neurodegeneration. However, direct evidence that melatonin deficiency leads to increased brain vulnerability is still lacking. We created melatonin deficiency in rats by pinealectomy and induced neurodegeneration by two models of focal brain ischemia/stroke and by glutamate receptor‐medi‐ ated, epilepsy‐like seizures. We observed greater neurodegeneration in melatonin‐deficient animals than in controls. Our results suggest that endogenous melatonin may play a neuroprotective role, and that melatonin deficiency might be a pathophysiological mechanism in neurodegenerative diseases.—Manev, H., Uz, T., Kharlamov, A., Joo, J.‐Y. Increased brain damage after stroke or excitotoxic seizures in mela‐ tonin‐deficient rats. FASEB J. 10, 1546‐1551