Pinealectomy causes hippocampal CA1 and CA3 cell loss: Reversal by melatonin supplementation
| Autor: | M. De Butte, Bruce A. Pappas |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Male
Aging medicine.medical_specialty Antioxidant Free Radicals Cell Survival Thiobarbituric acid medicine.medical_treatment Administration Oral Pinealectomy medicine.disease_cause Hippocampus Pineal Gland Rats Sprague-Dawley Lipid peroxidation Melatonin chemistry.chemical_compound Internal medicine medicine TBARS Animals Dose-Response Relationship Drug Pyramidal Cells General Neuroscience Glutathione Rats Endocrinology chemistry Dietary Supplements Lipid Peroxidation Neurology (clinical) Geriatrics and Gerontology Oxidative stress Developmental Biology medicine.drug |
| Zdroj: | Neurobiology of Aging. 28:306-313 |
| ISSN: | 0197-4580 |
| Popis: | This experiment determined if the loss of endogenous melatonin via pinealectomy affected rat CA1 and CA3 pyramidal neuron numbers over a 20-month span. Since pinealectomy eliminates many neurohormones, some rats received daily melatonin supplementation to determine if this would reverse its effects. CA1 pyramidal cells were significantly reduced between 2 and 4 months after pinealectomy. CA3 loss was evident at 2 months post-pinealectomy. Melatonin replacement in the drinking water prevented these effects and seemingly promoted the genesis of CA1 cells. Analyses of hippocampal thiobarbituric acid reactive substances (TBARS) levels at 3 and 20 months post-surgery, revealed no significant group differences in lipid peroxidation. However, hippocampal TBARS were higher at 20 than at 3 months in all groups. Pinealectomized rats exhibited a significantly higher ratio of reduced to oxidized glutathione at 3 months but not 20 months, when compared to the sham and melatonin-supplemented rats. This suggests that pinealectomy caused oxidative stress and a subsequent compensatory change in the glutathione system. These results indicate that endogenous melatonin is neuroprotective. |
| Databáze: | OpenAIRE |
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