Abstract
Alcohol exposure during brain development induces neuronal cell death in the brain. Several neuroactive peptides have been shown to protect against alcohol-induced cell death. Secretin is a peptide hormone, and the secretin receptor is expressed in the gut and the brain. To explore a potential role of secretin signal against ethanol neurotoxicity during brain development, secretin receptor-deficient mice were exposed to ethanol on postnatal day 4. We identified significant ethanol-induced apoptosis in the external granular layer of the secretin receptor-deficient cerebellum and in the striatum after ethanol treatment. During the early postnatal period, there is a proliferation of granular cell progenitors that reside in the external granular layer. The results suggest that secretin signal plays a neuroprotective role of neuronal progenitor cells against the neurotoxicity of ethanol.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects
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Cell Proliferation / drug effects
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Central Nervous System Depressants / toxicity
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Cerebellum / drug effects*
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Cerebellum / growth & development
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Cerebellum / metabolism
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Cerebellum / pathology
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Corpus Striatum / drug effects*
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Corpus Striatum / growth & development
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Corpus Striatum / metabolism
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Corpus Striatum / pathology
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Ethanol / toxicity*
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In Situ Nick-End Labeling
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Mice
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Mice, Transgenic
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Nerve Degeneration / chemically induced
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Nerve Degeneration / metabolism
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Nerve Degeneration / pathology*
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Neurons / cytology*
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Neurons / drug effects
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Neurons / physiology
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Receptors, G-Protein-Coupled / genetics
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Receptors, G-Protein-Coupled / metabolism*
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Receptors, Gastrointestinal Hormone / genetics
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Receptors, Gastrointestinal Hormone / metabolism*
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Secretin / metabolism*
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Stem Cells / drug effects
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Stem Cells / physiology
Substances
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Central Nervous System Depressants
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Receptors, G-Protein-Coupled
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Receptors, Gastrointestinal Hormone
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secretin receptor
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Secretin
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Ethanol