Ulk1 protects against ethanol-induced neuronal stress and cognition-related behavioral deficits.
Neurosci Res
; 117: 54-61, 2017 Apr.
Article
em En
| MEDLINE
| ID: mdl-28017600
ABSTRACT
Alcoholism is a psychiatric condition that develops through neuroadaptations in response to neuronal stresses caused by chronic ethanol intake. Neurons can adapt to ethanol-induced metabolic changes by activating cellular protective mechanisms, including autophagy. Here we show that expression of Ulk1, a gene critical to the regulation of autophagy, was affected in the prefrontal cortex (PFC) of mice following chronic intermittent ethanol (CIE) exposure. Consequently, overall levels of Ulk1 activity in the PFC were downregulated, leading to accumulation of p62, a protein that serves as a target for autophagic degradation. In addition, Ulk1-null mice demonstrated decline in the exploratory activity, deficits in the ability to recognize novel objects following CIE exposure, and reduced rate of voluntary ethanol drinking. The data suggest the neuroprotective role for Ulk1-mediated autophagy in the suppression of neuropsychiatric manifestation during ethanol exposure.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Comportamento Animal
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Transtornos Cognitivos
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Etanol
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Proteína Homóloga à Proteína-1 Relacionada à Autofagia
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Neurônios
Limite:
Animals
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article