Ulk1 protects against ethanol-induced neuronal stress and cognition-related behavioral deficits.

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.

journal_name

Neurosci Res

journal_title

Neuroscience research

authors

Sumitomo A,Ueta K,Mauchi S,Hirai K,Horike K,Hikida T,Sakurai T,Sawa A,Tomoda T

doi

10.1016/j.neures.2016.12.004

subject

Has Abstract

pub_date

2017-04-01 00:00:00

pages

54-61

eissn

0168-0102

issn

1872-8111

pii

S0168-0102(16)30283-8

journal_volume

117

pub_type

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