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 Resjournal_title
Neuroscience researchauthors
Sumitomo A,Ueta K,Mauchi S,Hirai K,Horike K,Hikida T,Sakurai T,Sawa A,Tomoda Tdoi
10.1016/j.neures.2016.12.004subject
Has Abstractpub_date
2017-04-01 00:00:00pages
54-61eissn
0168-0102issn
1872-8111pii
S0168-0102(16)30283-8journal_volume
117pub_type
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