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

Akiko Sumitomo, Keisho Ueta, Sayaka Mauchi, Kazuko Hirai, Kouta Horike, Takatoshi Hikida, Takeshi Sakurai, Akira Sawa, Toshifumi Tomoda

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)54-61
Number of pages8
JournalNeuroscience Research
StatePublished - Apr 2017


  • Alcoholism
  • Autophagy
  • Ethanol
  • Ulk1
  • p62

ASJC Scopus subject areas

  • Neuroscience(all)


Dive into the research topics of 'Ulk1 protects against ethanol-induced neuronal stress and cognition-related behavioral deficits'. Together they form a unique fingerprint.

Cite this