Chronic Alcohol Drinking Impairs Recognition Memory And Insulin-Associated Genes In The Medial Prefrontal Cortex.

Area of Science:

• Neuroscience
• Behavioral Science
• Genetics

Background:

• Chronic alcohol consumption is linked to cognitive deficits, but the underlying mechanisms are not fully understood.
• The medial prefrontal cortex (mPFC) is crucial for cognitive functions affected by alcohol use disorder.
• Insulin signaling pathways are being explored for potential therapeutic interventions in alcohol use disorder.

Purpose of the Study:

• To investigate the effects of chronic alcohol consumption on working and recognition memory in alcohol-preferring rats.
• To examine the impact of chronic alcohol exposure on insulin/IGF-1 signaling genes in the mPFC and hippocampus.
• To explore alterations in genes associated with brain plasticity and memory.

Main Methods:

• Male and female Marchigian Sardinian alcohol-preferring (msP) rats were given access to alcohol or water for several weeks.
• Working memory was assessed using the radial arm maze, and recognition memory was evaluated with the novel object recognition task.
• Gene expression analysis of insulin/IGF-1 signaling components and plasticity-related genes was performed in the prelimbic (PL), infralimbic (IL) cortex, and hippocampus CA1.

Main Results:

• Chronic alcohol consumption selectively impaired recognition memory in males but not working memory in either sex.
• Alcohol exposure altered the transcription of insulin/IGF-1 signaling genes, including decreased Insr in females and Igf1r in males within the IL region.
• Downstream effector Irs2 was decreased across both sexes and regions, alongside observed changes in plasticity-related genes like Bdnf and Pkmζ.

Conclusions:

• Chronic alcohol drinking impairs recognition memory in male rats and broadly disrupts metabolic and plasticity-associated genes in the mPFC and hippocampus.
• Sex differences exist in alcohol consumption and its effects on memory and gene expression.
• Findings suggest that disruptions in insulin/IGF-1 signaling and brain plasticity pathways contribute to alcohol-induced cognitive deficits.