MLRisherLab

Our laboratory is interested in understanding how adolescent binge drinking influences brain function and contributes to the development of alcohol use disorder. In rodent models of adolescent binge drinking (chronic intermittent ethanol exposure), our laboratory and others have demonstrated that there are acute and long-term changes to neuronal structure, function, and behavior across multiple cognitive domains.

Over the last few decades it has become apparent that non-neuronal cells called astrocytes which outnumber neurons and ensheathe many neuronal connections, play an important role in synapse formation, synapse maintenance across the life-span, and synaptic recovery following injury. However, how astrocytes contribute to changes in neuronal/synaptic structure and function following ethanol exposure is not fully understood.

Using multiple ethanol exposure paradigms in rat and mouse models of adolescent binge drinking we investigate:

1. How acute and long-term binge ethanol exposure influences astrocyte function.

2. The role of astrocytes in the development of alcohol-induced deficits in cognition and the emergence of AUD.

3. Long-term consequences of adolescent binge drinking on brain function and recovery from secondary insult

Techniques used to answer these questions include: intracranial surgeries, immunohistochemistry, Western blot, PCR, organotypic slice culture, confocal and STED microscopy, 3D image analysis, spatial transcriptomics, fiberoptics, and many, many different behavioral paradigms including conditioned place preference, fear conditioning, social interaction, and set-shifting.

Understanding how astrocytes contribute to the long-term effects of adolescent binge drinking in a rodent model is crucial for understanding the impact that underage alcohol exposure can have on the adult brain and how early onset drinking may contribute to the development of alcohol dependence later in life.

What We've Achieved