Brian Mathur
University of Maryland, Baltimore, MD·Neuroscience
Drinking compulsively, continuing despite harm, is a defining feature of alcohol use disorder, and few treatments target it well. The dorsolateral striatum is a deep brain region involved in habits.
- Fields
Neuroscience
Pharmacology
Physiology
- Topics
alcohol use disorder
compulsive drinking
ethanol
- Grants
- 1 known grant, through Feb 2028
What they work on
- Determine the circuit-specific synaptic mechanisms by which acute ethanol strengthens GABAergic (inhibitory) input to dorsolateral striatum fast-spiking interneurons (FSIs), using molecular tools and whole-cell patch clamp electrophysiology.
- Track the fate of inhibitory inputs to FSIs that are lost after chronic intermittent ethanol exposure, using advanced cellular and molecular imaging techniques.
- Test whether breakdown of perineuronal nets, the protective matrix around FSIs, causes the loss of inhibition and drives compulsive drinking, using slice electrophysiology, net imaging, in vivo chemogenetics, and drinking behavior analysis.
More about the research
The lab has shown that one small group of neurons in this region is needed for compulsive alcohol drinking. These are fast-spiking interneurons (FSIs), cells that fire rapidly and act as local controllers of striatal activity. This project asks how alcohol changes these cells at the levels of molecules, circuits, and behavior.
Why it matters
Alcohol use disorder is a major public health burden, and treatment for compulsive drinking is especially inadequate. Showing how chronic alcohol strips inhibitory control from striatal fast-spiking interneurons, possibly through perineuronal net breakdown, could point to new drug targets for compulsive drinking. It may also inform other psychiatric disorders that involve the dorsal striatum.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Christopher Kroenke
Oregon Health & Science University, OR·Neuroscience
Test whether chronic intermittent ethanol exposure combined with forced swim stress shifts the excitatory-to-inhibitory balance of input to medium spiny neurons in the mouse dorsolateral striatum, using ex vivo slice electrophysiology.
Brady Atwood
University of Minnesota, MN·Neuroscience
Test whether oxycodone increases tau protein expression, phosphorylation and oligomerization (clumping) in the mouse prefrontal cortex, and whether these changes cause synaptic dysfunction.
Subhash Pandey
University of Illinois Chicago, IL·Neuroscience
Test whether EZH2, an enzyme that adds methyl tags to histones, controls synaptic genes, electrical activity, synapse structure and anxiety-like behavior in the central amygdala of male and female rats during alcohol withdrawal, and examine these genes in postmortem human AUD amygdala.
The school
University of Maryland, Baltimore: 23 labs on PI Pages, $1.5B a year on research, 79 research doctorates a year.
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