Jun Wang
Texas A&M University-College Station, TX·Neuroscience
Addiction makes behavior rigid. People keep seeking alcohol or cocaine despite harm, and many relapse even after quitting.
- Fields
Neuroscience
Pharmacology
- Topics
alcohol use disorder
cocaine use disorder
addiction
- Grants
- 3 known grants, through Apr 2031
What they work on
- Define how cocaine-strengthened inhibition from dMSNs onto cholinergic interneurons reduces thalamic excitation of these interneurons and acetylcholine release, using dual-channel optogenetics, electrophysiology and genetically encoded ACh sensors.
- Determine how cocaine disrupts cholinergic interneuron control of prefrontal cortex inputs onto striatal medium spiny neurons, which may underlie impaired updating of action–outcome learning.
- Measure acetylcholine dip–rebound dynamics during reversal learning in cocaine-exposed animals with in vivo photometry, and test whether optogenetic CIN excitation or LTD induction at dMSN-to-CIN synapses restores flexible behavior.
- Test whether chronic alcohol intake amplifies the dMSN-induced pause and rebound of cholinergic interneuron firing, and whether blocking the resulting acetylcholine dip reduces dopamine release and alcohol drinking.
- Examine whether the acetylcholine rebound in the dorsomedial striatum controls the shift from alcohol seeking to alcohol taking, using optogenetics, neurotransmitter biosensors and live-tissue imaging.
- Test whether operant alcohol self-administration causes lasting corticostriatal plasticity in dMSN ensembles that drives relapse, using ArcTRAP and Cal-Light to tag behavior-activated neurons.
- Determine whether extinction training reduces relapse by strengthening thalamostriatal inputs onto iMSN ensembles, iMSN-to-dMSN inhibition, or the effects of iMSNs on habenula-projecting globus pallidus neurons.
More about the research
This research asks how drugs rewire the dorsomedial striatum (DMS), a deep brain region that supports learning from rewards and switching strategies when circumstances change. Two cell types in the DMS are central to this work: - medium spiny neurons (MSNs), the region's main output cells; direct-pathway MSNs (dMSNs) promote actions, while indirect-pathway MSNs (iMSNs) hold them back; - cholinergic interneurons (CINs), cells that release the signaling molecule acetylcholine (ACh).
Why it matters
Alcohol and cocaine use disorders have few effective treatments, and relapse remains a major clinical problem. By identifying specific striatal connections and acetylcholine signals that drugs disrupt, this work may point to new circuit-based treatment targets. These could include repurposed drugs that act on nicotinic acetylcholine receptors, or approaches that strengthen what extinction training does in the brain. Such treatments could help people with addiction regain flexible control over drug use and lower their risk of relapse.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Alexandra Nelson
University of California-San Francisco, CA·Neuroscience
Test whether local inhibitory synapses within the striatum, and inhibitory inputs from the globus pallidus, are altered in and contribute to levodopa-induced dyskinesia, using in vivo and ex vivo electrophysiology, optogenetics, and chemogenetics in parkinsonian mice.
Eduardo Gallo
Fordham University, NY·Neuroscience
Test whether dopamine D2 receptors on cholinergic interneurons of the nucleus accumbens control impulsive choice, by using cell type-specific genetic tools in mice to both increase and decrease receptor levels and measuring performance on a delay discounting task.
Giuseppe Giannotti
Washington State University, WA·Neuroscience·Early-career
Track the real-time activity of PVT neurons tagged with TRAP during spontaneous versus naloxone-precipitated withdrawal, using in vivo calcium imaging while rodents respond to heroin-linked cues.
The school
Texas A&M University-College Station: 23 labs on PI Pages, $1.4B a year on research, 768 research doctorates a year.
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