Marianne Seney
University of Pittsburgh, PA·Neuroscience
Addiction is rarely about one substance, and it rarely stops at the drug itself: people struggling with opioids or alcohol also report intense cravings, loss of pleasure in everyday life, disrupted sleep, and withdrawal from other people. Research in this lab asks what happens in the brain's own cells to produce those lasting symptoms, by pairing postmortem human brain tissue from people who had a substance use disorder with experiments in mice.
- Fields
Neuroscience
Pharmacology
Genetics
- Topics
opioid use disorder
alcohol use disorder
polysubstance use
- Grants
- 2 known grants, through Mar 2031
What they work on
- Determine whether somatostatin-expressing neurons in human prefrontal cortex show pronounced transcriptional changes in people with opioid use disorder who also used nicotine, using postmortem brain tissue.
- Define the persistent molecular and synaptic adaptations in prefrontal somatostatin inhibitory neurons of mice after combined nicotine and opioid exposure, testing the circuit in which nicotine-sensitive VIP neurons release these cells' brake on output neurons.
- Test whether directly modulating somatostatin interneuron activity in mice reduces combined nicotine and opioid use and eases withdrawal-related social anhedonia, the loss of interest in interacting with others.
- Map how 24-hour molecular rhythms are altered in individual cell types of the nucleus accumbens in alcohol use disorder, using single-nucleus RNA sequencing of postmortem human tissue ordered by each donor's time of death.
- Test whether disrupting rhythms in specific nucleus accumbens cell types in mice causally increases alcohol drinking, following the finding that clock genes such as CRY1 and PER2 lose rhythmicity in AUD.
More about the research
A shared strategy runs through both projects: measure gene activity in specific, individually identified cell types rather than in whole chunks of tissue, then go back into mice to test whether changing those cells changes drinking or drug-taking behavior.
Why it matters
Current medications for opioid use disorder leave most people vulnerable to relapse, and alcohol use contributes to over 200 health conditions and an estimated 5.1% of the global burden of disease and injury. By showing how nicotine reshapes opioid effects on prefrontal circuits — a factor omitted from most preclinical work — and which brain cell types lose their daily rhythms in alcohol use disorder, these studies could point to new treatment targets and to time-of-day-dependent dosing strategies.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
James M Otis
Medical University of South Carolina, SC·Neuroscience
Track single posterior paraventricular thalamus neurons that project to the nucleus accumbens across heroin self-administration, extinction, and reinstatement in mice, using two-photon calcium imaging.
Camron Bryant
Northeastern University, MA·Genetics
Sequence the whole genomes of SHR/NCrl and SHR/NHsd rat substrains and map behavioral QTLs for impulsivity, compulsivity, and cocaine self-administration traits in an F2 reduced complexity cross.
Yasmin L. Hurd
Icahn School of Medicine at Mount Sinai, NY·Neuroscience
Determine how prenatal cannabis or THC exposure disturbs immune-related genes in the placenta and brain, using placentas from women who used cannabis during pregnancy and rats exposed to THC during development.
The school
University of Pittsburgh: 83 labs on PI Pages, $1.5B a year on research, 403 research doctorates a year.
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