Giuseppe Giannotti
Washington State University, WA·Neuroscience·Early-career
When people stop using opioids, they go through withdrawal, a painful physical and emotional state that can last well beyond the first days. Relieving that distress becomes a powerful reason to use again.
- Fields
Neuroscience
Pharmacology
- Topics
opioid use disorder
opioid withdrawal
heroin self-administration
- Grants
- 2 known grants, through May 2031
What they work on
- 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.
- Test whether each withdrawal-tagged PVT neuron group is needed for heroin seeking, using optogenetic silencing timed to the presentation of drug cues.
- Measure how inputs from the prelimbic cortex and ventral subiculum change withdrawal-tagged PVT neurons, and how D1 and D2 accumbens neurons adapt, using slice electrophysiology.
- Monitor dynorphin release onto withdrawal-tagged PVT neurons with the kLight1.3 sensor and dual-color fiber photometry, to see how kappa opioid receptor signaling shapes their activity.
- Determine whether the PVT-to-nucleus accumbens pathway is necessary and sufficient for aversion, hyperalgesia and relapse during heroin withdrawal, using optogenetics and chemogenetics.
- Test whether a long-term depression protocol, which weakens synapses along the prelimbic cortex-PVT-accumbens circuit, reduces heroin seeking and pain sensitivity, after measuring synaptic strength with AMPA/NMDA ratios.
More about the research
As a result, withdrawal drives craving and relapse in opioid use disorder (OUD), even after long periods without the drug. Current treatments often fail to prevent relapse in the long run. This research looks for the brain circuits that link withdrawal to drug seeking. Both projects center on the paraventricular thalamus (PVT), a small brain region that acts as a relay hub, and study rats or mice that have learned to give themselves heroin.
Why it matters
Withdrawal-driven relapse is a major reason opioid use disorder treatments fail over the long term. By mapping how thalamic circuits link withdrawal to heroin seeking, this work could identify circuit-level and dynorphin/kappa opioid receptor targets for new therapies. Such therapies may help people with opioid addiction break the withdrawal-relapse cycle.
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.
Heath Schmidt
University of Pennsylvania, PA·Neuroscience
Define how amylin receptors on specific cell types, dopamine and GABA neurons of the ventral tegmental area and D1- or D2-receptor medium spiny neurons of the nucleus accumbens, control oxycodone self-administration and relapse-like seeking, using viral gene delivery in transgenic rats.
Mary Kay Lobo
University of Maryland, Baltimore, MD·Neuroscience
Map cellular, synaptic plasticity and molecular changes in defined cell subtypes of the medial prefrontal cortex and nucleus accumbens in mice exposed to fentanyl during the equivalent of human gestation, from weaning through adolescence.
The school
Washington State University: 22 labs on PI Pages, $403M a year on research, 259 research doctorates a year.
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