Matthew B. Pomrenze

The paper identifies Tshz1 neurons in the nucleus accumbens as critical for withdrawal aversion by modulating dopamine release and mGluR8 activity, offering a new therapeutic target for opioid use disorder.

The paper shows dopamine and serotonin regulate striatal output pathways through distinct neuronal populations, achieving opponent effects.

This study identifies a mechanism by which serotonin suppresses aggression by modulating nucleus accumbens circuits in mice.

This paper investigates how 5-HT2C receptors in the nucleus accumbens modulate MDMA's rewarding effects and prosocial behaviors through interactions with serotonin and dopamine release.

The paper shows that cholinergic modulation of dopamine release enhances effortful behavior by amplifying dopamine responses to high-effort rewards.

This study investigates psilocybin's effects on mouse behavior through a multi-laboratory collaboration, finding robust acute effects but inconsistent persistent effects.

This study shows that integrating inverse dopamine and serotonin signals in the striatum is essential for associative learning.

The paper shows that myelin plasticity in the ventral tegmental area, regulated by dopaminergic activity, is essential for opioid reward and dopamine release dynamics.

The paper identifies opioid receptor-expressing neurons in the central amygdala as mediators of ketamine's behavioral effects in mice, showing they are not direct targets of ketamine.

This study examines how psilocybin and environment affect brain-wide immediate early gene expression in mice using c-Fos immunofluorescence and light sheet microscopy.

This study shows that CCK released from somatodendritic regions of VTA dopamine neurons enhances GABAergic synapses and influences food consumption behaviors.

This study shows that acute social stress enhances learning of appetitive cues via synergistic CRF and NE signaling in the VTA, promoting Pavlovian reward conditioning.

This study identifies CeA CRF neurons and their projections to the BNST as drivers of excessive alcohol drinking and withdrawal in rats.