Arnab Barik

The paper identifies two molecularly distinct MCH neuron subpopulations in the LHA and characterizes their unique and overlapping anatomical projections using genetic and imaging approaches.

This study identifies how dopamine receptor-expressing neurons in the nucleus accumbens regulate scratching behavior during acute and chronic itch.

The paper introduces Scratcher, a computational tool for automated analysis of scratching behavior in mice, and demonstrates its use in studying itch-related neural circuits.

This study identifies a central mechanism by which stress modulates itch through LHA neurons projecting to brainstem regions.

The paper identifies an ascending neural pathway from the RVM to LHA that drives stress-induced anxiety, revealing a new role for RVM beyond pain modulation.

This study shows that modulating dopamine D1 receptor (D1R) activity in the anterior cingulate cortex (ACC) can alleviate chronic neuropathic pain in mice by altering neuronal excitability and circuit connectivity.

This study identifies a neural circuit between the periaqueductal gray and lateral septum that mediates acute restraint stress-induced analgesia through synaptic interactions.

This study identifies two thalamic nuclei mediating different aspects of cold pain responses in mice through viral genetics and physiology.

This study identifies a brain circuit involving the dorsal lateral septum and lateral hypothalamic area that drives stress-induced analgesia through opioid-dependent modulation of pain pathways.

The paper investigates how competing inputs in the lateral parabrachial nucleus (LPBN) modulate licking behavior in mice with chemotherapy-induced peripheral neuropathy (CIPN) in response to cold pain.

This study identifies a brainstem circuit involving LPBN and RVM neurons that mediates pain-induced suppression of itch in mice.

The paper uses deep learning to analyze mouse behavior on a thermal-plate test to study pain hypersensitivity mechanisms.

The paper identifies a spinoparabrachial circuit involving Tacr1-expressing neurons that modulates ongoing pain responses and suppresses itch.