Sarah E. Ross

The paper identifies a novel subset of IL-1R1+ nociceptors in mice using multimodal transcriptomics and calcium imaging, revealing their role in inflammatory pain.

The paper demonstrates that long-range GABAergic neurons expressing Tacr1 mediate neurovascular coupling through vasodilation and capillary pericyte activity.

This study identifies and characterizes wide-field amacrine cells in mouse retina that encode stimulus orientation through molecular and functional analysis.

The paper identifies a GRPR-expressing spinal neuron population that encodes itch and shows that kappa opioid receptor agonists inhibit itch by targeting these neurons.

This study shows that delta-opioid receptor agonists suppress itch while antagonists induce itch, revealing DOR's role in itch modulation in the spinal cord.

The paper examines how cortical and thalamic inputs target specific inhibitory neurons in mouse motor cortex, revealing distinct laminar and cell-type-specific connectivity patterns.

The paper investigates the role of mu-opioid receptor-expressing neurons in the periaqueductal gray in modulating pain and itch behaviors through optogenetic and chemogenetic manipulations.

This study investigates the role of Tacr1-expressing ON cells in the RVM in modulating pruriceptive transmission, finding they inhibit itch despite being pronociceptive.

The paper identifies RVM neurons expressing the kappa-opioid receptor that inhibit pain and itch via a descending circuit in mice.

The paper uses two-photon calcium imaging and pharmacological profiling to identify neuronal populations involved in capsaicin-induced central sensitization.

This study investigates the role of NK1R spinal neurons in itch using a Tacr1CreER mouse line, showing their involvement in modulating itch behavior through coexpression with GRPR.

The paper uses optogenetics to assess how non-peptidergic C-fiber afferents contribute to aversive behaviors before and after nerve injury.

The paper identifies distinct neural pathways from the lateral parabrachial nucleus that mediate different aspects of the pain response, including escape behaviors and aversive memory.

The paper identifies a cold-specific neural pathway from the periphery to the parabrachial nucleus, characterized by unique physiological and connectivity properties.