Bryan A. Copits

The paper investigates alternative splicing plasticity of neurexin family genes in human sensory neurons and finds it is dynamic and conserved across species.

This study investigates the role of H3R in DRG neurons and shows that an H3R inverse agonist reduces mechanical hypersensitivity in neuropathic pain without affecting thermal pain.

This study investigates the role of mu opioid receptors in glutamatergic and GABAergic neurons of the rostral ventromedial medulla in neuropathic pain, finding that MOR signaling modulates early hypersensitivity but not chronic pain intensity.

This paper creates a multi-omic atlas of human autonomic and sensory ganglia, identifying cell-type-specific features and disease associations in peripheral neuropathies.

This paper constructs a human dorsal root ganglion reference atlas, identifying 22 neuronal subtypes and 10 non-neuronal cell types, and reveals functional differences between human and mouse DRG neurons.

The paper maps molecular features of human spinal cord dorsal and ventral horns, identifying neuronal types and sex-specific glial differences using single-nucleus sequencing and spatial transcriptomics.

The paper identifies impaired SK channel function in mesolimbic dopamine neurons as a mechanism driving reward seeking adaptations in chronic neuropathic pain.

This study creates a single-nucleus multi-omic atlas of human dorsal root ganglia, identifying novel regulatory mechanisms and therapeutic targets for pain.

This study links electrical properties to transcriptional identities in human sensory neurons, identifying associations between pain history and specific electrophysiological subtypes.

The paper investigates FGFR3 expression in human peripheral nervous system tissues and finds no detectable mRNA or protein expression in nerve or dorsal root ganglia, suggesting FGFR3 autoantibodies may not directly cause neuropathy.

The paper builds harmonized cross-species cell atlases of DRG and TG, identifies 29 cell types across 6 species, and shows transcriptomic similarities and differences in sensory neurons.

The paper develops a CRISPR/Cas9 gene editing strategy using a single AAV vector and Cre-dependent Cas9 in mice to enable cell-type specific editing and tool delivery in the nervous system.

This study introduces an optogenetic GDI tool to induce Gβγ signaling independently of GPCRs and demonstrates its ability to trigger macrophage migration.

This paper identifies PdCO as a bistable GPCR with high temporal precision for optogenetic control of neural circuits in vivo.

The paper identifies the cellular and subcellular localization of Kv2.1 and Kv2.2 channels in DRG neurons, showing similarities between mice and humans.

This study characterizes bradykinin receptor expression and function in human dorsal root ganglia neurons, finding conserved acute hyperexcitability and age/pain history-related B1 receptor expression.

This study shows that sustained depolarization reduces excitability in mouse and human sensory neurons through decreased voltage-gated sodium currents, suggesting homeostatic plasticity may be altered in chronic pain.

This study shows that oral oxycodone self-administration in mice leads to features of opioid addiction, including escalation, dependence, and relapse behavior.

This study identifies itch-activated neurons in the central amygdala (CeA) and their role in itch sensation, avoidance, and comorbidities like anxiety, using RNA-sequencing and viral tracing.

This paper introduces parapinopsin (PPO), a photoswitchable GPCR-based opsin that enables rapid and reversible presynaptic inhibition, and demonstrates its utility in vivo.

This paper introduces an oral oxycodone self-administration paradigm in mice to model prescription opioid use and its transition to abuse.

The paper uses spatial transcriptomics to characterize human sensory neurons, comparing them to mouse and non-human primate data to identify similarities and divergences in drug targets.

This study identifies macrophage AT2R activation as a key driver of neuropathic pain through ROS/NO-mediated TRPA1 activation in sensory neurons.