A5066832260- Neurotransmitter Receptor Influence on Behavior
- Neuropeptides and Animal Physiology
- Neuroscience and Neuropharmacology Research
- Receptor Mechanisms and Signaling
- Pain Mechanisms and Treatments
- Stress Responses and Cortisol
- Memory and Neural Mechanisms
- Pain Management and Placebo Effect
- Pharmacological Receptor Mechanisms and Effects
- Ion channel regulation and function
- Neuroendocrine regulation and behavior
- Neuroscience of respiration and sleep
- Nicotinic Acetylcholine Receptors Study
- Pain Management and Opioid Use
- Neural dynamics and brain function
- Anesthesia and Neurotoxicity Research
- Cancer, Stress, Anesthesia, and Immune Response
- Anesthesia and Sedative Agents
- Biochemical effects in animals
- Neurobiology and Insect Physiology Research
- Eicosanoids and Hypertension Pharmacology
- Pediatric Pain Management Techniques
- Birth, Development, and Health
- Renin-Angiotensin System Studies
- Mindfulness and Compassion Interventions
William Penn University
2025
University of Pennsylvania
2020-2024
University of North Carolina at Chapel Hill
2011-2022
University of Minnesota System
2021
Indiana University School of Medicine
2012-2016
University of Minnesota
2015-2016
University of North Carolina Health Care
2016
Colby College
2011-2015
G-protein-gated inwardly rectifying K + (GIRK/Kir3) channel activation underlies key physiological effects of opioids, including analgesia and dependence. GIRK has also been implicated in the opioid-induced inhibition midbrain GABA neurons consequent disinhibition dopamine (DA) ventral tegmental area (VTA). Drug-induced VTA DA linked to reward-related behaviors motor activation. Here, we demonstrate that mouse express a formed by GIRK1 GIRK2 subunits. Nevertheless, neither constitutive...
The basolateral amygdala (BLA) is essential for assigning positive or negative valence to sensory stimuli. Noxious stimuli that cause pain are encoded by an ensemble of
Pain is a dynamic and nonlinear experience shaped by injury contextual factors, including expectations of future pain or relief. While mu opioid receptors are central to the analgesic effects drugs, endogenous neurocircuitry underlying placebo analgesia remains poorly understood. The ventrolateral column posterior periaqueductal gray critical hub for nociception mediated signaling. However, significant gaps remain in understanding cell-type identities, sub-second neural dynamics involved...
With concurrent global epidemics of chronic pain and opioid use disorders, there is a critical need to identify, target manipulate specific cell populations expressing the mu-opioid receptor (MOR). However, available tools transgenic models for gaining long-term genetic access MOR+ neural types circuits involved in modulating pain, analgesia addiction across species are limited. To address this, we developed catalog MOR promoter (MORp) based constructs packaged into adeno-associated viral...
Dopamine (DA) neurons of the VTA have been widely implicated in cellular and behavioral responses to drugs abuse. Inhibitory G protein signaling mediated by GABA B receptors (GABA Rs) D 2 DA (D regulates excitability neurons, neurotransmission, behaviors modulated DA. Most somatodendritic inhibitory effect R activation on reflects protein-gated inwardly rectifying K + (GIRK) channels. Furthermore, GIRK-dependent can be weakened exposure psychostimulants strengthened phasic neuron firing. The...
The anterior cingulate cortex plays a pivotal role in the cognitive and affective aspects of pain perception. Both endogenous exogenous opioid signaling within mitigate cortical nociception, reducing unpleasantness. However, specific functional molecular identities cells mediating analgesia remain elusive. Given complexity as sensory emotional experience, richness ethological pain-related behaviors, we developed standardized, deep-learning platform for deconstructing behavior dynamics...
A large literature has demonstrated that neuropeptide Y (NPY) regulates many emotional and reward-related behaviors via its primary receptors, Y1R Y2R. Classically, NPY actions at postsynaptic decrease anxiety, depression, alcohol drinking, while presynaptic Y2R produce the opposite behavioral phenotypes. However, emerging evidence suggests activation of can also anxiolysis in a brain region neurotransmitter system-dependent fashion. Further, numerous human rodent studies have reported...
Drugs of abuse engage overlapping but distinct molecular and cellular mechanisms to enhance dopamine (DA) signaling in the mesocorticolimbic circuitry. DA neurons ventral tegmental area (VTA) are key substrates drugs have been implicated addiction-related behaviors. Enhanced VTA neurotransmission evoked by can inhibitory G-protein-dependent feedback pathways, mediated GABAB receptors (GABABRs) D2 (D2Rs). Chemogenetic inhibition potently suppressed baseline motor activity, as well...
ABSTRACT Fear is an adaptive state that drives defensive behavioral responses to specific and imminent threats. The central nucleus of the amygdala (CeA) a critical site adaptations are required for acquisition expression fear, in part due alterations activity inputs CeA. Here, we characterize novel GABAergic input CeA from ventral periaqueductal gray area (vPAG) using fiber photometry ex vivo whole-cell slice electrophysiology combined with optogenetics pharmacology. GABA transmission this...