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For the Spring semester, The Department of Psychology will be open Monday through Thursday from 10 am to 3 pm. Advising will be conducted through email and MS Teams. For general questions, please contact us at (817-272-2281)

The University of Texas at ArlingtonThe University of Texas at Arlington

Psychology

Behavioral Neuroscience and Neurophysiology Laboratories

Perry N. Fuchs, Ph.D.

Description of Research

The main focus of my overall research is aimed at exploring the basic, underlying central and peripheral nervous system mechanisms associated with rewarding and aversive stimuli. Experimental models, such as peripheral inflammation and neural injury, produce aversive behavioral responses that are associated with pain. A noxious stimulus usually engages in specific peripheral mechanisms, causing several conscious sensations consisting of judgments regarding the location and extent of tissue damage. Typically, there is also an alteration in effect and an induction of subconscious somatic and autonomic responses. Using a variety of experimental models, central mechanisms of pain processing are elucidated using focal electrical stimulation, microinjection, and lesion techniques. Research on peripheral mechanisms focuses on the coupling between the sympathetic and somatic nervous systems.

Yuan Bo Peng, M.D., Ph.D. 

Description of Research

Physiological mechanisms of pain

My lab is interested in studying the neurophysiological mechanisms of nociception by means of electrophysiological techniques in both the peripheral and central nervous systems.  We have been studying in these areas: (1) Dorsal root reflexes in peripheral inflammation; (2) Cortical modulation of spinal dorsal horn neuronal activity; (3) Pain mechanisms of experimental autoimmune encephalomyelitis; (4) Detection of neuronal activities by optic spectroscopy; (5) Development and application of telemetry system for recording and stimulating in the nervous system.

Qing Lin, M.D., Ph.D.

Description of Research 

Mechanisms of Neurogenic Inflammation Induced Pain - The National Institute of Health (NIH) funded the research project. Neurogenic inflammation is the process by which inflammatory mediators released from sensory nerve terminals produce inflammation in their target tissue. This process exacerbates pain. Neurogenic inflammation contributes to many clinically relevant states, including arthritis, inflammatory bowel disease, complex regional pain syndrome (CRPS), chronic bronchitis, migraine, and interstitial cystitis. One of the mechanisms by which neurogenic inflammation is induced, is the effector function of primary nociceptive afferent fibers. It is hypothesized that antidromic activity in primary afferents triggers the release of inflammatory mediators from these terminals when peripheral tissue is damaged, which helps develop neurogenic inflammatory pain. An increasing number of studies demonstrate that the antidromic activity of primary afferent fibers is centrally mediated by way of dorsal root reflexes (DRRs). In order to investigate its mechanisms, we have experimentally established an acute model of neurogenic inflammation by using intradermal capsaicin (CAP) injection. The long-term goal of the proposed studies is to elucidate how neurogenic inflammation is initiated by action of the peripheral nociceptive molecule, the transient receptor potential vanilloid-1 (TRPV1) activated by CAP, then maintained by triggering the centrally mediated antidromic activity, DRRs, to exacerbate inflammatory pain, and how the released inflammatory mediators driven by DRRs participate in the process of pain sensation. Currently, our specific goals are 1) to determine if neurogenic inflammation following CAP injection involves triggering DRRs that cause the release of calcitonin gene-related peptide and/or substance P from primary afferent nociceptors and if this process would, in turn, enhance the CAP-induced sensitization of primary afferent nociceptors, as well as analyze if this process is initiated by activation of TRPV1 receptors; 2) to examine if activation of the TRPV1 receptors in primary afferent nociceptors plays an important role in enhancing DRRs by activating GABAergic interneurons in dorsal horn circuits; 3) to determine if phosphorylation of protein kinase C (PKC) takes place in the primary afferent neurons when neurogenic inflammation is initiated and develops and if TRPV1 receptors are upregulated by the phosphorylation of PKC.

Electrophysiology, neuropharmacology, neurochemistry, immunocytochemistry (confocal imaging analysis), Western blots, and laser Doppler blood flow meter are utilized to perform these studies. In addition, we are currently developing molecular biological techniques, such as PCR, aiming at a deeper study of ionic and molecular targets by which the DRRs mediate inflammatory pain.

Uncovering these mechanisms will be critical for pharmaceutical manufacturers and clinicians to develop new anti-inflammatory therapies and improve the healthcare for patients. 

 

Linda I. Perrotti, Ph.D.

Description of Research

My primary research interests are focused on the neural mechanisms underlying sex differences in the behavioral and molecular responses to psychostimulant and opioid drugs. The overall goal of my work is to clarify interactions among the neuroendocrine system and dopamine reward system using rodent models of addictive behaviors. 

The second area of interest is the further examination of the “tail of the ventral tegmental area” or “rostromedial tegmental nucleus” (tVTA/RMTg) as a major nucleus modulating dopamine-driven drug reward. Using rodents as model organisms, I investigate
the initiation, acquisition, expression, extinction and reacquisition of conditioned drug reward. I am particularly interested in the biochemical and neuroendocrine factors which predispose certain individuals to respond differentially to drugs of abuse. The goal of our research is to better understand the biological basis of this disease and to identify major biological targets for potential therapeutic intervention to promote abstinence and prevention.

Dr. Perrotti

From left to right: Blake Brady (undergraduate research assistant), Houda Chamseddine (second-year graduate student), Dr. Linda Perrotti (PI), Saurabh Kokane (doctoral candidate), and Clinton Coelho (first-year graduate student)

 

Contact Information

Dr. Perry Fuchs
817-272-3427
fuchs@uta.edu

Dr. Yuan Bo Peng
817-272-5222
ypeng@uta.edu 

Dr. Linda Perrotti
817-272-1202
perrotti@uta.edu 

Dr. Qing Lin
817-272-0154
qilin@uta.edu