Behavioral Neuroscience

Behavioral Neuroscience and Neurophysiology Laboratories

The Behavioral Neuroscience and Neurophysiology Laboratories are a component of the UTA Department of Psychology. The laboratories use modern behavioral and electrophysiological analyses to explore the underlying relationship between neuronal function and behavior. This integrative approach involves the use of molecular biology, biochemistry, immunocytohistochemistry, neurophysiology, anatomy, and a wide range of behavioral methodology to understand the function of the nervous system. Members of the neuroscience subprogram use these approaches to explore behavior, pain processing, learning and memory, anxiety, depression and mechanisms underlying drug abuse and addiction.

Pain Research

Pain is a significant national health problem. It is the most common reason individuals seek medical care, with 40 million medical visits annually, costing the American public more than $100 billion each year. Thus, both clinical and basic studies share equal importance in helping benefit patients suffering various conditions of pain. There are various tools to address the pain problem. Here at UTA, we are studying pain by means of basic research and biopsychosocial research. The major interest of our basic research focuses on studying the neurophysiological mechanisms of nociception by means of electrophysiological and behavioral neuroscience techniques.

Yuan Bo Peng, M.D., Professor

Dr. Peng’s research interests include physiological mechanisms of pain. His lab is interested in studying the neurophysiological mechanisms of nociception by means of electrophysiological techniques in both the peripheral and central nervous systems. His lab has 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., Associate Professor

Mechanisms of Neurogenic Inflammation Induced Pain is a research project funded by the National Institutes of Health (NIH). 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 Perrotti, Professor

Dr. Perrotti’s 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 her work is to clarify interactions among the neuroendocrine system and dopamine reward system using rodent models of addictive behaviors. Her 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, She investigates the initiation, acquisition, expression, extinction and reacquisition of conditioned drug reward. She is particularly interested in the biochemical and neuroendocrine factors which predispose certain individuals to respond differentially to drugs of abuse. The goal of her lab’s 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.

NEURAL - NET MODELING AND DECISION MAKING 

Daniel Levine, Professor of Research

Dr. Levine's laboratory deals with both experimental and theoretical studies of decision making, cognitive-emotional interactions, and cognitive dissonance. Current research projects include:

• Simulated gambling tasks in which the participant has to decide between two alternatives that provide different probabilities of winning or losing different amounts of (virtual, not actual) money. Dr. Levine and his students look at the effects of various personality variables on gambling choices. They also consider the effect of how the alternatives are presented and how preferences are elicited.
• Studying how emotion contributes to perceived value of resources. Responses of the same participants are compared on two analogous tasks, both involving an unexpected loss after a sequence of gains. Preliminary results suggest the amount of time participants are willing to invest could differ between the two tasks.
• Studying different methods people use to reduce cognitive dissonance. Typically, cognitive dissonance studies assess the degree to which people will change relatively trivial attitudes or beliefs to be consonant with their behavior. However, when attitudes are particularly central to the person’s core identity, it is believed that they will use different methods to resolve cognitive dissonance than attitude change.

The laboratory also has a long-term goal of understanding how interactions among several brain regions (frontal lobes, amygdala, basal ganglia, etc.) contribute to emotionally-influenced decision making. To that end, the laboratory is involved in a collaborative project with a brain imaging laboratory at UT Southwestern to discern relationships between brain region activations and decision style on a probability maximization task. Also, the lab has a long history of pioneering work in brain-based neural network modeling of cognition and behavior (see Dr. Levine), and current modeling efforts are being integrated with the behavioral and physiological studies described above. For information about applying to work in Dr. Levine’s lab, contact him at levine@uta.edu or 817-272-3598.

Stephen G. Lomber, Professor

Cortical plasticity is the neural mechanism by which the cerebrum adapts itself to its environment, while at the same time making it vulnerable to impoverished sensory or developmental experiences.  Like the visual system, auditory development passes through a series of sensitive periods in which circuits and connections are established and then refined by experience.  Current research is expanding our understanding of cerebral processing and organization in the deaf.  In the congenitally deaf, higher-order areas of "deaf" auditory cortex demonstrate significant crossmodal plasticity with neurons responding to visual and somatosensory stimuli.  This crucial cerebral function results in compensatory plasticity.  Not only can the remaining inputs reorganize to substitute for those lost, but this additional circuitry also confers enhanced abilities to the remaining systems.  Work in our lab seeks to understand the structure and function of “deaf” auditory cortex using psychophysical, electrophysiological, and connectional anatomy approaches and consider how this knowledge informs our expectations of the capabilities of cochlear implants in the developing brain.

Website: www.cerebralsystems.ca