center for molecular and behavioral neuroscience contributing faculty and research
Biopsychosocial Models of Risk for PTSD
Researcher: Matthew Morris, Ph.D.
Funding Source: National Institute of Child Health/Human Dev. (NICHD)
Project Summary: This project seeks to identify cognitive and neurobiological markers of risk for posttraumatic stress disorder (PTSD) and/or major depressive disorder (MDD) in the acute aftermath of trauma. The study will investigate longitudinal pathways leading from interpersonal violence (IPV) exposure to PTSD and/or MDD in a sample of 60 women recently exposed to IPV and 40 non-exposed women using four waves of data collection (within one month after exposure to IPV, and at one, three, and six months following the initial assessment). Although women are twice as likely as men to develop PTSD and/or MDD after exposure to trauma, the mechanisms underlying this increased risk remain unclear. Identifying individuals at elevated risk for these disorders is critical for developing effective early intervention programs.
Twum Ansah, Ph.D.
Department of Neuroscience and Pharmacology
The research in Dr. Twum Ansah's laboratory seeks to understand the neurobiological mechanisms that mediate neurological disorders, such as Parkinson's Disease as well as psychiatric disorders such as depression and drug abuse, all of which involve the dopaminergic system and its regulation by other systems, such as the serotonergic system. His major research efforts are being devoted to systematically investigate alterations in the serotonergic system and to understand its role in the hypokinesia produced by lesioning of the dopaminergic system with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The objective is to understand the role of serotonin in the neurobiology of Parkinson's Disease and how manipulating the serotonergic system might alter the course of the disease, as a prelude to identification of novel therapeutic targets for the disease.
Clivel George Charlton, Ph.D.
Professor and Chairman
Department of Neurobiology and Neurotoxicology
Dr. Charlton's laboratory is exploring the possible causal relationship between excess methylation in the brain and Parkinson's disease. Methylation depletes the amount of the essential neurotransmitter dopamine and increases levels of lyso-phosphatidyl choline, which disrupts the structure of biological membranes in the microcompartment where this occurs. Dr. Charlton and his colleagues have observed that injection of the methyl donor, S-adenosyl-methionine (SAM), into the brain of rodents results in extensive brain methylation and causes transient tremor, hypokinesia, rigidity, and abnormal posture, changes that resemble the motor deterioration that accompanies Parkinson's. Consistent with their hypothesis of a role of methylation in the pathway leading to Parkinson's disease is the finding that MPP+, a toxic metabolite linked to Parkinson's disease development in human beings, increases SAM-dependent methylation in the brain. The laboratory is exploring possible therapeutic interventions to alter these methylation processes. Interestingly, a current Parkinson's therapy, L-dopa, diminishes the Parkinson's-like symptoms in SAM-injected rats. However, there are considerable side effects and loss of effects of L-dopa when given therapeutically. Dr. Charlton and his colleagues are also exploring the molecular basis for these unwanted treatment sequelae.
Sukhbir Mokha, Ph.D.
Professor, Meharry Department of Neuroscience and Pharmacology
Adjunct Professor of Pharmacology, Vanderbilt University
Director of Graduate Studies, Neuroscience Program
Dr. Mokha's laboratory is investigating the neurobiology of pain and analgesia in normal and pathological states using electrophysiological, behavioral, cellular, and molecular techniques. Many painful syndromes/disorders such as migraine, trigeminal neuralgia, temporomandibular joint disorder (TMJ/TMD), and irritable bowel syndrome (IBS) are more prevalent in women than in men. Dr. Mokha and his colleagues are interested in understanding the biological mechanisms that generate the higher prevalence of painful syndromes in women. Specifically, the laboratory is investigating whether activation of endogenous noradrenergic or serotonergic pathways involving G protein–coupled receptors (opioid, noradrenergic, and serotonergic) produce estrogen-dependent, sex-specific inhibition of pain mechanisms , in both spinal and trigeminal systems. Estrogen-dependent decreased inhibition in the female could contribute to the higher prevalence of painful syndromes in women. They have already provided evidence that estrogen decreases the analgesic effects produced by activation of α₂-adrenoceptors and opiod or opiod-like receptors (ORL1) in the spinal cord and trigeminal system and have shown that estrogen alters the expression of the gene encoding ORL1.
Mitchell Parks, M.D.
Assistant Professor, Department of Psychiatry & Behavioral Sciences
Dr. Parks's research examines the nexus of two health disparities in African-American women: their documented increased incidence of alcohol use disorders and their prevalence of HIV infection. The technique employed to address the question of why these two disparities occur in this population is functional magnetic resonance imaging (fMRI). fMRI utilizes hemoglobin as a natural tracer to differentially determine activity in brain areas. Dr. Parks's previous work with chronic alcoholic patients determined their different utilization of frontal and parietal regions in response to simple motor tasks. The objective in the work with African-American women is to use fMRI to determine whether routine or binge ingestion of alcohol incurs changes in brain physiology that might lead to HIV infection risk.