Neurotoxicology and Alcohol Study Section – NAL
The Neurotoxicology and Alcohol [NAL] Study Section reviews applications that address the effects of environmental toxicants or alcohol on the central nervous system in animal models and humans.
Environmental toxicants include air pollution (diesel exhaust, organic compounds, ambient particulate matter) metals, plasticizers, pesticides, and others. The emphasis of the alcohol research in this study section is on the negative consequences of alcohol exposure throughout development and in adulthood, rather than motivational aspects of alcohol addiction. The approaches include molecular, cellular, pharmacological, physiological, behavioral, neuroimaging, genetic, and computational.
Review Dates
Topics
- Neuroteratology: effects of acute or chronic prenatal or early exposure to environmental toxins on development of the central nervous system.
- Fetal alcohol spectrum disorders: anatomical and behavioral effects of prenatal alcohol exposure on the central nervous system, and associated phenotypes.
- Neurodegeneration: effects of acute or chronic exposure to neurotoxins or alcohol on oxidative stress, neuroinflammation, neurodegeneration, cognitive deficits, motor impairment and development of neurodegenerative diseases (e.g. Parkinson’s disease, Alzheimer’s disease, ALS, etc.).
- Gene environment interaction: genetic factors responsible for increased vulnerability to neurotoxicants or alcohol use disorder.
- Alcohol dependence: epigenetic, molecular, and cellular effects of alcohol exposure; synaptic, structural, and behavioral adaptations resulting from chronic or repeated alcohol exposure, and associated with symptoms of alcohol withdrawal and negative affect, such as anxiety and depression.
- Interaction between stress and alcohol: maladaptive responses to acute, chronic or developmental stress associated with increased alcohol consumption and relapse to alcohol abuse.
Shared Interests and Overlaps
Applications with a focus on behavioral mechanisms of alcohol abuse, such as discriminative and reinforcing effects of alcohol, social influences, and behavioral economic approaches may be reviewed by Biobehavioral Regulation, Learning and Ethology Study Section [BRLE].
Applications examining the reward circuitry and motivational aspects of alcohol addiction may be reviewed by Neurobiology of Motivated Behavior (NMB).
Applications including alcohol or neurotoxicology, but focused on neuroimmunology may be reviewed in Behavioral Neuroendocrinology, Neuroimmunology, Rhythms, and Sleep [BNRS].
There are shared interests in human subject studies of behavioral neuropharmacology/behavioral toxicology particularly the effects of chronic exposure to alcohol with Neural Basis of Psychopathology, Addictions, and Sleep Disorders (NPAS). Applications that emphasize the use of animal models and humans with an emphasis on the negative consequences of alcohol exposure throughout development and in adulthood, rather than motivational aspects of alcohol addiction are reviewed in NAL. Applications that emphasize etiology, pathophysiology, and treatment of alcoholism and are clinically-oriented are reviewed in NPAS.
There are shared interests in neurotoxicology with Child Psychopathology and Developmental Disabilities (CPDD). Applications that emphasize the general effects of environmental toxicants (such as pesticides or metals) or alcohol on the central nervous system are reviewed in NAL. Applications that emphasize infant and child developmental outcomes following early teratogen exposure are more reviewed in CPDD.
There are shared interests in the effects of toxicants (e.g., organophosphates, heavy metals) that effect the nervous system with Environmental Determinants of Disease (EDD). Applications that emphasize neurotoxicology in model systems or that address the effects of environmental toxicants or alcohol on the central nervous system in animal models and humans are reviewed in NAL. Applications that focus on the effects of environmental toxicants outside the central nervous system are reviewed in EDD.