Master of Arts (MA)
First Committee Member
Second Committee Member
Third Committee Member
Fourth Committee Member
Frank Van Breukelen
Number of Pages
Schizophrenia is a debilitating mental disorder that affects up to 3% of the world population. The behavioral symptoms are categorized into positive and negative symptoms, which appear during late adolescence/early adulthood. Unfortunately, the underlying cellular and molecular mechanisms of the disease are poorly understood. Several hypotheses exist to explain mechanisms contributing to these behavioral alterations. One model proposes that a reduced function of the NMDA glutamate receptor on specific GABAergic interneurons may be responsible for deficits in schizophrenia. Post-mortem investigations provide evidence of reductions in both glutamate and GABA-related proteins in patients with schizophrenia. Further, GABAergic interneurons that are activated by glutamate via NMDA receptors are important for oscillatory activity involved with sensory processing and cognitive function. Alterations in the function of NMDA receptors on GABAeric interneurons are implicated in regulating neural network activity and, if disrupted, could potentially lead to altered brain function and deficits seen in schizophrenia. Several investigations have demonstrated reduction in NMDA receptor function or GABA receptor function induces deficits consistent with schizophrenia. Recent approaches have also focused on changes in NMDA or GABA function related to schizophrenia as a neurodevelopmental disorder. This approach suggests that alterations in either system during brain development may result in behavioral deficits later in life. The purpose of the below studies was to determine if changes in NMDA receptor function or alterations in downstream GABA receptor function during development in rodent pups results in behavioral or biochemical alterations in adulthood that are relevant to schizophrenia. The data reveal that altering these receptor systems in development produce deficits in adulthood. Changes in sensorimotor gating, spatial learning and memory, and differential expression of multiple GABA related proteins in the brain tissue were observed in these animals.
Development; GABA; GABA – Receptors; Methyl aspartate; NMDA; Prepulse inhibition; Schizophrenia; Water maze
Biology | Medical Neurobiology | Neuroscience and Neurobiology | Neurosciences | Psychology
University of Nevada, Las Vegas
Bolton, Monica, "Alternations of NMDA and GABAB Receptor Function in Development: A Potential Animal Model of Schizophrenia" (2013). UNLV Theses, Dissertations, Professional Papers, and Capstones. 1918.
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