John F. MarshallProfessor, Neurobiology and Behavior Joint Appointment, Pharmacology |
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Research Interests |
Recovery of function after brain injury; cellular factors contributing to neurodegeneration; organization of basal ganglia motor systems; computer-assisted quanlitative localization of transmitter receptors in central nervous system | |
| URLs | darwin.bio.uci.edu/neurobio/Faculty/Marshall/marshall.htm | |
| Neurobiology & Behavior Home Page | ||
| Pharmacology Home Page | ||
| PUB MED | ||
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Academic Distinctions |
1974-1975 Fellow, Foundations Fund for Research in Psychiatry 1980-1982 Fellow in Neuroscience, Alfred N. Sloan Foundation 2005 Elected Fellow, American Association for the Advancement of Science |
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Research Abstract |
Our research centers on the capacity for reorganization in the central nervous system. Animals that sustain sudden injury to particular brain pathways can exhibit remarkable improvement in sensory and motor functions. Although the models of strutural and chemical reorganization in the brain-damaged animals provided new insight into the remarkable diversity of neuronal mechanisms that permit restoration of function, human neurodegenerative disorders (especially those associated with aging-such as Parkinson's and Alzheimer's diseases) are insidious in onset. Two major forefronts of research are to identify the processes that dispose certain neurons to degenerate in these diseases, and to determine means by which the brain's compensatory mechanisms may be induced to retard slow degenerative processes or to counteract their function consequences. These considerations have prompted an analysis of patterns of brain dopaminergic innervation of the basal ganglia and studies of the distribution of the major subtypes of dopamine receptor (D-1 and D-2) in this motor area. In particular, using quantitative autoradiographic markers for the dopamine nerve terminals as well as for the D-1 and D-2 receptors, a complete picture has emerged of the organization of dopaminergic synapses in this structure. Important new information has emerged from our research concerning how this synaptic neurochemistry reorganizes itself in rodent and nonhuman primate models of Parkinson's disease. Similar analyses have been performed on postmortem human basal ganglia tissue, and experiments are planned to extend these studies to postmortem tissue derived from patients with diagnosed Parkinsonism. Our research also is actively investigating factors responsible for the neurodegeneration occurring in Parkinsonism by using animals that undergo injury to the nigrostriatal dopamine projection as a consequence of exposure to neurotoxic agents (6-hydroxydopamine, MPTP, methamphetamine) or as a mutation ("weaver" mouse). Just as in Parkinson's disease, rodents undergoing degeneration to this pathway show considerable heterogeneity in their pathology, with certain dopamine-containing neurons being more vulnerable than others to injury. Cellular markers that distinguish vulnerable from resistant neurons have been identified. |
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| Publications |
Recent Publications: McPherson, R.J. and Marshall, J.F. Substantia nigra glutamate antagonists produce contralateral turning and basal ganglia Fos expression: Interactions with D1 and D2 dopamine receptor agonists. Synapse 36: 194-204, 2000. O’Dell, S.J. and Marshall, J.F. Repeated administration of methamphetamine damages cells in the somatosensory cortex: Overlap with cytochrome oxidase-rich barrels. Synapse 37: 32-37, 2000. Schuller, J.J. and Marshall, J.F. Acute immediate-early gene response to 6-hydroxydopamine lesions of the medial forebrain bundle. Neuroscience 96: 51-58, 2000. Neisewander, J.L., Baker, D.A., Fuchs, R.A., Tran-Nguyen, L.T.L., Palmer, A., and Marshall, J.F. Fos protein expression in rats following exposure to cocaine and cocaine-paired environmental stimuli. Journal of Neuroscience 20: 798-805, 2000. LaHoste, G.J., Henry, B.L., and Marshall, J.F. Dopamine D1 receptors synergize with D2, but not D3 or D4, receptors in the striatum without the involvement of action potentials. Journal of Neuroscience 20: 6666-6671, 2000. Marshall, J.F., Henry, B.L., Billings, L.M., and Hoover, B.R. The role of globus pallidus D2 subfamily of dopamine receptors in pallidal immediate early gene expression. Neuroscience 105: 365-378, 2001. Marshall, J.F., Hoover, B.R. and Schuller, J.J. The enkephalin-expressing cells of the rodent globus pallidus. In The Basal Ganglia VI (Graybiel, A.N., DeLong, M.R., and Kitai, S.T., Eds.) Kluwer Press, 2002. O’Dell, S.J. and Marshall, J.F. Effects of vibrissae removal on methamphetamine-induced damage to rat somatosensory cortical neurons. Synapse 43: 122-130, 2002. Hoover, B.R. and Marshall, J.F. Further characteristics of preproenkephalin mRNA-containing cells in the rodent globus pallidus. Neuroscience 111: 111-125, 2002. Schröder, N., O'Dell, S.J., Marshall, J.F. Neurotoxic methamphetamine regimen severely impairs recognition memory in rats. Synapse 49: 89-96, 2003. Billings, L.M., Marshall, J.F. D2 antagonist-induced c-fos in an identified subpopulation of globus pallidus neurons by a direct intrapallidal action. Brain Research. 964: 237-243, 2003. Hoover, B.R. and Marshall, J.F. Molecular, chemical, and anatomical characterization of globus pallidus dopamine D2 receptor mRNA-containing neurons. Synapse 52: 100-113, 2004. Billings, L.M. and Marshall, J.F. Glutamic acid decarboxylase 67 mRNA regulation in two globus pallidus neuron populations by dopamine and the subthalamic nucleus. Journal of Neuroscience 24: 3094-3103, 2004. Miller C.A. and Marshall J.F. Altered prelimbic cortex output during cue-elicited drug seeking. Journal of Neuroscience 24: 6889-97, 2004. O’Dell, S.J. and Marshall, J.F. Neurotoxic regimens of methamphetamine induce persistent expression of phospho-c-Jun in somatosensory cortex and substantia nigra. Synapse, 55: 137-147, 2004. Trevitt, J.T., Morrow, J. and Marshall, J.F., Dopamine manipulation alters immediate early gene response of striatal parvalbumin interneurons to cortical stimulation. Brain Research 1035: 41-50, 2005. Miller C.A. and Marshall J.F. Altered Fos expression in neural pathways underlying cue-elicited drug seeking in the rat. European Journal of Neuroscience 21: 1385-1393, 2005. Belcher, A.M., O’Dell, S.J. and Marshall, J.F. Impaired object recognition memory following methamphetamine but not p-chloroamphetamine or d-amphetamine-induced neurotoxicity. Neuropsychopharmacology 30(11):2026-34, 2005. Miller, C.A. Marshall, J.F., Molecular substrates for retrieval and reconsolidation of cocaine-associated contextual memory. Neuron. 47(6):873-84, 2005. Belcher AM, O'Dell SJ, Marshall JF., A sensitizing regimen of methamphetamine causes impairments in a novelty preference task of object recognition. Behav Brain Res. 170:167-172, 2006. Marshall, J.F., Belcher, A.M., Feinstein, E.M. and O’Dell, S.J., Animal models of long-term neural and cognitive changes after methamphetamine administration. Addiction (Submitted). O’Dell, S.J., Gross, N.B., Fricks, A.N., Casiano, B.D., Nguyen, T.B., and Marshall, J.F. Running wheel exercise enhances recovery from nigrostriatal dopamine injury without inducing neuroprotection, Neuroscience (Accepted pending final revision). |
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Professional Societies |
2005 Molecular and Cellular Cognition Society 1999 International Basal Ganglia Society 1991 International Brain Research Organization 1991 New York Academy of Sciences 1989 Integrative/Behavioral Neuroscience Group 1978 Brain Neurochemicals and Behavior Society 1977 Society for Neuroscience 1973 American Association for the Advancement of Scie 1972 Society of Sigma Xi 1970 Phi Beta Kappa |
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| Graduate Programs |
Neurobiology and Behavior Pharmacology and Toxicology |
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| Link to this profile | http://www.faculty.uci.edu/profile.cfm?faculty_id=2141 | |
| Last updated | 10/12/2007 | |