James H. Meador‐Woodruff

ORCID: 0000-0002-3015-281X
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Receptor Mechanisms and Signaling
  • Ion channel regulation and function
  • Neurotransmitter Receptor Influence on Behavior
  • Schizophrenia research and treatment
  • Tryptophan and brain disorders
  • Amino Acid Enzymes and Metabolism
  • Memory and Neural Mechanisms
  • Neural dynamics and brain function
  • Nicotinic Acetylcholine Receptors Study
  • Glycosylation and Glycoproteins Research
  • Cellular transport and secretion
  • Functional Brain Connectivity Studies
  • Neuropeptides and Animal Physiology
  • Treatment of Major Depression
  • Biochemical Analysis and Sensing Techniques
  • Genetics and Neurodevelopmental Disorders
  • Diet and metabolism studies
  • Neurogenesis and neuroplasticity mechanisms
  • Endoplasmic Reticulum Stress and Disease
  • Neurological disorders and treatments
  • Smoking Behavior and Cessation
  • Bipolar Disorder and Treatment
  • RNA Research and Splicing
  • Carbohydrate Chemistry and Synthesis

University of Alabama at Birmingham
2014-2023

Icahn School of Medicine at Mount Sinai
2015

Behavioral Pharma (United States)
2015

University of Arizona
2012-2013

Civitan International
2012

In-Q-Tel
2010

University of Michigan
1999-2009

Memorial Sloan Kettering Cancer Center
2006

Yale University
2006

University of Maryland, Baltimore
2006

The distribution of mRNA coding for the D2 dopamine receptor was studied in rat brain by situ hybridization. A cDNA probe corresponding to putative third cytosolic loop and sixth seventh transmembrane domains used generate an 35S-labeled riboprobe hybridize mRNA. found both projection fields regions associated with dopamine-containing cell bodies, suggesting postsynaptic presynaptic autoreceptor localization. Highest concentrations were neostriatum, olfactory tubercle, substantia nigra,...

10.1073/pnas.86.19.7625 article EN Proceedings of the National Academy of Sciences 1989-10-01

Both thalamic and glutamatergic dysfunction have been implicated in the pathophysiology of schizophrenia. The authors examined ionotropic glutamate receptor expression postmortem samples from patients with schizophrenia comparison subjects, using hypothesis that differs limbic nuclei thalamus schizophrenia.N-Methyl-D-aspartate (NMDA), AMPA, kainate was determined six 12 subjects DSM-III-R diagnoses eight psychiatrically normal individuals. used situ hybridization to determine NMDAR1,...

10.1176/appi.ajp.157.11.1811 article EN American Journal of Psychiatry 2000-11-01

OBJECTIVE: Recent investigations of schizophrenia have targeted glutamatergic neurotransmission, since phencyclidine, an N-methyl-d-aspartate (NMDA) receptor antagonist, can induce schizophreniform psychosis. The authors previously reported alterations in thalamic NMDA subunit expression schizophrenia, consistent with the hypothesis that hypofunction may contribute to pathophysiology this illness. In study they generalized include other molecules glutamate synapse, specifically excitatory...

10.1176/appi.ajp.158.9.1393 article EN American Journal of Psychiatry 2001-09-01

Abstract We investigated the expression of metabotropic glutamate receptors (mGluR) in prefrontal cortex (PFC) and striatum schizophrenia. mGluRs modulate release reuptake synaptic mediate some molecular correlates neuroplasticity, including long‐term potentiation. The are expressed widely PFC striatum, regions often implicated pathophysiology Thus, we hypothesized that abnormal might contribute to glutamatergic dysfunction observed Accordingly, measured (mGluRs) Brodmann areas 9, 11, 32, 46...

10.1002/syn.20164 article EN Synapse 2005-06-08
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