J
James M. Tepper
Researcher at Rutgers University
Publications - 88
Citations - 8483
James M. Tepper is an academic researcher from Rutgers University. The author has contributed to research in topics: Medium spiny neuron & GABAergic. The author has an hindex of 46, co-authored 87 publications receiving 7932 citations. Previous affiliations of James M. Tepper include Hungarian Academy of Sciences.
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Inhibitory control of neostriatal projection neurons by GABAergic interneurons.
Tibor Koós,James M. Tepper +1 more
TL;DR: Paired whole-cell recordings are used to show that inhibitory synaptic potentials generated from single interneurons are sufficiently powerful to delay or entirely block the generation of action potentials in a large number of projection neurons simultaneously.
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Functional diversity and specificity of neostriatal interneurons.
James M. Tepper,J. Paul Bolam +1 more
TL;DR: The role of cholinergic interneurons is to modulate the sub- and supra-threshold responses of spiny neurons to cortical and/or thalamic excitation, particularly in reward-related activities.
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GABAergic microcircuits in the neostriatum
TL;DR: New data are incompatible with current "winner-take-all" models of lateral inhibitory function in the neostriatum, and they force a modification of established concepts of the functional roles of feedback inhibition in this nucleus.
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Heterogeneity and diversity of striatal GABAergic interneurons.
TL;DR: The anatomy, neurochemistry, electrophysiology, synaptic connections, and function of the three “classic” striatal GABAergic interneurons are reviewed, based on more recent data derived from in vitro recordings from BAC transgenic mice as well as recent in vivo data.
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GABAA receptor-mediated inhibition of rat substantia nigra dopaminergic neurons by pars reticulata projection neurons
TL;DR: A model in which the firing pattern of nigral dopaminergic neurons in vivo is modulated differentially by disin inhibition of GABAA inputs arising from pars reticulata projection neuron axon collaterals and disinhibition of pallidonigral GABAergic inputs mediated by GABAB receptors is proposed.