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Max L. Schiff

Researcher at Vanderbilt University

Publications -  13
Citations -  603

Max L. Schiff is an academic researcher from Vanderbilt University. The author has contributed to research in topics: Receptive field & Auditory cortex. The author has an hindex of 8, co-authored 13 publications receiving 561 citations. Previous affiliations of Max L. Schiff include Salk Institute for Biological Studies & Center for Neural Science.

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Tyrosine-kinase-dependent recruitment of RGS12 to the N-type calcium channel

TL;DR: Results indicate that RGS12 is a multifunctional protein capable of direct interactions through its PTB domain with the tyrosine-phosphorylated calcium channel, and recruitment of RGS proteins to G-protein effectors may represent an additional mechanism for signal termination in G- protein-coupled pathways.
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Synaptic mechanisms underlying auditory processing.

TL;DR: These findings challenge existing models of auditory processing in which broadly tuned lateral inhibition is used to limit excitatory receptive fields and suggest new mechanisms by which inhibition and short term plasticity shape neural responses.
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Linking the response properties of cells in auditory cortex with network architecture: cotuning versus lateral inhibition.

TL;DR: It is found that the amplitude of synaptic responses in AI varies non-monotonically with the intensity of the stimulation in the medial geniculate nucleus (MGv).
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Anatomical Identification of Extracellularly Recorded Cells in Large-Scale Multielectrode Recordings

TL;DR: A novel approach to the central problem of anatomically identifying recorded cells, based on the electrical image: the spatiotemporal pattern of voltage deflections induced by spikes on a large-scale, high-density multielectrode array.
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Regulators of G Protein Signaling Proteins as Determinants of the Rate of Desensitization of Presynaptic Calcium Channels

TL;DR: It is found that recombinant Gα interacting protein (GAIP) and regulators of G protein signaling (RGS)4 selectively accelerate the rate of desensitization of Go- and Gi-mediated pathways, respectively.