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Anita K. Roopun

Researcher at Newcastle University

Publications -  17
Citations -  2190

Anita K. Roopun is an academic researcher from Newcastle University. The author has contributed to research in topics: Population & Bursting. The author has an hindex of 15, co-authored 17 publications receiving 2045 citations. Previous affiliations of Anita K. Roopun include University of Leeds & University of Newcastle.

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Single-column thalamocortical network model exhibiting gamma oscillations, sleep spindles, and epileptogenic bursts

TL;DR: It is shown that epileptiform bursts, including double and multiple bursts, containing VFO occur in rat auditory cortex in vitro, in the presence of kainate, when both GABA(A) and GABA(B) receptors are blocked.
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A beta2-frequency (20–30 Hz) oscillation in nonsynaptic networks of somatosensory cortex

TL;DR: A beta2 frequency oscillation occurring in vitro in networks of layer V pyramidal cells, the cells of origin of the corticospinal tract, depends on gap junctional coupling, but it survives a cut through layer 4 and, hence, does not depend on apical dendritic electrogenesis.
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Temporal Interactions between Cortical Rhythms

TL;DR: A frequency transformation in which activity in two co-active local circuits may combine sequentially to generate a third frequency whose period is the concatenation sum of the original two is discussed, suggesting a robust mechanism for combining information processed on multiple concurrent spatiotemporal scales.
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A role for fast rhythmic bursting neurons in cortical gamma oscillations in vitro

TL;DR: It is demonstrated that fast rhythmic bursting neurons may function by providing a large-scale input to an axon plexus consisting of gap-junctionally connected axons from both FRB neurons and their anatomically similar counterparts regular spiking neurons.
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Region-Specific Changes in Gamma and Beta2 Rhythms in NMDA Receptor Dysfunction Models of Schizophrenia

TL;DR: It is concluded that many observed changes in markers for GABAergic function in schizophrenia may be secondary to deficits in NMDA receptor-mediated excitatory synaptic activity, and the broad range of changes in cortical dynamics seen in schizophrenia might be more directly attributable to underlying deficits in glutamatergic neuronal communication.