ORCID Profile
0000-0002-0247-1362
Current Organisation
University of York
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Publisher: Wiley
Date: 22-03-2005
Publisher: American Physiological Society
Date: 08-2005
Abstract: Persistent gamma frequency (30–70 Hz) network oscillations occur in hippoc al slices under conditions of metabotropic glutamate receptor (mGluR) activation. Excessive mGluR activation generated a bistable pattern of network activity during which epochs of gamma oscillations of increasing litude were terminated by synchronized bursts and very fast oscillations ( Hz). We provide experimental evidence that, during this behavior, pyramidal cell-to-interneuron synaptic depression takes place, occurring spontaneously during the gamma rhythm and associated with the onset of epileptiform bursts. We further provide evidence that excitatory postsynaptic potentials (EPSPs) in pyramidal cells are potentiated during the interburst gamma oscillation. When these two types of synaptic plasticity are incorporated, phenomenologically, into a network model previously shown to account for many features of persistent gamma oscillations, we find that epochs of gamma do indeed alternate with epochs of very fast oscillations and epileptiform bursts. Thus the same neuronal network can generate either gamma oscillations or epileptiform bursts, in a manner depending on the degree of network drive and network-induced fluctuations in synaptic efficacies.
Publisher: Springer Science and Business Media LLC
Date: 02-1995
DOI: 10.1038/NG0295-197
Abstract: The prion protein (PrP) is central to the aetiology of the prion diseases, transmissible neurodegenerative conditions of humans and animals. PrP null mice show abnormalities of synaptic neurophysiology, in particular weakened GABAA receptor-mediated fast inhibition and impaired long-term potentiation in the hippoc us. Here we demonstrate that this PrP null phenotype is rescued in mice with a high copy number of a transgene encoding human PrP but not in low copy number mice, confirming the specificity of the phenotype for loss of function of PrP. The ability of human PrP to compensate for loss of murine PrP will allow direct study of the functional consequences of the 18 human PrP mutations, which cause the inherited prion diseases this phenotype can now form the basis of the first functional assay for PrP.
Publisher: American Physiological Society
Date: 04-2007
Abstract: Generation of gamma rhythms in reciprocally connected areas of cortex produces synchronous neuronal firing, although little is known about the consequences of gamma rhythms when generated in nonreciprocally connected regions. This nonreciprocity exists in hippoc us, where gamma rhythms are generated in area CA3 in vitro and in vivo and nonreciprocally projected to area CA1 by the Schaffer collateral pathway. Here we demonstrate how this CA3 gamma rhythm generates two different patterns of local CA1 oscillation dependent on the degree of output from area CA1. 1) In conditions where activity projected to area CA1 produces only very low principal cell recruitment the local population rhythm mimics the gamma rhythm projected from CA3. This activity is generated predominantly by recruitment of CA1 basket cells in a manner dependent on phasic, feedforward excitation of this interneuron subclass. Interneurons in stratum oriens, not receiving CA3 feedforward input, fired at theta frequencies. 2) In the presence of serotonin CA1 principal cell recruitment was appreciably enhanced, resulting in dual activation of CA1 basket cells through both feedforward and feedback excitations. Feedback excitation to CA1 stratum oriens interneurons was also enhanced. The resulting change in interneuron network dynamics generated a beta-frequency CA1 rhythm (as a near-subharmonic of the gamma rhythm projected from CA3). These findings demonstrate that in nonreciprocally connected networks, the frequency of population rhythms in target areas serves to code for degree of principal cell recruitment by afferent input.
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Miles Adrian Whittington.