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Gavin Woodhall - Aston University. Birmingham, , GB

Gavin Woodhall Gavin Woodhall

Professor, Aston Pharmacy School | Aston University

Birmingham, UNITED KINGDOM

Professor Woodhall researches electrophysiological studies on neurones of the entorhinal cortex (EC) and the hippocampus.

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What causes epilepsy? That is the question - Professor Gavin Woodhall

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Biography

Professor Woodhall researches electrophysiological studies on neurons of the entorhinal cortex (EC) and the hippocampus.

Additional interests include the role of glutamate and GABA receptors in epilepsy in the brain; the role of homeodynamic synaptic scaling in epileptogenesis in the temporal lobe. Autoimmune epilepsies, psychosis and neuronal network dynamics; the relationship between epilepsy and affective disorders. The role of cannabinoids in epilepsy treatment (collaboration with GW Pharma). The role of the primary motor cortex in epilepsy and Parkinson’s disease (in collaboration with Dr. Stuart Greenhill).

The temporal lobe is a brain region which is especially prone to epilepsy. His research focuses on how epilepsy is established, and how dynamic changes in receptor expression and function lead to changes in neuronal network behaviour that may underlie epileptic seizures. Additionally, he is interested in how neuronal network dynamics alter in schizophrenia, and how epilepsy and schizophrenia relate to each other in terms of pathological network function.

Areas of Expertise (4)

Neuronal Network Dynamics

Schizophrenia

Epilepsy

Hippocampus

Education (1)

University of Southampton: PhD 1994

Media Appearances (2)

Aston Institute of Health and Neurodevelopment officially launches new £2.8m MRI scanner

EurekAlert!  online

2022-04-26

After an official ribbon-cutting ceremony hosted by the Institute co-directors Professor Jackie Blissett and Professor Gavin Woodhall, guests were invited to take a tour of the new MRI scanner facilities where imaging researchers were on hand to showcase and discuss their research for which the new MRI scanner is a vital facility.

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What causes epilepsy? That is the question - Professor Gavin Woodhall

Epilepsy Sparks Insights  online

2021-08-12

Meet Prof. Gavin Woodhall, a neuropharmacologist, epilepsy researcher, and director for the Institute for Health and Neurodevelopment at Aston University, Birmingham, UK. Or, as Gavin would say “Mostly, I just run a lab!”. Gavin is particularly interested in severe epilepsy syndromes. A key question of his is “What makes a brain develop epilepsy (epileptogenesis)?”

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Articles (3)

The AMPA receptor antagonist perampanel suppresses epileptic activity in human focal cortical dysplasia

Epilepsia Open

2022 Focal cortical dysplasia (FCD) is one of the most common malformations causing refractory epilepsy. Dysregulation of glutamatergic systems plays a critical role in the hyperexcitability of dysplastic neurons in FCD lesions. The pharmacoresistant nature of epilepsy associated with FCD may be due to a lack of well-tolerated and precise antiepileptic drugs that can target glutamate receptors. Here, for the first time in human FCD brain slices, we show that the established, noncompetitive α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist, perampanel has potent antiepileptic action. Moreover, we demonstrate that this effect is due to a reduction in burst firing behavior in human FCD microcircuits. These data support a potential role for the treatment of refractory epilepsy associated with FCD in human patients.

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Encephalitis patient-derived monoclonal GABAA receptor antibodies cause epileptic seizures

Journal of Experimental Medicine

2021 Autoantibodies targeting the GABAA receptor (GABAAR) hallmark an autoimmune encephalitis presenting with frequent seizures and psychomotor abnormalities. Their pathogenic role is still not well-defined, given the common overlap with further autoantibodies and the lack of patient-derived mAbs. Five GABAAR mAbs from cerebrospinal fluid cells bound to various epitopes involving the α1 and γ2 receptor subunits, with variable binding strength and partial competition. mAbs selectively reduced GABAergic currents in neuronal cultures without causing receptor internalization. Cerebroventricular infusion of GABAAR mAbs and Fab fragments into rodents induced a severe phenotype with seizures and increased mortality, reminiscent of encephalitis patients’ symptoms. Our results demonstrate direct pathogenicity of autoantibodies on GABAARs independent of Fc-mediated effector functions and provide an animal model for GABAAR encephalitis. They further provide the scientific rationale for clinical treatments using antibody depletion and can serve as tools for the development of antibody-selective immunotherapies.

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Multimodal electrophysiological analyses reveal that reduced synaptic excitatory neurotransmission underlies seizures in a model of NMDAR antibody-mediated encephalitis

Communications Biology

2021 Seizures are a prominent feature in N-Methyl-D-Aspartate receptor antibody (NMDAR antibody) encephalitis, a distinct neuro-immunological disorder in which specific human autoantibodies bind and crosslink the surface of NMDAR proteins thereby causing internalization and a state of NMDAR hypofunction. To further understand ictogenesis in this disorder, and to test a potential treatment compound, we developed an NMDAR antibody mediated rat seizure model that displays spontaneous epileptiform activity in vivo and in vitro. Using a combination of electrophysiological and dynamic causal modelling techniques we show that, contrary to expectation, reduction of synaptic excitatory, but not inhibitory, neurotransmission underlies the ictal events through alterations in the dynamical behaviour of microcircuits in brain tissue. Moreover, in vitro application of a neurosteroid, pregnenolone sulphate, that upregulates NMDARs, reduced established ictal activity. This proof-of-concept study highlights the complexity of circuit disturbances that may lead to seizures and the potential use of receptor-specific treatments in antibody-mediated seizures and epilepsy.

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