Search

Joint Institutions are created from two different universities joining together to create a collaborative research and education effort. Compared to traditional universities, several unique challenges present themselves from this arrangement. We are especially interested in the student experience at UK-China Joint Institutes. We therefore organized a conference with the UK-China Joint Institute Alliance to aggregate knowledge on this issue. This paper summarizes the topics presented and discussed at the conference including: student learning and methods with which to measure and improve it, monitoring and incentivizing student engagement, the transition period from high school to university, teaching evaluations of staff, and lastly, learning and teaching during the COVID-19 pandemic. [ABSTRACT FROM AUTHOR]

Objective Absence seizures in childhood absence epilepsy are initiated in the thalamocortical ( TC) system. We investigated if these seizures result from altered development of the TC system before the appearance of seizures in mice containing a point mutation in γ-aminobutyric acid A ( GABAA) receptor γ2 subunits linked to childhood absence epilepsy (R43Q). Findings from conditional mutant mice indicate that expression of normal γ2 subunits during preseizure ages protect from later seizures. This indicates that altered development in the presence of the R43Q mutation is a key contributor to the R43Q phenotype. We sought to identify the cellular processes affected by the R43Q mutation during these preseizure ages. Methods We examined landmarks of synaptic development at the end of the critical period for somatosensory TC plasticity using electrophysiologic recordings in TC brain slices from wild-type mice and R43Q mice. Results We found that the level of TC connectivity to layer 4 (L4) principal cells and the properties of TC synapses were unaltered in R43Q mice. Furthermore, we show that, although TC feedforward inhibition and the total level of GABAergic inhibition were normal, there was a reduction in the local connectivity to cortical interneurons. This reduction leads to altered inhibition during bursts of cortical activity. Significance This altered inhibition demonstrates that alterations in cortical circuitry precede the onset of seizures by more than a week. [ABSTRACT FROM AUTHOR]

Inhibitory synaptic transmission in the hippocampus in mediated by a wide variety of different interneuron classes which are assumed to play different roles in network activity. Activation of presynaptic kainate receptors (KARs) has been shown to reduce inhibitory transmission but the interneuron class(es) at which they act is only recently beginning to emerge. Using paired recordings we show that KAR activation causes a decrease in presynaptic release from cholecystokinin (CCK)- but not parvalbumin-containing interneurons and that this decrease is observed when pyramidal cells, but not interneurons, are the postsynaptic target. We also show that although the synchronous release component is reduced, the barrage of asynchronous GABA release from CCK interneurons during sustained firing is unaffected by KAR activation. This indicates that presynaptic KARs preserve and act in concert with asynchronous release to switch CCK interneurons from a phasic inhibition mode to produce prolonged inhibition during periods of intense activity. [ABSTRACT FROM AUTHOR]

Objective: Absence seizures in childhood absence epilepsy are initiated in the thalamocortical (TC) system. We investigated if these seizures result from altered development of the TC system before the appearance of seizures in mice containing a point mutation in γ-aminobutyric acid A (GABA A ) receptor γ2 subunits linked to childhood absence epilepsy (R43Q). Findings from conditional mutant mice indicate that expression of normal γ2 subunits during preseizure ages protect from later seizures. This indicates that altered development in the presence of the R43Q mutation is a key contributor to the R43Q phenotype. We sought to identify the cellular processes affected by the R43Q mutation during these preseizure ages., Methods: We examined landmarks of synaptic development at the end of the critical period for somatosensory TC plasticity using electrophysiologic recordings in TC brain slices from wild-type mice and R43Q mice., Results: We found that the level of TC connectivity to layer 4 (L4) principal cells and the properties of TC synapses were unaltered in R43Q mice. Furthermore, we show that, although TC feedforward inhibition and the total level of GABAergic inhibition were normal, there was a reduction in the local connectivity to cortical interneurons. This reduction leads to altered inhibition during bursts of cortical activity., Significance: This altered inhibition demonstrates that alterations in cortical circuitry precede the onset of seizures by more than a week., (© 2017 The Authors. Epilepsia published by Wiley Periodicals Inc. on behalf of International League Against Epilepsy.)