[BIC-announce] FW: Killam Lecture - Dr. Vincenzo Crunelli-Pathophysiological Mechanisms of Absence Seizures

[Jennifer Chew, Ms.]

PLEASE DISCARD IF THIS IS A DUPLICATE.  THANK YOU.  Jennifer

From: MNISTAFF - Montreal Neurological Institute Staff [mailto:MNISTAFF at LISTS.MCGILL.CA] On Behalf Of Enza Ferracane, Ms.
Sent: Monday, June 10, 2013 8:51 AM
To: MNISTAFF at LISTS.MCGILL.CA
Subject: Killam Lecture - Dr. Vincenzo Crunelli

Killam Lecture

Speaker:  Vincenzo Crunelli, PhD
Cardiff School of Biosciences
Cardiff, UK

Title:  Pathophysiological Mechanisms of Absence Seizures

Date:  Tuesday, June 11, 2013

Time:  4 pm

Place:  de Grandpre Communications Centre

Killam's Lecture, June 11, 2013

PATHOPHYSIOLOGICAL MECHANISMS OF TYPICAL ABSENCE SEIZURES

Vincenzo Crunelli
Neuroscience Division, Cardiff University, UK

Our understanding of the pathophysiological mechanisms that bring about typical absence seizures is still patchy. Whereas it is established that these non-convulsive seizures originate from abnormal activity within neocortical and thalamic territories, the precise genetic, molecular, cellular and network alterations underlying absence seizures are still a matter of intense debate and controversy.

Dr. Crunelli's lecture will summarize the current status of human and experimental research on this type of epilepsy, focusing on two transmitter-gated channels (i.e. GABA-A and GABA-B receptors) and one voltage-gated channel (the T-type calcium channel) that have attracted much attention over the last 25 years. In particular, he will discuss how both human and experimental evidence strongly supports the view of brain region-specific changes in phasic and tonic GABA-A receptor-mediated inhibition in typical absence seizures, with a decreased phasic GABA-A inhibition in neocortical neurons, and an enhanced tonic GABA-A inhibition in thalamocortical neurons, which results from a malfunction in the astrocytic GABA transporter GAT-1. Indeed, recent work from Dr. Crunelli's laboratory suggests that the ability of GABA-B receptor agonists and antagonists to increase and abolish, respectively, absence seizures is likely to be related to their indirect modulation of extrasynaptic GABA-A receptor function. Moreover, in contrast to current text-book views, unpublished work in undrugged, freely moving rats indicate that during spontaneous, genetically-determined absence seizures there is a reduction in the overall firing of thalamocortical and reticular thalamic neurons and only very few T-type calcium channel-mediated high frequency bursts of action potentials are present.

Thus, the long-standing view of a widespread GABAergic loss-of-function in typical absence seizures is no longer tenable and model systems that use an indiscriminate block of GABAA receptors (with the resulting increase of high frequency action potential bursts in thalamocortical neurons) are of no value for understanding the cellular and network mechanisms operating in cortico-thalamic-cortical circuits during typical absence seizures.

Dr. Crunelli is the Head of the Neuroscience Division in the School of Bioscience at Cardiff University in Wales (UK). With a PhD in Chemistry and a strong background in CNS physiology and pharmacology, his research interests are the system and cellular mechanisms operating in the thalamocortical network during non-REM sleep and in absence epilepsy. Dr. Crunelli's research group uses a combination of pharmacological and electrophysiological methods including large ensemble recordings and microdialysis in freely moving animals, patch and sharp electrode recordings in brain slices from normal animals and different mouse and rat genetic models of absence epilepsy, and 2-photon laser scanning imaging combined with dendritic recordings.


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