Literature DB >> 18028408

Multiple roles of midline dorsal thalamic nuclei in induction and spread of limbic seizures.

Edward H Bertram1, DeXing Zhang, John M Williamson.   

Abstract

PURPOSE: Studies have suggested that the medial dorsal nucleus of the thalamus plays a role in the behavioral expression of limbic seizures, but it is unclear whether this region is a key component for the primary seizure circuitry or a path for seizure spread from one region to another. This study was undertaken to determine the potential role of this region in limbic seizure activity.
METHODS: Adult male rats received kindling stimulation either under urethane anesthesia or while awake. Glutamate or its agonists or the GABA antagonist bicuculline or agonist muscimol were infused into the medial dorsal nucleus. In another series, kindling acquisition was compared among three thalamic sites as well as with the amygdala and hippocampus
RESULTS: Drugs that enhanced excitatory drive or blocked GABA resulted in significant prolongation of electrographic seizure activity compared to saline infused controls. Enhanced GABA activity resulted in a significant reduction of seizure duration. Infusion of the compounds lateral to the medial dorsal nucleus did not affect seizure duration. In the kindling studies the medial dorsal region is the only thalamic nucleus from which hippocampal seizures can be induced, but with an elevated afterdischarge threshold compared to the two limbic sites. However, the seizures generalized more rapidly from the medial dorsal region.
CONCLUSIONS: This study demonstrates that the medial dorsal nucleus and other dorsal midline nuclei have a significant role in the primary seizure circuits of limbic seizures as well as in spread of seizure activity to other regions.

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Year:  2007        PMID: 18028408     DOI: 10.1111/j.1528-1167.2007.01408.x

Source DB:  PubMed          Journal:  Epilepsia        ISSN: 0013-9580            Impact factor:   5.864


  41 in total

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3.  Increased GABAergic inhibition in the midline thalamus affects signaling and seizure spread in the hippocampus-prefrontal cortex pathway.

Authors:  David M Sloan; DeXing Zhang; Edward H Bertram
Journal:  Epilepsia       Date:  2011-01-04       Impact factor: 5.864

4.  Chemogenetic silencing of the midline and intralaminar thalamus blocks amygdala-kindled seizures.

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Review 5.  Neuronal circuits in epilepsy: do they matter?

Authors:  Edward H Bertram
Journal:  Exp Neurol       Date:  2012-02-08       Impact factor: 5.330

6.  Involvement of the thalamocortical network in TLE with and without mesiotemporal sclerosis.

Authors:  Susanne G Mueller; Kenneth D Laxer; Jerome Barakos; Ian Cheong; Daniel Finlay; Paul Garcia; Valerie Cardenas-Nicolson; Michael W Weiner
Journal:  Epilepsia       Date:  2009-12-01       Impact factor: 5.864

7.  Altered pharmacology and GABA-A receptor subunit expression in dorsal midline thalamic neurons in limbic epilepsy.

Authors:  Karthik Rajasekaran; Chengsan Sun; Edward H Bertram
Journal:  Neurobiol Dis       Date:  2008-10-17       Impact factor: 5.996

8.  Thalamic structural connectivity in medial temporal lobe epilepsy.

Authors:  Daniel S Barron; Nitin Tandon; Jack L Lancaster; Peter T Fox
Journal:  Epilepsia       Date:  2014-05-06       Impact factor: 5.864

9.  An acquired channelopathy involving thalamic T-type Ca2+ channels after status epilepticus.

Authors:  John D Graef; Brian K Nordskog; Walter F Wiggins; Dwayne W Godwin
Journal:  J Neurosci       Date:  2009-04-08       Impact factor: 6.167

10.  Effects of quetiapine on monoamine, GABA, and glutamate release in rat prefrontal cortex.

Authors:  Satoshi Yamamura; Keiko Ohoyama; Tatsuya Hamaguchi; Kanae Kashimoto; Masanori Nakagawa; Shinichi Kanehara; Dai Suzuki; Takuya Matsumoto; Eishi Motomura; Takashi Shiroyama; Motohiro Okada
Journal:  Psychopharmacology (Berl)       Date:  2009-07-03       Impact factor: 4.530

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