Format

Send to:

Choose Destination
See comment in PubMed Commons below
Brain Dev. 1998 Mar;20(2):75-9.

Mechanisms of generalized absence epilepsy.

Author information

  • 1Department of Neurology, Children's Hospital and Harvard Medical School, Boston, MA 02115, USA.

Abstract

Absence seizures represent bilaterally synchronous burst-firing of an ensemble of reciprocally connected neuronal populations located in the thalamus and neocortex. Recent studies demonstrate that neurons in the reticular thalamic nucleus (nRt), thalamic relay neurons (RNs), and neocortical pyramidal cells comprise a circuit that sustains the thalamocortical oscillatory burst-firing of absence seizures. Recent studies have focused on three intrinsic neuronal mechanisms that increase the likelihood of thalamocortical oscillations. The first mechanism involves T-currents elicited by activating the T-type calcium channel, which appear to trigger sustained burst-firing of thalamic neurons during absence seizures. A second intrinsic mechanism is GABA B receptors which can elicit longstanding hyperpolarization in thalamic neurons required to 'prime' T-channels for sustained burst-firing. A third mechanism involves the ability of GABA A receptors, located on nRt neurons, to mediate recurrent inhibition. Enhanced activation of GABA A receptors on nRt neurons decreases the pacemaking capacity of these cells, therefore decreasing the likelihood of generating absence seizures. Cholinergic mechanisms through modulating cortical excitability and excitatory amino acid mediated mechanisms through depolarizing thalamic neurons also play a role in absence seizures.

PMID:
9545175
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk