Abstract：
:Burst firing of the thalamic neurons is driven by the low threshold Ca2+ spike generated by Ca2+ influx through T-type Ca2+ channels when these channels are activated by membrane hyperpolarization due to inhibitory inputs. The major inhibitory inputs to the thalamocortical (TC) neurons are from the GABAergic neurons in the thalamic reticular nucleus. Thalamic burst firings have long been implicated in the pathogenesis of absence epilepsy. The recent progress in genetic approaches has provided with an opportunity to examine this issue at the level of an organism. In this review I describe results primarily obtained from the analysis of the mice deficient for the alpha1G locus which is the predominant gene underlying the low threshold Ca2+ currents in the TC neurons. Current results so far demonstrate the essential role of the thalamocortical bursts in certain forms of absence seizures. Understanding of the pathophysiological mechanisms of absence epilepsy may help develop drugs to control the disease.
journal_name
Cell Calciumjournal_title
Cell calciumauthors
Shin HSdoi
10.1016/j.ceca.2006.04.023subject
Has Abstractpub_date
2006-08-01 00:00:00pages
191-6issue
2eissn
0143-4160issn
1532-1991pii
S0143-4160(06)00088-1journal_volume
40pub_type
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