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Neuropharmacology. 2009 Mar;56(3):665-75. doi: 10.1016/j.neuropharm.2008.11.005. Epub 2008 Dec 6.

Calcium channel dysfunction in inferior colliculus neurons of the genetically epilepsy-prone rat.

Author information

1
Department of Pediatrics, Georgetown University Medical Center, 3900 Reservoir Rd, NW, Washington, DC 20057, United States. pn@georgetown.edu

Abstract

Voltage-gated calcium (Ca(2+)) channels are thought to play an important role in epileptogenesis and seizure generation. Here, using the whole cell configuration of patch-clamp techniques, we report on the modifications of biophysical and pharmacological properties of high threshold voltage-activated Ca(2+) channel currents in inferior colliculus (IC) neurons of the genetically epilepsy-prone rats (GEPR-3s). Ca(2+) channel currents were measured by depolarizing pulses from a holding potential of - 80 mV using barium (Ba(2+)) as the charge carrier. We found that the current density of high threshold voltage-activated Ca(2+) channels was significantly larger in IC neurons of seizure-naive GEPR-3s compared to control Sprague-Dawley rats, and that seizure episodes further enhanced the current density in the GEPR-3s. The increased current density was reflected by both a - 20 mV shifts in channel activation and a 25% increase in the non-inactivating fraction of channels in seizure-naive GEPR-3s. Such changes were reduced by seizure episodes in the GEPR-3s. Pharmacological analysis of the current density suggests that upregulation of L-, N- and R-type of Ca(2+) channels may contribute to IC neuronal hyperexcitability that leads to seizure susceptibility in the GEPR-3s.

PMID:
19084544
PMCID:
PMC2638996
DOI:
10.1016/j.neuropharm.2008.11.005
[Indexed for MEDLINE]
Free PMC Article

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