Evaluation of the α(2A)adrenergic receptor gene in a heritable form of temporal lobe epilepsy

M. H. Wilson; R. S. Puranam; Ruth Ottman; C. Gilliam; L. E. Limbird; A. L. George; J. O. McNamara

doi:10.1212/WNL.51.6.1730

Evaluation of the α(2A)adrenergic receptor gene in a heritable form of temporal lobe epilepsy

M. H. Wilson^*, R. S. Puranam, Ruth Ottman, C. Gilliam, L. E. Limbird, A. L. George, J. O. McNamara

^*Corresponding author for this work

Pharmacology

Research output: Contribution to journal › Article › peer-review

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Abstract

An autosomal dominant form of human temporal lobe epilepsy (TLE) has been mapped to a region of chromosome 10q that contains the intronless α(2A)-adrenergic receptor (α(2A) AR) gene. Because mutation of the α(2A)AR gene in the mouse fosters epileptogenesis, we developed methods for analysis of the α(2A)AR coding region applicable to any pathophysiologic state in which the α(2A)AR could be implicated in the disease mechanism. This study rules out mutations in the 2a(2A)AR coding region as causal for this form of autosomal dominant TLE.

Original language	English (US)
Pages (from-to)	1730-1731
Number of pages	2
Journal	Neurology
Volume	51
Issue number	6
DOIs	https://doi.org/10.1212/WNL.51.6.1730
State	Published - Dec 1998

ASJC Scopus subject areas

Clinical Neurology

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abstract = "An autosomal dominant form of human temporal lobe epilepsy (TLE) has been mapped to a region of chromosome 10q that contains the intronless α(2A)-adrenergic receptor (α(2A) AR) gene. Because mutation of the α(2A)AR gene in the mouse fosters epileptogenesis, we developed methods for analysis of the α(2A)AR coding region applicable to any pathophysiologic state in which the α(2A)AR could be implicated in the disease mechanism. This study rules out mutations in the 2a(2A)AR coding region as causal for this form of autosomal dominant TLE.",

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AU - Wilson, M. H.

AU - Puranam, R. S.

AU - Ottman, Ruth

AU - Gilliam, C.

AU - Limbird, L. E.

AU - George, A. L.

AU - McNamara, J. O.

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AB - An autosomal dominant form of human temporal lobe epilepsy (TLE) has been mapped to a region of chromosome 10q that contains the intronless α(2A)-adrenergic receptor (α(2A) AR) gene. Because mutation of the α(2A)AR gene in the mouse fosters epileptogenesis, we developed methods for analysis of the α(2A)AR coding region applicable to any pathophysiologic state in which the α(2A)AR could be implicated in the disease mechanism. This study rules out mutations in the 2a(2A)AR coding region as causal for this form of autosomal dominant TLE.

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Evaluation of the α(2A)adrenergic receptor gene in a heritable form of temporal lobe epilepsy

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