Louise Parker
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Louise Parker has a total of 4 co-authors. Here are the top co-authors by number of shared publications:
Ke Dong
Department of Environmental Science, Policy and Management, University of California, Berkeley, California 94720, ‡Department of Molecular and Cell Biology, University of California, Berkeley, California 94720 and †Department of Entomology, Michigan State University, East Lansing, Michigan 48824
1 shared publicationMark A Tanouye
Department of Environmental Science, Policy and Management, University of California, Berkeley, California 94720, ‡Department of Molecular and Cell Biology, University of California, Berkeley, California 94720 and †Department of Entomology, Michigan State University, East Lansing, Michigan 48824
1 shared publicationMiguel Padilla
Department of Environmental Science, Policy and Management, University of California, Berkeley, California 94720, ‡Department of Molecular and Cell Biology, University of California, Berkeley, California 94720 and †Department of Entomology, Michigan State University, East Lansing, Michigan 48824
1 shared publicationYuzhe Du
Department of Environmental Science, Policy and Management, University of California, Berkeley, California 94720, ‡Department of Molecular and Cell Biology, University of California, Berkeley, California 94720 and †Department of Entomology, Michigan State University, East Lansing, Michigan 48824
1 shared publication
Latest Publications
- 1 February 2011
- Published by Oxford University Press (OUP) in Genetics
- Vol. 187 (2) , 523-534
Drosophila as a Model for Epilepsy:bssIs a Gain-of-Function Mutation in the Para Sodium Channel Gene That Leads to Seizures
We report the identification of bang senseless (bss), a Drosophila melanogaster mutant exhibiting seizure-like behaviors, as an allele of the paralytic (para) voltage-gated Na+ (NaV) channel gene. Mutants are more prone to seizure episodes than normal flies because of a lowered seizure threshold. The bss phenotypes are due to a missense mutation in a segment previously implicated in inactivation, termed the “paddle motif” of the NaV fourth homology domain. Heterologous expression of cDNAs containing the bss1 lesion, followed by electrophysiology, shows that mutant channels display altered voltage dependence of inactivation compared to wild type. The phenotypes of bss are the most severe of the bang-sensitive mutants in Drosophila and can be ameliorated, but not suppressed, by treatment with anti-epileptic drugs. As such, bss-associated seizures resemble those of pharmacologically resistant epilepsies caused by mutation of the human NaV SCN1A, such as severe myoclonic epilepsy in infants or intractable childhood epilepsy with generalized tonic-clonic seizures.
- 1 February 2011
- Published by Oxford University Press (OUP) in Genetics
- Vol. 187 (2) , 523-534
Drosophila as a Model for Epilepsy:bssIs a Gain-of-Function Mutation in the Para Sodium Channel Gene That Leads to Seizures
We report the identification of bang senseless (bss), a Drosophila melanogaster mutant exhibiting seizure-like behaviors, as an allele of the paralytic (para) voltage-gated Na+ (NaV) channel gene. Mutants are more prone to seizure episodes than normal flies because of a lowered seizure threshold. The bss phenotypes are due to a missense mutation in a segment previously implicated in inactivation, termed the “paddle motif” of the NaV fourth homology domain. Heterologous expression of cDNAs containing the bss1 lesion, followed by electrophysiology, shows that mutant channels display altered voltage dependence of inactivation compared to wild type. The phenotypes of bss are the most severe of the bang-sensitive mutants in Drosophila and can be ameliorated, but not suppressed, by treatment with anti-epileptic drugs. As such, bss-associated seizures resemble those of pharmacologically resistant epilepsies caused by mutation of the human NaV SCN1A, such as severe myoclonic epilepsy in infants or intractable childhood epilepsy with generalized tonic-clonic seizures.