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Titolo:
Genetic comparison of seizure control by norepinephrine and neuropeptide Y
Autore:
Weinshenker, D; Szot, P; Miller, NS; Rust, NC; Hohmann, JG; Pyati, U; White, SS; Palmiter, RD;
Indirizzi:
Univ Washington, Howard Hughes Med Inst, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 ghes Med Inst, Seattle, WA 98195 USA Univ Washington, Dept Biochem, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 Dept Biochem, Seattle, WA 98195 USA Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 t & Behav Sci, Seattle, WA 98195 USA Univ Washington, Ctr Geriatr Res Educ & Clin, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 s Educ & Clin, Seattle, WA 98195 USA Univ Washington, Program Neurobiol & Behav, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 obiol & Behav, Seattle, WA 98195 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 19, volume: 21, anno: 2001,
pagine: 7764 - 7769
SICI:
0270-6474(20011001)21:19<7764:GCOSCB>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
DOPAMINE-BETA-HYDROXYLASE; LOCUS COERULEUS NEURONS; CENTRAL NERVOUS-SYSTEM; MESSENGER-RNA; TYROSINE-HYDROXYLASE; NORADRENERGIC SYSTEM; TRANSIENT CHANGES; RAT-BRAIN; EXPRESSION; MICE;
Keywords:
norepinephrine; NPY; dopamine beta-hydroxylase; mice; epilepsy; seizure; pentylenetetrazole; flurothyl; kainic acid; mice; knock-out; in situ hybridization; neurotransmitter;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Palmiter, RD Univ Washington, Howard Hughes Med Inst, Box 357370, Seattle,WA 98195 USA Univ Washington Box 357370 Seattle WA USA 98195 WA 98195 USA
Citazione:
D. Weinshenker et al., "Genetic comparison of seizure control by norepinephrine and neuropeptide Y", J NEUROSC, 21(19), 2001, pp. 7764-7769

Abstract

Epilepsy is a disease of neuronal hyperexcitability, and pharmacological and genetic studies have identified norepinephrine (NE) and neuropeptide Y (NPY) as important endogenous regulators of neuronal excitability. Both transmitters signal through G-protein-coupled receptors, are expressed either together or separately, and are, abundant in brain regions implicated in seizure generation. NPY knock-out (NPY KO) and dopamine g-hydroxylase. knock-out (DBH KO) mice that lack NE are susceptible to seizures, and agonists of NE and NPY receptors protect against seizures. Tb examine the relative contributions of NE and NPY to neuronal excitability, we tested Dbh;Npy double knock-out (DKO) mice for seizure sensitivity. In general, DBH KO mice were much more seizure-sensitive than NPY KO mice and had normal NPY expression,demonstrating that an NPY deficiency did not contribute to the DBH KO seizure phenotype. DKO mice were only slightly more sensitive than DBH KO mice to seizures induced by kainic acid, pentylenetetrazole, or flurothyl, although DKO mice were uniquely prone to handling-induced seizures. NPY contributed to the seizure phenotype of DKO mice at high doses of convulsant agentsand advanced stages of seizures. These data suggest that NE Is a more potent endogenous anticonvulsant than NPY, and that NPY has the greatest contribution under conditions of extreme neuronal excitability.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 19:37:23