Near-complete adaptation of the PRiMA knockout to the lack of central acetylcholinesterase

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11140%2F12%3A10126804" target="_blank" >RIV/00216208:11140/12:10126804 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11110/12:11484 RIV/46747885:24610/12:#0000011

Výsledek na webu

<a href="http://dx.doi.org/10.1111/j.1471-4159.2012.07856.x" target="_blank" >http://dx.doi.org/10.1111/j.1471-4159.2012.07856.x</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1111/j.1471-4159.2012.07856.x" target="_blank" >10.1111/j.1471-4159.2012.07856.x</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Near-complete adaptation of the PRiMA knockout to the lack of central acetylcholinesterase

Popis výsledku v původním jazyce

J. Neurochem. (2012) 122, 10651080. Abstract Acetylcholinesterase (AChE) rapidly hydrolyzes acetylcholine. At the neuromuscular junction, AChE is mainly anchored in the extracellular matrix by the collagen Q, whereas in the brain, AChE is tethered by theproline-rich membrane anchor (PRiMA). The AChE-deficient mice, in which AChE has been deleted from all tissues, have severe handicaps. Surprisingly, PRiMA KO mice in which AChE is mostly eliminated from the brain show very few deficits. We now report that most of the changes observed in the brain of AChE-deficient mice, and in particular the high levels of ambient extracellular acetylcholine and the massive decrease of muscarinic receptors, are also observed in the brain of PRiMA KO. However, the two groups of mutants differ in their responses to AChE inhibitors. Since PRiMA-KO mice and AChE-deficient mice have similar low AChE concentrations in the brain but differ in the AChE content of the peripheral nervous system, these results su

Název v anglickém jazyce

Near-complete adaptation of the PRiMA knockout to the lack of central acetylcholinesterase

Popis výsledku anglicky

J. Neurochem. (2012) 122, 10651080. Abstract Acetylcholinesterase (AChE) rapidly hydrolyzes acetylcholine. At the neuromuscular junction, AChE is mainly anchored in the extracellular matrix by the collagen Q, whereas in the brain, AChE is tethered by theproline-rich membrane anchor (PRiMA). The AChE-deficient mice, in which AChE has been deleted from all tissues, have severe handicaps. Surprisingly, PRiMA KO mice in which AChE is mostly eliminated from the brain show very few deficits. We now report that most of the changes observed in the brain of AChE-deficient mice, and in particular the high levels of ambient extracellular acetylcholine and the massive decrease of muscarinic receptors, are also observed in the brain of PRiMA KO. However, the two groups of mutants differ in their responses to AChE inhibitors. Since PRiMA-KO mice and AChE-deficient mice have similar low AChE concentrations in the brain but differ in the AChE content of the peripheral nervous system, these results su

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

ED - Fyziologie

OECD FORD obor

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Projekt

<a href="/cs/project/GA309%2F09%2F0406" target="_blank" >GA309/09/0406: Mechanismy regulace muskarinových receptorů</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2012

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Neurochemistry

ISSN

0022-3042

e-ISSN

—

Svazek periodika

122

Číslo periodika v rámci svazku

5

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

16

Strana od-do

1065-1080

Kód UT WoS článku

000307969700019

EID výsledku v databázi Scopus

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