Extracellular acidosis and high levels of carbon dioxide suppress synaptic transmission and prevent the induction of long-term potentiation in the CA1 region of rat hippocampal slices
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11120%2F98%3A43901775" target="_blank" >RIV/00216208:11120/98:43901775 - isvavai.cz</a>
Výsledek na webu
<a href="http://dx.doi.org/10.1002/(SICI)1098-1063(1998)8:1<24::AID-HIPO3>3.0.CO;2-7" target="_blank" >http://dx.doi.org/10.1002/(SICI)1098-1063(1998)8:1<24::AID-HIPO3>3.0.CO;2-7</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1002/(SICI)1098-1063(1998)8:1<24::AID-HIPO3>3.0.CO;2-7" target="_blank" >10.1002/(SICI)1098-1063(1998)8:1<24::AID-HIPO3>3.0.CO;2-7</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Extracellular acidosis and high levels of carbon dioxide suppress synaptic transmission and prevent the induction of long-term potentiation in the CA1 region of rat hippocampal slices
Popis výsledku v původním jazyce
Long-term potentiation (LTP) is a long-lasting increase in synaptic strength induced by high frequency stimulation. LTP may participate in learning and memory formation, In many synaptic systems, LTP is dependent on intact function of M-methyl-D-aspartate (NMDA) receptors, NMDA receptors may be inhibited in different conditions involving also extracellular acidosis. A decrease in the extracellular pH accompanies many pathological states such as ischemia, hypoxia, and the CNS injury. The study was designed to determine whether comparable extracellular acid-base imbalances are able to interfere with the LTP induction. Hippocampal slices from adult rats were stimulated with high frequency stimulation (1 x 100 Hz/1 s) at Schaffer collateral-commissural synaptic system in the environment with different pH (6.7-7.8) and the field responses were recorded in CA1. Acidosis was achieved by supplying excessive CO2 or by HCO(3)(-)decrease in standard bicarbonate-containing buffer or by a direct ac
Název v anglickém jazyce
Extracellular acidosis and high levels of carbon dioxide suppress synaptic transmission and prevent the induction of long-term potentiation in the CA1 region of rat hippocampal slices
Popis výsledku anglicky
Long-term potentiation (LTP) is a long-lasting increase in synaptic strength induced by high frequency stimulation. LTP may participate in learning and memory formation, In many synaptic systems, LTP is dependent on intact function of M-methyl-D-aspartate (NMDA) receptors, NMDA receptors may be inhibited in different conditions involving also extracellular acidosis. A decrease in the extracellular pH accompanies many pathological states such as ischemia, hypoxia, and the CNS injury. The study was designed to determine whether comparable extracellular acid-base imbalances are able to interfere with the LTP induction. Hippocampal slices from adult rats were stimulated with high frequency stimulation (1 x 100 Hz/1 s) at Schaffer collateral-commissural synaptic system in the environment with different pH (6.7-7.8) and the field responses were recorded in CA1. Acidosis was achieved by supplying excessive CO2 or by HCO(3)(-)decrease in standard bicarbonate-containing buffer or by a direct ac
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
ED - Fyziologie
OECD FORD obor
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Návaznosti výsledku
Projekt
<a href="/cs/project/GA305%2F95%2F0588" target="_blank" >GA305/95/0588: Extracelulární pH moduluje aktivitu neuronů, neuronální plasticitu a epileptické záchvaty</a><br>
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
1998
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Hippocampus
ISSN
1050-9631
e-ISSN
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Svazek periodika
8
Číslo periodika v rámci svazku
1
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
9
Strana od-do
24-32
Kód UT WoS článku
000072269000003
EID výsledku v databázi Scopus
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