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• W1608318158 endingPage "921" @default.
• W1608318158 startingPage "907" @default.
• W1608318158 abstract "Mechanisms of pain‐related plasticity in the amygdala, a key player in emotionality, were studied at the cellular and molecular levels in a model of arthritic pain. The influence of the arthritis pain state induced in vivo on synaptic transmission and N ‐methyl‐ d ‐aspartate (NMDA) receptor function was examined in vitro using whole‐cell voltage‐clamp recordings of neurones in the latero‐capsular part of the central nucleus of the amygdala (CeA), which is now defined as the ‘nociceptive amygdala’. Synaptic transmission was evoked by electrical stimulation of afferents from the pontine parabrachial area (part of the spino‐parabrachio‐amygdaloid pain pathway) in brain slices from control rats and from arthritic rats. This study shows that pain‐related synaptic plasticity is accompanied by protein kinase A (PKA)‐mediated enhanced NMDA‐receptor function and increased phosphorylation of NMDA‐receptor 1 (NR1) subunits. Synaptic plasticity in the arthritis pain model, but not normal synaptic transmission in control neurones, was inhibited by a selective NMDA receptor antagonist. Accordingly, an NMDA receptor‐mediated synaptic component was recorded in neurones from arthritic animals, but not in control neurones, and was blocked by inhibition of PKA but not protein kinase C (PKC). Exogenous NMDA evoked a larger inward current in neurones from arthritic animals than in control neurones, indicating a postsynaptic effect. Paired‐pulse facilitation, a measure of presynaptic mechanisms, was not affected by an NMDA‐receptor antagonist. Increased levels of phosphorylated NR1 protein, but not of total NR1, were measured in the CeA of arthritic rats compared to controls. Our results suggest that pain‐related synaptic plasticity in the amygdala involves a critical switch of postsynaptic NMDA receptor function through PKA‐dependent NR1 phosphorylation." @default.
• W1608318158 created "2016-06-24" @default.
• W1608318158 creator A5030512706 @default.
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• W1608318158 date "2005-04-21" @default.
• W1608318158 modified "2023-10-14" @default.
• W1608318158 title "Protein kinase A‐dependent enhanced NMDA receptor function in pain‐related synaptic plasticity in rat amygdala neurones" @default.
• W1608318158 cites W1533926750 @default.
• W1608318158 cites W1565438915 @default.
• W1608318158 cites W1570725062 @default.
• W1608318158 cites W1575571855 @default.
• W1608318158 cites W1594563757 @default.
• W1608318158 cites W1618945825 @default.
• W1608318158 cites W1628708546 @default.
• W1608318158 cites W1755902553 @default.
• W1608318158 cites W1761628643 @default.
• W1608318158 cites W1771301420 @default.
• W1608318158 cites W1826560869 @default.
• W1608318158 cites W1846766371 @default.
• W1608318158 cites W1918669680 @default.
• W1608318158 cites W1946000001 @default.
• W1608318158 cites W1950317766 @default.
• W1608318158 cites W1951970154 @default.
• W1608318158 cites W1969730957 @default.
• W1608318158 cites W1972161349 @default.
• W1608318158 cites W1979231658 @default.
• W1608318158 cites W1980135097 @default.
• W1608318158 cites W1980400989 @default.
• W1608318158 cites W1983681057 @default.
• W1608318158 cites W1986469313 @default.
• W1608318158 cites W1988059170 @default.
• W1608318158 cites W1988111588 @default.
• W1608318158 cites W1990264946 @default.
• W1608318158 cites W1991739295 @default.
• W1608318158 cites W1992384753 @default.
• W1608318158 cites W1992875076 @default.
• W1608318158 cites W1998108399 @default.
• W1608318158 cites W2001558837 @default.
• W1608318158 cites W2003646312 @default.
• W1608318158 cites W2004159036 @default.
• W1608318158 cites W2004337408 @default.
• W1608318158 cites W2009401184 @default.
• W1608318158 cites W2009796900 @default.
• W1608318158 cites W2015602085 @default.
• W1608318158 cites W2017848817 @default.
• W1608318158 cites W2017934537 @default.
• W1608318158 cites W2027072793 @default.
• W1608318158 cites W2037204220 @default.
• W1608318158 cites W2039101107 @default.
• W1608318158 cites W2040623908 @default.
• W1608318158 cites W2047910499 @default.
• W1608318158 cites W2049517532 @default.
• W1608318158 cites W2053263437 @default.
• W1608318158 cites W2059380500 @default.
• W1608318158 cites W2059958157 @default.
• W1608318158 cites W2062644960 @default.
• W1608318158 cites W2064348349 @default.
• W1608318158 cites W2067849553 @default.
• W1608318158 cites W2070037006 @default.
• W1608318158 cites W2074264994 @default.
• W1608318158 cites W2074340804 @default.
• W1608318158 cites W2077348695 @default.
• W1608318158 cites W2079311820 @default.
• W1608318158 cites W2079403841 @default.
• W1608318158 cites W2081793810 @default.
• W1608318158 cites W2093090171 @default.
• W1608318158 cites W2095577553 @default.
• W1608318158 cites W2102396911 @default.
• W1608318158 cites W2110724392 @default.
• W1608318158 cites W2118398750 @default.
• W1608318158 cites W2121853679 @default.
• W1608318158 cites W2129108032 @default.
• W1608318158 cites W2140899588 @default.
• W1608318158 cites W2142738038 @default.
• W1608318158 cites W2143046795 @default.
• W1608318158 cites W2144933081 @default.
• W1608318158 cites W2146958131 @default.
• W1608318158 cites W2148365115 @default.
• W1608318158 cites W2148389554 @default.
• W1608318158 cites W2150224367 @default.
• W1608318158 cites W2152541148 @default.
• W1608318158 cites W2155520726 @default.
• W1608318158 cites W2158553737 @default.
• W1608318158 cites W2168226677 @default.
• W1608318158 cites W2171037951 @default.
• W1608318158 cites W2265262946 @default.
• W1608318158 cites W2309025722 @default.
• W1608318158 cites W2329382998 @default.
• W1608318158 cites W38310539 @default.
• W1608318158 cites W4319053752 @default.
• W1608318158 cites W49989104 @default.
• W1608318158 doi "https://doi.org/10.1113/jphysiol.2005.084780" @default.
• W1608318158 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1464474" @default.
• W1608318158 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15760935" @default.

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