FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2400629514> ?p ?o ?g. }

• W2400629514 endingPage "5762" @default.
• W2400629514 startingPage "5748" @default.
• W2400629514 abstract "Dependence is a hallmark feature of opiate addiction and is defined by the emergence of somatic and affective withdrawal signs. The nucleus accumbens (NAc) integrates dopaminergic and glutamatergic inputs to mediate rewarding and aversive properties of opiates. Evidence suggests that AMPA glutamate-receptor-dependent synaptic plasticity within the NAc underlies aspects of addiction. However, the degree to which NAc AMPA receptors (AMPARs) contribute to somatic and affective signs of opiate withdrawal is not fully understood. Here, we show that microinjection of the AMPAR antagonist NBQX into the NAc shell of morphine-dependent rats prevented naloxone-induced conditioned place aversions and decreases in sensitivity to brain stimulation reward, but had no effect on somatic withdrawal signs. Using a protein cross-linking approach, we found that the surface/intracellular ratio of NAc GluA1, but not GluA2, increased with morphine treatment, suggesting postsynaptic insertion of GluA2-lacking AMPARs. Consistent with this, 1-naphthylacetyl spermine trihydrochloride (NASPM), an antagonist of GluA2-lacking AMPARs, attenuated naloxone-induced decreases in sensitivity to brain stimulation reward. Naloxone decreased the surface/intracellular ratio and synaptosomal membrane levels of NAc GluA1 in morphine-dependent rats, suggesting a compensatory removal of AMPARs from synaptic zones. Together, these findings indicate that chronic morphine increases synaptic availability of GluA1-containing AMPARs in the NAc, which is necessary for triggering negative-affective states in response to naloxone. This is broadly consistent with the hypothesis that activation of NAc neurons produces acute aversive states and raises the possibility that inhibiting AMPA transmission selectively in the NAc may have therapeutic value in the treatment of addiction. SIGNIFICANCE STATEMENT Morphine dependence and withdrawal result in profound negative-affective states that play a major role in the maintenance of addiction. However, the underlying neurobiological mechanisms are not fully understood. We use a rat model of morphine dependence to show that GluA1 subunits of AMPA glutamate receptors in the nucleus accumbens (NAc), a brain region critical for modulating affective states, are necessary for aversive effects of morphine withdrawal. Using biochemical methods in NAc tissue, we show that morphine dependence increases cell surface expression of GluA1, suggesting that neurons in this area are primed for increased AMPA receptor activation upon withdrawal. This work is important because it suggests that targeting AMPA receptor trafficking and activation could provide novel targets for addiction treatment." @default.
• W2400629514 created "2016-06-24" @default.
• W2400629514 creator A5004706282 @default.
• W2400629514 creator A5006143104 @default.
• W2400629514 creator A5010261582 @default.
• W2400629514 creator A5015331692 @default.
• W2400629514 creator A5024383091 @default.
• W2400629514 creator A5067961117 @default.
• W2400629514 creator A5088862857 @default.
• W2400629514 date "2016-05-25" @default.
• W2400629514 modified "2023-10-13" @default.
• W2400629514 title "Nucleus Accumbens AMPA Receptors Are Necessary for Morphine-Withdrawal-Induced Negative-Affective States in Rats" @default.
• W2400629514 cites W1487599137 @default.
• W2400629514 cites W1566858817 @default.
• W2400629514 cites W1590162153 @default.
• W2400629514 cites W1658796519 @default.
• W2400629514 cites W1854766247 @default.
• W2400629514 cites W1901309030 @default.
• W2400629514 cites W1962727914 @default.
• W2400629514 cites W1966425023 @default.
• W2400629514 cites W1966879038 @default.
• W2400629514 cites W1969509559 @default.
• W2400629514 cites W1970007744 @default.
• W2400629514 cites W1976176845 @default.
• W2400629514 cites W1976587743 @default.
• W2400629514 cites W1977266070 @default.
• W2400629514 cites W1977313055 @default.
• W2400629514 cites W1980915383 @default.
• W2400629514 cites W1981891173 @default.
• W2400629514 cites W1986660167 @default.
• W2400629514 cites W1989416066 @default.
• W2400629514 cites W1990927532 @default.
• W2400629514 cites W1993135690 @default.
• W2400629514 cites W2000607451 @default.
• W2400629514 cites W2003016330 @default.
• W2400629514 cites W2004416831 @default.
• W2400629514 cites W2005352154 @default.
• W2400629514 cites W2005520124 @default.
• W2400629514 cites W2011748173 @default.
• W2400629514 cites W2012659957 @default.
• W2400629514 cites W2013285413 @default.
• W2400629514 cites W2014415095 @default.
• W2400629514 cites W2015011123 @default.
• W2400629514 cites W2015506510 @default.
• W2400629514 cites W2017187845 @default.
• W2400629514 cites W2021594631 @default.
• W2400629514 cites W2021782736 @default.
• W2400629514 cites W2022361809 @default.
• W2400629514 cites W2023079553 @default.
• W2400629514 cites W2024031866 @default.
• W2400629514 cites W2027436298 @default.
• W2400629514 cites W2031163840 @default.
• W2400629514 cites W2033440445 @default.
• W2400629514 cites W2034022242 @default.
• W2400629514 cites W2047535883 @default.
• W2400629514 cites W2048647443 @default.
• W2400629514 cites W2049683554 @default.
• W2400629514 cites W2051508663 @default.
• W2400629514 cites W2052836803 @default.
• W2400629514 cites W2054498589 @default.
• W2400629514 cites W2056607057 @default.
• W2400629514 cites W2058571616 @default.
• W2400629514 cites W2059117412 @default.
• W2400629514 cites W2062904490 @default.
• W2400629514 cites W2066038116 @default.
• W2400629514 cites W2067046066 @default.
• W2400629514 cites W2067814202 @default.
• W2400629514 cites W2075432773 @default.
• W2400629514 cites W2075597274 @default.
• W2400629514 cites W2079872791 @default.
• W2400629514 cites W2084903850 @default.
• W2400629514 cites W2100423235 @default.
• W2400629514 cites W2103124605 @default.
• W2400629514 cites W2111954958 @default.
• W2400629514 cites W2114938879 @default.
• W2400629514 cites W2116344152 @default.
• W2400629514 cites W2125437891 @default.
• W2400629514 cites W2139358036 @default.
• W2400629514 cites W2148799498 @default.
• W2400629514 cites W2150375400 @default.
• W2400629514 cites W2153961293 @default.
• W2400629514 cites W2161282151 @default.
• W2400629514 cites W2167295928 @default.
• W2400629514 cites W2168019923 @default.
• W2400629514 cites W2168384606 @default.
• W2400629514 cites W2170276695 @default.
• W2400629514 cites W2171758189 @default.
• W2400629514 cites W2231467691 @default.
• W2400629514 cites W2270599390 @default.
• W2400629514 cites W2317914721 @default.
• W2400629514 doi "https://doi.org/10.1523/jneurosci.2875-12.2016" @default.
• W2400629514 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4879196" @default.
• W2400629514 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27225765" @default.
• W2400629514 hasPublicationYear "2016" @default.
• W2400629514 type Work @default.
• W2400629514 sameAs 2400629514 @default.
• W2400629514 citedByCount "60" @default.
• W2400629514 countsByYear W24006295142016 @default.

• next