We are analyzing https://link.springer.com/article/10.1186/1756-6606-1-2.

Title:
Cingulate NMDA NR2B receptors contribute to morphine-induced analgesic tolerance | Molecular Brain
Description:
Morphine is widely used to treat chronic pain, however its utility is hindered by the development of tolerance to its analgesic effects. While N-methyl-D-aspartate (NMDA) receptors are known to play roles in morphine tolerance and dependence, less is known about the roles of individual NMDA receptor subtypes. In this study, Ro 256981, an antagonist of the NMDA receptor subunit NR2B, was used to reduce the expression of analgesic tolerance to morphine. The mechanisms altered with chronic drug use share similarities with those underlying the establishment of long-tem potentiation (LTP) and behavioral memory. Since NMDA NR2B receptors in the anterior cingulate cortex (ACC) play roles in the establishment of LTP and fear memory, we explored their role in changes that occur in this region after chronic morphine. Both systemic and intra-ACC inhibition of NR2B in morphine-tolerant animals inhibited the expression of analgesic tolerance. Electrophysiological recordings revealed a significant increase in the NR2B component of NMDA receptor mediated excitatory postsynaptic currents (EPSCs), at both synaptic and extra-synaptic sites. However, there was no change in alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor mediated EPSCs. This study suggests that selective inhibition of NMDA NR2B receptors may prove useful in combating the development of analgesic tolerance to morphine and proposes a novel role for the ACC in opioid tolerance and morphine induced changes in synaptic plasticity.
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Keywords {🔍}

morphine, nrb, mice, nmda, tolerance, pubmed, google, scholar, cas, acc, receptor, analgesic, receptors, saline, treated, significant, day, figure, treatment, role, chronic, antagonists, responses, pain, ltp, response, synaptic, opioid, mgkg, study, expression, analgesia, effects, brain, compared, cingulate, memory, component, results, acute, development, antagonist, epscs, induced, enhanced, antinociception, difference, article, nmethyldaspartate, cortex,

Topics {✒️}

recombinant n-methyl-d-aspartate receptors n-methyl-d-aspartate receptor antagonists alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid n-methyl-d-aspartate receptor n-methyl-d-aspartate long-jun wu ampa receptor-mediated responses nmda receptor-mediated epscs nmda receptor-mediated component jessica quan & min zhuo ng-nitro-l-arginine trigger long-term upregulation open access article anterior cingulate cortex thermally-controlled metal plate article download pdf excitatory postsynaptic currents latency-baseline response latency prefrontal long-term potentiation l-methadone-induced antinociception author information authors layer ii/iii neurons nmda receptor antagonists nmda receptor antagonist acute morphine-induced analgesia student-newmann-keuls test morphine-induced analgesic tolerance acute mu-opioid analgesia hot-plate response latencies receptor mediated epscs rat cingulate cortex morphine-tolerant animals inhibited nmda nr2b subunit nmda subunit nr2b nr2b receptor function central nervous system cue-induced cocaine craving nmda receptor responses total nmda current nmda receptor activity long-term depression search mu opioid receptor privacy choices/manage cookies patch clamp recordings authors’ original file long-term potentiation canada research chair post hoc comparison ro256981+morphine treated mice

Questions {❓}

Trujillo KA: Are NMDA receptors involved in opiate-induced neural and behavioral plasticity?

Schema {🗺️}

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         description:Morphine is widely used to treat chronic pain, however its utility is hindered by the development of tolerance to its analgesic effects. While N-methyl-D-aspartate (NMDA) receptors are known to play roles in morphine tolerance and dependence, less is known about the roles of individual NMDA receptor subtypes. In this study, Ro 256981, an antagonist of the NMDA receptor subunit NR2B, was used to reduce the expression of analgesic tolerance to morphine. The mechanisms altered with chronic drug use share similarities with those underlying the establishment of long-tem potentiation (LTP) and behavioral memory. Since NMDA NR2B receptors in the anterior cingulate cortex (ACC) play roles in the establishment of LTP and fear memory, we explored their role in changes that occur in this region after chronic morphine. Both systemic and intra-ACC inhibition of NR2B in morphine-tolerant animals inhibited the expression of analgesic tolerance. Electrophysiological recordings revealed a significant increase in the NR2B component of NMDA receptor mediated excitatory postsynaptic currents (EPSCs), at both synaptic and extra-synaptic sites. However, there was no change in alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor mediated EPSCs. This study suggests that selective inhibition of NMDA NR2B receptors may prove useful in combating the development of analgesic tolerance to morphine and proposes a novel role for the ACC in opioid tolerance and morphine induced changes in synaptic plasticity.
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      description:Morphine is widely used to treat chronic pain, however its utility is hindered by the development of tolerance to its analgesic effects. While N-methyl-D-aspartate (NMDA) receptors are known to play roles in morphine tolerance and dependence, less is known about the roles of individual NMDA receptor subtypes. In this study, Ro 256981, an antagonist of the NMDA receptor subunit NR2B, was used to reduce the expression of analgesic tolerance to morphine. The mechanisms altered with chronic drug use share similarities with those underlying the establishment of long-tem potentiation (LTP) and behavioral memory. Since NMDA NR2B receptors in the anterior cingulate cortex (ACC) play roles in the establishment of LTP and fear memory, we explored their role in changes that occur in this region after chronic morphine. Both systemic and intra-ACC inhibition of NR2B in morphine-tolerant animals inhibited the expression of analgesic tolerance. Electrophysiological recordings revealed a significant increase in the NR2B component of NMDA receptor mediated excitatory postsynaptic currents (EPSCs), at both synaptic and extra-synaptic sites. However, there was no change in alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor mediated EPSCs. This study suggests that selective inhibition of NMDA NR2B receptors may prove useful in combating the development of analgesic tolerance to morphine and proposes a novel role for the ACC in opioid tolerance and morphine induced changes in synaptic plasticity.
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