ArticleThe Journal of pharmacology and experimental therapeutics2009
Rewarding morphine-induced synaptic function of delta-opioid receptors on central glutamate synapses.
Article in The Journal of pharmacology and experimental therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 60 citations in OpenAlex.
- Key differences in regulation of opioid receptors localized to presynaptic terminals compared to somas: Relevance for novel therapeutics.Neuropharmacology · 2023Review
- Opioid Receptor-Mediated Regulation of Neurotransmission in the Brain.Frontiers in molecular neuroscience · 2022Review
- Amyloid Fibril-Induced Astrocytic Glutamate Transporter Disruption Contributes to Complement C1q-Mediated Microglial Pruning of Glutamatergic Synapses.Molecular neurobiology · 2020Article
- Silver nanoparticles (Ag-NPs) in the central amygdala protect the rat conditioned by morphine from withdrawal attack due to naloxone via high-level nitric oxide.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Pharmacotherapeutic management of co-morbid alcohol and opioid use.Expert opinion on pharmacotherapy · 2020Review
- The amygdalar opioid system.Handbook of behavioral neuroscience · 2020Article
- Activation of mGluR1 Mediates C1q-Dependent Microglial Phagocytosis of Glutamatergic Synapses in Alzheimer's Rodent Models.Molecular neurobiology · 2019Article
- Article
- Brain Circuits Mediating Opposing Effects on Emotion and Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Molecular Pharmacology of δ-Opioid Receptors.Pharmacological reviews · 2016Review
- Amygdala pain mechanisms.Handbook of experimental pharmacology · 2015Review
- The role of δ-opioid receptors in learning and memory underlying the development of addiction.British journal of pharmacology · 2015Review
- Persistent pain facilitates response to morphine reward by downregulation of central amygdala GABAergic function.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
- Epigenetic suppression of neuroligin 1 underlies amyloid-induced memory deficiency.Nature neuroscience · 2014Article
- Synergistic activity between the delta-opioid agonist SNC80 and amphetamine occurs via a glutamatergic NMDA-receptor dependent mechanism.Neuropharmacology · 2014Article
- Acute morphine alters GABAergic transmission in the central amygdala during naloxone-precipitated morphine withdrawal: role of cyclic AMP.Frontiers in integrative neuroscience · 2014Article
- Pharmacological traits of delta opioid receptors: pitfalls or opportunities?Psychopharmacology · 2013Review
- Central amygdala GluA1 facilitates associative learning of opioid reward.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Upregulation of nerve growth factor in central amygdala increases sensitivity to opioid reward.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012Article
- Sex differences in the neural mechanisms mediating addiction: a new synthesis and hypothesis.Biology of sex differences · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The rewarding effect of opioids, the driving force for compulsive behaviors of opioid abuse and addiction, is primarily mediated by the mu-opioid receptor. However, the role of the delta-opioid receptor (DOR) in opioid reward and addiction is still poorly understood. The recently discovered adaptive DOR property of exocytotic translocation in sensory neurons after chronic opioid exposure provides a new avenue of conceptual thoughts to exploring the DOR function in this psychoneurological disease. In this study, we investigated potential adaptive function of DOR in neurons of the central nucleus of the amygdala (CeA), a forebrain structure increasingly recognized for mediating stimulus reward learning in drug addiction. Using whole-cell recordings in CeA slices, we found that in rats displaying morphine-induced behavior of conditioned place preference, a behavioral measure of drug reward, the overall synaptic strength of glutamate synapses in CeA neurons was significantly enhanced. The selective DOR agonist [D-Pen(2),D-Pen(5)]-enkephalin, having no apparent effect on glutamatergic excitatory postsynaptic current (EPSC) in neurons from control rats, produced a significant, dose-dependent inhibition of the synaptic current in neurons from those morphine-treated rats. Detailed analyses of EPSC properties revealed that DOR activation inhibited the EPSC by reducing presynaptic release of glutamate, indicating functional DOR emerging on presynaptic glutamate terminals. The morphine treatment also significantly increased DOR proteins in CeA preparations of synaptosomes. These findings provide functional evidence for an adaptive modulation by presynaptic DOR of a key synaptic activity altered by morphine, thus implying likely important involvement of DOR in opioid reward and addiction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.