ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
μ-Opioid Receptor-Mediated Inhibition of Intercalated Neurons and Effect on Synaptic Transmission to the Central Amygdala.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 53 citations in OpenAlex.
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- Transcriptional response to chronic long-access fentanyl self-administration in rat habenula and amygdala.bioRxiv : the preprint server for biology · 2025Article
- Chronic Intermittent Ethanol and Withdrawal Suppress Evoked and Spontaneous GABA Release Onto Distinct Populations of Basolateral Amygdala Principal Neurons.Addiction biology · 2025Article
- Tricyclic antidepressants dose-dependently modulate the biphasic activity of the TRPC5 channel through opioid receptors.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Amygdala intercalated cells form an evolutionarily conserved system orchestrating brain networks.Nature neuroscience · 2025Review
- Pain-related cortico-limbic plasticity and opioid signaling.Neuropharmacology · 2023Review
- Shared Mechanisms of GABAergic and Opioidergic Transmission Regulate Corticolimbic Reward Systems and Cognitive Aspects of Motivational Behaviors.Brain sciences · 2023Review
- Opioid-Induced Reductions in Amygdala Lateral Paracapsular GABA Neuron Circuit Activity.International journal of molecular sciences · 2023Article
- Amygdala Intercalated Cells: Gate Keepers and Conveyors of Internal State to the Circuits of Emotion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Review
- Mechanism of opioid addiction and its intervention therapy: Focusing on the reward circuitry and mu-opioid receptor.MedComm · 2022Review
- Breakdown of utilitarian moral judgement after basolateral amygdala damage.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Current and Future Therapeutic Options in Pain Management: Multi-mechanistic Opioids Involving Both MOR and NOP Receptor Activation.CNS drugs · 2022Review
- Neurodegeneration Within the Amygdala Is Differentially Induced by Opioid and HIV-1 Tat Exposure.Frontiers in neuroscience · 2022Article
- Opioid Receptor-Mediated Regulation of Neurotransmission in the Brain.Frontiers in molecular neuroscience · 2022Review
- Selective δ-Opioid Receptor Agonist, KNT-127, Facilitates Contextual Fear ExtinctionFrontiers in behavioral neuroscience · 2022Article
- Incentive motivation: 'wanting' roles of central amygdala circuitry.Behavioural brain research · 2021Review
- Cross-reactivity of a pathogenic autoantibody to a tumor antigen in GABAProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Fear Memory Retrieval Is Associated With a Reduction in AMPA Receptor Density at Thalamic to Amygdala Intercalated Cell Synapses.Frontiers in synaptic neuroscience · 2021Article
- Deletion of ErbB4 Disrupts Synaptic Transmission and Long-Term Potentiation of Thalamic Input to Amygdalar Medial Paracapsular Intercalated Cells.Frontiers in synaptic neuroscience · 2021Article
- Multiple Sclerosis and the Endogenous Opioid System.Frontiers in neuroscience · 2021Review
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6 authors at 2 institutions in 2 countries.
Funding
Abstract
The amygdala is a key region for the processing of information underlying fear, anxiety, and fear extinction. Within the local neuronal networks of the amygdala, a population of inhibitory, intercalated neurons (ITCs) modulates the flow of information among various nuclei of amygdala, including the basal nucleus (BA) and the centromedial nucleus (CeM) of the amygdala. These ITCs have been shown to be important during fear extinction and are target of a variety of neurotransmitters and neuropeptides. Here we provide evidence that the activation of μ-opioid receptors (MORs) by the specific agonist DAMGO ([D-Ala2,N-Me-Phe4,Gly5-ol]-Enkephalin) hyperpolarizes medially located ITCs (mITCs) in acute brain slices of mice. Moreover, we use whole-cell patch-clamp recordings in combination with local electrical stimulation or glutamate uncaging to analyze the effect of MOR activation on local microcircuits. We show that the GABAergic transmission between mITCs and CeM neurons is attenuated by DAMGO, whereas the glutamatergic transmission on CeM neurons and mITCs is unaffected. Furthermore, MOR activation induced by theta burst stimulation in BA suppresses plastic changes of feedforward inhibitory transmission onto CeM neurons as revealed by the MOR antagonist CTAP d-Phe-Cys-Tyr-d-Trp-Arg-Thr-Pen-Thr-NH2. In summary, the mITCs constitute a target for the opioid system, and therefore, the activation of MOR in ITCs might play a central role in the modulation of the information processing between the basolateral complex of the amygdala and central nuclei of the amygdala.
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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.