ArticleScientific reports2019
µ-opioid receptor-mediated downregulation of midline thalamic pathways to basal and central amygdala.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- The Therapeutic Potential of Dual NMR (NOP/MOP) Agonism in Pain Management.Pain and therapy · 2026Review
- The Paraventricular Thalamic Nucleus and Its Projections in Regulating Reward and Context Associations.eNeuro · 2024Article
- Cell-type specific molecular architecture for mu opioid receptor function in pain and addiction circuits.Neuropharmacology · 2023Review
- Pain-related cortico-limbic plasticity and opioid signaling.Neuropharmacology · 2023Review
- Article
- Perioperative stress prolong post-surgical pain via miR-339-5p targetingThe Korean journal of pain · 2022Article
- Thalamocortical functional connectivity in infants with prenatal opioid exposure correlates with severity of neonatal opioid withdrawal syndrome.Neuroradiology · 2022Article
- Opioid Receptor-Mediated Regulation of Neurotransmission in the Brain.Frontiers in molecular neuroscience · 2022Review
- Brain circuits for pain and its treatment.Science translational medicine · 2021Review
- Optogenetic study of central medial and paraventricular thalamic projections to the basolateral amygdala.Journal of neurophysiology · 2021Article
- Glutamatergic Systems and Memory Mechanisms Underlying Opioid Addiction.Cold Spring Harbor perspectives in medicine · 2021Review
- The µ-opioid system in midline thalamic nuclei modulates defence strategies towards a conditioned fear stimulus in male mice.Journal of psychopharmacology (Oxford, England) · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain µ-opioid receptors (MOR) mediate reward and help coping with pain, social rejection, anxiety and depression. The dorsal midline thalamus (dMT) integrates visceral/emotional signals and biases behavior towards aversive or defensive states through projections to the amygdala. While a dense MOR expression in the dMT has been described, the exact cellular and synaptic mechanisms of µ-opioidergic modulation in the dMT-amygdala circuitry remain unresolved. Here, we hypothesized that MORs are important negative modulators of dMT-amygdala excitatory networks. Using retrograde tracers and targeted channelrhodopsin expression in combination with patch-clamp electrophysiology, we found that projections of dMT neurons onto both basal amygdala principal neurons (BA PN) and central amygdala (CeL) neurons are attenuated by stimulation of somatic or synaptic MORs. Importantly, dMT efferents to the amygdala drive feedforward excitation of centromedial amygdala neurons (CeM), which is dampened by MOR activation. This downregulation of excitatory activity in dMT-amygdala networks puts the µ-opioid system in a position to ameliorate aversive or defensive behavioral states associated with stress, withdrawal, physical pain or social rejection.
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