Marco Capogna

μ-Opioid Receptor-Mediated Inhibition of Intercalated Neurons and Effect on Synaptic Transmission to the Central Amygdala

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

  • Peter Blaesse, Institute of Physiology I, University of Münster, D-48149 Münster, Germany.
  • ,
  • Lena Goedecke, Institute of Physiology I, University of Münster, D-48149 Münster, Germany.
  • ,
  • Michaël Bazelot, MRC Brain Network Dynamics Unit, Department of Pharmacology, University of Oxford, Oxford, OX1 3TH, United Kingdom, and GW Pharmaceuticals, School of Chemistry, Food and Nutritional Science and Pharmacy, University of Reading, Whiteknights, Reading, RG6 6AP, United Kingdom.
  • ,
  • Marco Capogna
  • Hans-Christian Pape, Institute of Physiology I, University of Münster, D-48149 Münster, Germany.
  • ,
  • Kay Jüngling, Institute of Physiology I, University of Münster, D-48149 Münster, Germany, Kay.Juengling@gmx.de.

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.

Original languageEnglish
JournalThe Journal of neuroscience : the official journal of the Society for Neuroscience
Volume35
Issue19
Pages (from-to)7317-25
Number of pages9
ISSN0270-6474
DOIs
Publication statusPublished - 13 May 2015
Externally publishedYes

    Research areas

  • Analgesics, Opioid, Animals, Central Amygdaloid Nucleus, Enkephalin, Ala(2)-MePhe(4)-Gly(5)-, Excitatory Amino Acid Antagonists, Glutamate Decarboxylase, In Vitro Techniques, Mice, Mice, Inbred C57BL, Mice, Transgenic, Narcotic Antagonists, Neural Inhibition, Neurons, Peptides, Quinoxalines, Receptors, Opioid, mu, Sodium Channel Blockers, Synaptic Transmission, Tetrodotoxin, Valine, Journal Article, Research Support, Non-U.S. Gov't

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