Divergent opioid-mediated suppression of inhibition between hippocampus and neocortex across species and development.

Autor:	Caccavano AP; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., Vlachos A; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., McLean N; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., Kimmel S; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., Kim JH; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., Vargish G; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., Mahadevan V; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., Hewitt L; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., Rossi AM; Harvard Medical School, Blavatnik Institute, Department of Neurobiology, Boston, MA 02115, USA.; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Spineux I; Harvard Medical School, Blavatnik Institute, Department of Neurobiology, Boston, MA 02115, USA.; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Wu SJ; Harvard Medical School, Blavatnik Institute, Department of Neurobiology, Boston, MA 02115, USA.; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Furlanis E; Harvard Medical School, Blavatnik Institute, Department of Neurobiology, Boston, MA 02115, USA.; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Dai M; Harvard Medical School, Blavatnik Institute, Department of Neurobiology, Boston, MA 02115, USA.; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Garcia BL; Harvard Medical School, Blavatnik Institute, Department of Neurobiology, Boston, MA 02115, USA.; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Chittajallu R; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., London E; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., Yuan X; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., Hunt S; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., Abebe D; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., Eldridge MAG; National Institute of Mental Health (NIMH), NIH, Bethesda, MD 20892, USA., Cummins AC; National Institute of Mental Health (NIMH), NIH, Bethesda, MD 20892, USA., Hines BE; National Institute of Mental Health (NIMH), NIH, Bethesda, MD 20892, USA., Plotnikova A; National Institute of Mental Health (NIMH), NIH, Bethesda, MD 20892, USA., Mohanty A; National Institute of Mental Health (NIMH), NIH, Bethesda, MD 20892, USA., Averbeck BB; National Institute of Mental Health (NIMH), NIH, Bethesda, MD 20892, USA., Zaghloul K; National Institute of Neurological Disorders and Stroke (NINDS) Intramural Research Program, NIH, Bethesda, MD 20892, USA., Dimidschstein J; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Fishell G; Harvard Medical School, Blavatnik Institute, Department of Neurobiology, Boston, MA 02115, USA.; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Pelkey KA; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA., McBain CJ; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Section on Cellular and Synaptic Physiology, National Institutes of Health (NIH), Bethesda, MD 20892, USA.
Jazyk:	angličtina
Zdroj:	BioRxiv : the preprint server for biology [bioRxiv] 2024 Nov 02. Date of Electronic Publication: 2024 Nov 02.
DOI:	10.1101/2024.01.20.576455
Abstrakt:	Opioid receptors within the CNS regulate pain sensation and mood and are key targets for drugs of abuse. Within the adult rodent hippocampus (HPC), μ-opioid receptor agonists suppress inhibitory parvalbumin-expressing interneurons (PV-INs), thus disinhibiting the circuit. However, it is uncertain if this disinhibitory motif is conserved in other cortical regions, species, or across development. We observed that PV-IN mediated inhibition is robustly suppressed by opioids in hippocampus proper but not neocortex in mice and nonhuman primates, with spontaneous inhibitory tone in resected human tissue also following a consistent dichotomy. This hippocampal disinhibitory motif was established in early development when PV-INs and opioids were found to regulate primordial network rhythmogenesis. Acute opioid-mediated modulation was partially occluded with morphine pretreatment, with implications for the effects of opioids on hippocampal network activity important for learning and memory. Together, these findings demonstrate that PV-INs exhibit a divergence in opioid sensitivity across brain regions that is remarkably conserved across evolution and highlights the underappreciated role of opioids acting through immature PV-INs in shaping hippocampal development. Competing Interests: DECLARATION OF INTERESTS The authors declare no competing interests.
Databáze:	MEDLINE
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