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Nociceptin/orphanin FQ decreases glutamate transmission and blocks ethanol-induced effects in the central amygdala of naive and ethanol-dependent rats.
Neuropsychopharmacology. 2014 Apr; 39(5):1081-92.N

Abstract

The central nucleus of the amygdala (CeA) mediates several addiction-related processes and nociceptin/orphanin FQ (nociceptin) regulates ethanol intake and anxiety-like behaviors. Glutamatergic synapses, in the CeA and throughout the brain, are very sensitive to ethanol and contribute to alcohol reinforcement, tolerance, and dependence. Previously, we reported that in the rat CeA, acute and chronic ethanol exposures significantly decrease glutamate transmission by both pre- and postsynaptic actions. In this study, using electrophysiological techniques in an in vitro CeA slice preparation, we investigated the effects of nociceptin on glutamatergic transmission and its interaction with acute ethanol in naive and ethanol-dependent rats. We found that nociceptin (100-1000 nM) diminished basal-evoked compound glutamatergic receptor-mediated excitatory postsynaptic potentials (EPSPs) and spontaneous and miniature EPSCs (s/mEPSCs) by mainly decreasing glutamate release in the CeA of naive rats. Notably, nociceptin blocked the inhibition induced by acute ethanol (44 mM) and ethanol blocked the nociceptin-induced inhibition of evoked EPSPs in CeA neurons of naive rats. In neurons from chronic ethanol-treated (ethanol-dependent) rats, the nociceptin-induced inhibition of evoked EPSP amplitude was not significantly different from that in naive rats. Application of [Nphe1]Nociceptin(1-13)NH2, a nociceptin receptor (NOP) antagonist, revealed tonic inhibitory activity of NOP on evoked CeA glutamatergic transmission only in ethanol-dependent rats. The antagonist also blocked nociceptin-induced decreases in glutamatergic responses, but did not affect ethanol-induced decreases in evoked EPSP amplitude. Taken together, these studies implicate a potential role for the nociceptin system in regulating glutamatergic transmission and a complex interaction with ethanol at CeA glutamatergic synapses.

Authors+Show Affiliations

1] Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, USA [2] School of Pharmacy, Pharmacology Unit, University of Camerino, Camerino, Italy.Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, USA.Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, USA.1] Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, USA [2] Department of Pharmacology, Universidade Federal do Paraná, Jardim das Américas, Curitiba, Paraná, Brazil.Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, USA.Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, USA.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24169802

Citation

Kallupi, Marsida, et al. "Nociceptin/orphanin FQ Decreases Glutamate Transmission and Blocks Ethanol-induced Effects in the Central Amygdala of Naive and Ethanol-dependent Rats." Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, vol. 39, no. 5, 2014, pp. 1081-92.
Kallupi M, Varodayan FP, Oleata CS, et al. Nociceptin/orphanin FQ decreases glutamate transmission and blocks ethanol-induced effects in the central amygdala of naive and ethanol-dependent rats. Neuropsychopharmacology. 2014;39(5):1081-92.
Kallupi, M., Varodayan, F. P., Oleata, C. S., Correia, D., Luu, G., & Roberto, M. (2014). Nociceptin/orphanin FQ decreases glutamate transmission and blocks ethanol-induced effects in the central amygdala of naive and ethanol-dependent rats. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, 39(5), 1081-92. https://doi.org/10.1038/npp.2013.308
Kallupi M, et al. Nociceptin/orphanin FQ Decreases Glutamate Transmission and Blocks Ethanol-induced Effects in the Central Amygdala of Naive and Ethanol-dependent Rats. Neuropsychopharmacology. 2014;39(5):1081-92. PubMed PMID: 24169802.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nociceptin/orphanin FQ decreases glutamate transmission and blocks ethanol-induced effects in the central amygdala of naive and ethanol-dependent rats. AU - Kallupi,Marsida, AU - Varodayan,Florence P, AU - Oleata,Christopher S, AU - Correia,Diego, AU - Luu,George, AU - Roberto,Marisa, Y1 - 2013/10/30/ PY - 2013/09/05/received PY - 2013/10/08/revised PY - 2013/10/24/accepted PY - 2013/10/31/entrez PY - 2013/10/31/pubmed PY - 2014/12/15/medline SP - 1081 EP - 92 JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology JO - Neuropsychopharmacology VL - 39 IS - 5 N2 - The central nucleus of the amygdala (CeA) mediates several addiction-related processes and nociceptin/orphanin FQ (nociceptin) regulates ethanol intake and anxiety-like behaviors. Glutamatergic synapses, in the CeA and throughout the brain, are very sensitive to ethanol and contribute to alcohol reinforcement, tolerance, and dependence. Previously, we reported that in the rat CeA, acute and chronic ethanol exposures significantly decrease glutamate transmission by both pre- and postsynaptic actions. In this study, using electrophysiological techniques in an in vitro CeA slice preparation, we investigated the effects of nociceptin on glutamatergic transmission and its interaction with acute ethanol in naive and ethanol-dependent rats. We found that nociceptin (100-1000 nM) diminished basal-evoked compound glutamatergic receptor-mediated excitatory postsynaptic potentials (EPSPs) and spontaneous and miniature EPSCs (s/mEPSCs) by mainly decreasing glutamate release in the CeA of naive rats. Notably, nociceptin blocked the inhibition induced by acute ethanol (44 mM) and ethanol blocked the nociceptin-induced inhibition of evoked EPSPs in CeA neurons of naive rats. In neurons from chronic ethanol-treated (ethanol-dependent) rats, the nociceptin-induced inhibition of evoked EPSP amplitude was not significantly different from that in naive rats. Application of [Nphe1]Nociceptin(1-13)NH2, a nociceptin receptor (NOP) antagonist, revealed tonic inhibitory activity of NOP on evoked CeA glutamatergic transmission only in ethanol-dependent rats. The antagonist also blocked nociceptin-induced decreases in glutamatergic responses, but did not affect ethanol-induced decreases in evoked EPSP amplitude. Taken together, these studies implicate a potential role for the nociceptin system in regulating glutamatergic transmission and a complex interaction with ethanol at CeA glutamatergic synapses. SN - 1740-634X UR - https://www.unboundmedicine.com/medline/citation/24169802/Nociceptin/orphanin_FQ_decreases_glutamate_transmission_and_blocks_ethanol_induced_effects_in_the_central_amygdala_of_naive_and_ethanol_dependent_rats_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24169802/ DB - PRIME DP - Unbound Medicine ER -