Orexin type-2 receptor blockade prevents the nicotine-induced excitation of nucleus accumbens core neurons in rats: An electrophysiological perspective.


Journal

Pharmacological reports : PR
ISSN: 2299-5684
Titre abrégé: Pharmacol Rep
Pays: Switzerland
ID NLM: 101234999

Informations de publication

Date de publication:
Apr 2019
Historique:
received: 07 07 2018
revised: 11 12 2018
accepted: 29 12 2018
pubmed: 5 3 2019
medline: 18 6 2019
entrez: 5 3 2019
Statut: ppublish

Résumé

The nucleus accumbens core (NAcc) expresses both orexin and nicotinic acetylcholine receptors (nAChRs). Orexin is among important neurotransmitters, which regulates addictive properties of drugs of abuse including nicotine. The role of orexin-2 receptor (OX2R) in the regulation of NAcc neural activity in response to nicotine has not yet been studied. Hence, in this study, we examined whether the OX2R antagonist (TCS-OX2-29) can adjust the effects of nicotine on electrical activity of NAcc neurons, in urethane-anesthetized rats, using the single unit recording. Neuronal firing of NAcc was recorded for 15 min, then TCS-OX2-29 (OX2R-antagonist; 1, 3 and 10 ng/rat) or DMSO were microinjected into NAcc, just 5 min before subcutaneous (sc) administration of nicotine (0.5 mg/kg) or saline. The spontaneous firing activity was recorded for 70 min, after nicotine injection. The results demonstrated that nicotine significantly excites the NAcc neurons and interestingly, the administration of TCS-OX2-29 (3 and 10 ng/rat) into the NAcc, inhibited nicotine-induced increases of NAcc neuronal responses. Furthermore, administration of TCS-OX2-29 (10 ng/rat), just 5 min before sc administration of saline instead of nicotine, did not significantly alter the neuronal responses, compared to the saline-control group. Our results showed that, although OX2R blockade alone did not affect neuronal activity in the NAcc, it was able to prevent the exciting effects of nicotine on NAcc neuronal activity. Therefore, we proposed that orexin has a potential modulator effect, in response to nicotine.

Sections du résumé

BACKGROUND BACKGROUND
The nucleus accumbens core (NAcc) expresses both orexin and nicotinic acetylcholine receptors (nAChRs). Orexin is among important neurotransmitters, which regulates addictive properties of drugs of abuse including nicotine. The role of orexin-2 receptor (OX2R) in the regulation of NAcc neural activity in response to nicotine has not yet been studied. Hence, in this study, we examined whether the OX2R antagonist (TCS-OX2-29) can adjust the effects of nicotine on electrical activity of NAcc neurons, in urethane-anesthetized rats, using the single unit recording.
METHODS METHODS
Neuronal firing of NAcc was recorded for 15 min, then TCS-OX2-29 (OX2R-antagonist; 1, 3 and 10 ng/rat) or DMSO were microinjected into NAcc, just 5 min before subcutaneous (sc) administration of nicotine (0.5 mg/kg) or saline. The spontaneous firing activity was recorded for 70 min, after nicotine injection.
RESULTS RESULTS
The results demonstrated that nicotine significantly excites the NAcc neurons and interestingly, the administration of TCS-OX2-29 (3 and 10 ng/rat) into the NAcc, inhibited nicotine-induced increases of NAcc neuronal responses. Furthermore, administration of TCS-OX2-29 (10 ng/rat), just 5 min before sc administration of saline instead of nicotine, did not significantly alter the neuronal responses, compared to the saline-control group.
CONCLUSION CONCLUSIONS
Our results showed that, although OX2R blockade alone did not affect neuronal activity in the NAcc, it was able to prevent the exciting effects of nicotine on NAcc neuronal activity. Therefore, we proposed that orexin has a potential modulator effect, in response to nicotine.

Identifiants

pubmed: 30831442
pii: S1734-1140(18)30413-4
doi: 10.1016/j.pharep.2018.12.013
pii:
doi:

Substances chimiques

1-(3,4-dihydro-6,7-dimethoxy-2(1H)-isoquinolinyl)-3,3-dimethyl-2-((4-pyridinylmethyl)amino)-1-butanone 0
Isoquinolines 0
Orexin Receptor Antagonists 0
Orexin Receptors 0
Orexins 0
Pyridines 0
Nicotine 6M3C89ZY6R

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

361-366

Informations de copyright

Copyright © 2018 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.

Auteurs

Reza Fartootzadeh (R)

Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Fatemeh Azizi (F)

Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Hojjatallah Alaei (H)

Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Parham Reisi (P)

Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: p_reisi@med.mui.ac.ir.

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Classifications MeSH