CB1 cannabinoid receptor-mediated anandamide signaling mechanisms of the inferior colliculus modulate the haloperidol-induced catalepsy

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dc.citation.volume337
dc.contributor.authorMedeiros, Priscila [UNIFESP]
dc.contributor.authorde Freitas, R. L.
dc.contributor.authorSilva, M. O.
dc.contributor.authorCoimbra, N. C.
dc.contributor.authorMelo-Thomas, Liana [UNIFESP]
dc.coverageOxford
dc.date.accessioned2020-07-31T12:47:16Z
dc.date.available2020-07-31T12:47:16Z
dc.date.issued2016
dc.description.abstractThe inferior colliculus (IC), a midbrain structure that processes acoustic information of aversive nature, is distinguished from other auditory nuclei in the brainstem by its connections with structures of the motor system. Previous evidence relating the IC to motor behavior shows that glutamatergic and GABAergic mechanisms in the IC exert influence on systemic haloperidol-induced catalepsy. There is substantial evidence supporting a role played by the endocannabinoid system as a modulator of the glutamatergic neurotransmission, as well as the dopaminergic activity in the basal nuclei and therefore it may be considered as a potential pharmacological target for the treatment of movement disorders. The present study evaluated if the endocannabinoid system in the IC plays a role in the elaboration of systemic haloperidol-induced catalepsy. Male Wistar rats received intracollicular microinjection of either the endogenous cannabinoid anandamide (AEA) at different concentrations (5, 50 or 100 pmol/0.2 mu l), the CB1 cannabinoid receptor antagonist AM251 at 50, 100 or 200 pmol/0.2 mu l or vehicle, followed by intraperitoneal (IP) administration of either haloperidol at 0.5 or 1 mg/kg or physiological saline. Systemic injection of haloperidol at both doses (0.5 or 1 mg/kg, IP) produced a cataleptic state, compared to vehicle/physiological saline-treated group, lasting 30 and 50 min after systemic administration of the dopaminergic receptors non-selective antagonist. The midbrain microinjection of AEA at 50 pmol/0.2 mu l increased the latency for stepping down from the horizontal bar after systemic administration of haloperidol. Moreover, the intracollicular administration of AEA at 50 pmol/0.2 mu l was able to increase the duration of catalepsy as compared to AEA at 100 pmol/0.2-mu l-treated group. Intracollicular pretreatment with AM251 at the intermediate concentration (100 pmol/0.2 mu l) was able to decrease the duration of catalepsy after systemic administration of haloperidol. However, neither the intracollicular microinjection of AM251 at the lowest (50 pmol/0.2 mu l) nor at the highest (200 pmol/0.2 mu l) concentration was able to block the systemic haloperidol-induced catalepsy. Furthermore, the intracollicular administration of AM251 at 100 pmol/0.2 mu l was able to decrease the duration of catalepsy as compared to AM251 at 50 pmol/0.2 mu l- and AM251 at 200 pmol/0.2-mu l-treated group. The latency for stepping down from the horizontal bar-induced by haloperidol administration-was decreased when microinjection of AEA at 50 pmol/0.2 mu l was preceded with blockade of CB1 receptor with AM251 (100 pmol/0.2 mu l). Our results strengthen the involvement of CB1-signaled endocannabinoid mechanisms of the IC in the neuromodulation of catalepsy induced by systemic administration of the dopaminergic receptors non-selective antagonist haloperidol. (C) 2016 IBRO. Published by Elsevier Ltd. All rights reserved.en
dc.description.affiliationUniv Marburg, Lab Expt & Physiol Psychol, Gutenbergstr 18, D-35032 Marburg, Germany
dc.description.affiliationUniv Sao Paulo, Ribeirao Preto Med Sch, FMRP, Lab Neuroanat & Neuropsychobiol,Dept Pharmacol, Av Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP, Brazil
dc.description.affiliationUniv Sao Paulo, Ribeirao Preto Med Sch, FMRP, Neurobiol Emot Res Ctr NAP USP NuPNE, Av Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP, Brazil
dc.description.affiliationBehav Neurosci Inst INeC, Av Cafe 2450, BR-14050220 Ribeirao Preto, SP, Brazil
dc.description.affiliationUniv Sao Paulo, FMRP, Ribeirao Preto Med Sch, Dept Neuroci & Behav Sci,Div Neurol,Postgrad Sect, Av Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP, Brazil
dc.description.affiliationUniv Sao Paulo, Dept Surg & Anat, Ribeirao Preto Med Sch, Neuroelectrophysiol Multiuser Ctr, Av Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP, Brazil
dc.description.affiliationUniv Sao Paulo, Dept Surg & Anat, Ribeirao Preto Med Sch, Neurobiol Pain & Emot Lab, Av Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP, Brazil
dc.description.affiliationUniv Fed Sao Paulo, UNIFESP, Dept Biosci, Av D Ana Costa 95, BR-11060001 Santos, SP, Brazil
dc.description.affiliationUnifespDepartment of Biosciences, Universidade Federal de São Paulo (UNIFESP), Av. D. Ana Costa, 95, Vila Mathias, Santos, São Paulo 11060-001, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipGerman Federation of Industrial Research Associations
dc.description.sponsorshipIDFAPESP: 2011/01409-4
dc.description.sponsorshipIDFAPESP: 2012/25167-2
dc.description.sponsorshipIDFAPESP: 2013/12916-0
dc.description.sponsorshipIDFAPESP: 2014/11869-0
dc.description.sponsorshipIDFAPESP: 02/01497-1
dc.description.sponsorshipIDCNPq: 301905/2010-0
dc.description.sponsorshipIDCNPq: 301341/2015-0
dc.description.sponsorshipIDCNPq: 501858/2005-9
dc.description.sponsorshipIDCNPq: 372654/2006-1
dc.description.sponsorshipIDCNPq: 372810/2008-0
dc.description.sponsorshipIDCNPq: 372877/2010-9
dc.description.sponsorshipIDGerman Federation of Industrial Research Associations: KF2780403JL3
dc.format.extent17-26
dc.identifierhttp://dx.doi.org/10.1016/j.neuroscience.2016.08.047
dc.identifier.citationNeuroscience. Oxford, v. 337, p. 17-26, 2016.
dc.identifier.doi10.1016/j.neuroscience.2016.08.047
dc.identifier.issn0306-4522
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/56708
dc.identifier.wosWOS:000386337600003
dc.language.isoeng
dc.publisherPergamon-Elsevier Science Ltd
dc.relation.ispartofNeuroscience
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjecthaloperidol catalepsyen
dc.subjectendocannabinoidsen
dc.subjectanandamideen
dc.subjectAM251en
dc.subjectCB1 cannabinoid receptoren
dc.subjectinferior colliculusen
dc.titleCB1 cannabinoid receptor-mediated anandamide signaling mechanisms of the inferior colliculus modulate the haloperidol-induced catalepsyen
dc.typeinfo:eu-repo/semantics/article
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