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CB1 cannabinoid receptor-mediated anandamide signaling mechanisms of the inferior colliculus modulate the haloperidol-induced catalepsy.
Neuroscience. 2016 Nov 19; 337:17-26.N

Abstract

The 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 100pmol/0.2μl), the CB1 cannabinoid receptor antagonist AM251 at 50, 100 or 200pmol/0.2μl or vehicle, followed by intraperitoneal (IP) administration of either haloperidol at 0.5 or 1mg/kg or physiological saline. Systemic injection of haloperidol at both doses (0.5 or 1mg/kg, IP) produced a cataleptic state, compared to vehicle/physiological saline-treated group, lasting 30 and 50min after systemic administration of the dopaminergic receptors non-selective antagonist. The midbrain microinjection of AEA at 50pmol/0.2μl increased the latency for stepping down from the horizontal bar after systemic administration of haloperidol. Moreover, the intracollicular administration of AEA at 50pmol/0.2μl was able to increase the duration of catalepsy as compared to AEA at 100pmol/0.2-μl-treated group. Intracollicular pretreatment with AM251 at the intermediate concentration (100pmol/0.2μl) was able to decrease the duration of catalepsy after systemic administration of haloperidol. However, neither the intracollicular microinjection of AM251 at the lowest (50pmol/0.2μl) nor at the highest (200pmol/0.2μl) concentration was able to block the systemic haloperidol-induced catalepsy. Furthermore, the intracollicular administration of AM251 at 100pmol/0.2μl was able to decrease the duration of catalepsy as compared to AM251 at 50pmol/0.2μl- and AM251 at 200pmol/0.2-μl-treated group. The latency for stepping down from the horizontal bar - induced by haloperidol administration - was decreased when microinjection of AEA at 50pmol/0.2μl was preceded with blockade of CB1 receptor with AM251 (100pmol/0.2μl). 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.

Authors+Show Affiliations

Laboratory of Neuroanatomy and Neuropsychobiology, Department of Pharmacology, Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, 14049-900 São Paulo, Brazil; Department of Neurocience and Behavioral Sciences, Division of Neurology, Post-Graduation Section, Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, São Paulo 14049-900, Brazil; Neuroelectrophysiology Multiuser Center and Neurobiology of Pain and Emotions Laboratory, Department of Surgery and Anatomy, Ribeirão Preto Medical School of the University of São Paulo, Av. Bandeirantes, 3900, Ribeirão Preto, São Paulo 14049-900, Brazil; Department of Biosciences, Federal University of São Paulo (UNIFESP), Av. D. Ana Costa, 95, Vila Mathias, Santos, São Paulo 11060-001, Brazil.Laboratory of Neuroanatomy and Neuropsychobiology, Department of Pharmacology, Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, 14049-900 São Paulo, Brazil; Neurobiology of Emotions Research Center (NAP-USP-NuPNE), Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, 14049-900 São Paulo, Brazil; Neuroelectrophysiology Multiuser Center and Neurobiology of Pain and Emotions Laboratory, Department of Surgery and Anatomy, Ribeirão Preto Medical School of the University of São Paulo, Av. Bandeirantes, 3900, Ribeirão Preto, São Paulo 14049-900, Brazil.Laboratory of Neuroanatomy and Neuropsychobiology, Department of Pharmacology, Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, 14049-900 São Paulo, Brazil; Neuroelectrophysiology Multiuser Center and Neurobiology of Pain and Emotions Laboratory, Department of Surgery and Anatomy, Ribeirão Preto Medical School of the University of São Paulo, Av. Bandeirantes, 3900, Ribeirão Preto, São Paulo 14049-900, Brazil.Laboratory of Neuroanatomy and Neuropsychobiology, Department of Pharmacology, Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, 14049-900 São Paulo, Brazil; Neurobiology of Emotions Research Center (NAP-USP-NuPNE), Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, 14049-900 São Paulo, Brazil; Behavioural Neurosciences Institute (INeC), Av. do Café, 2450, Ribeirão Preto, 14050-220 São Paulo, Brazil; Department of Neurocience and Behavioral Sciences, Division of Neurology, Post-Graduation Section, Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, São Paulo 14049-900, Brazil; Neuroelectrophysiology Multiuser Center and Neurobiology of Pain and Emotions Laboratory, Department of Surgery and Anatomy, Ribeirão Preto Medical School of the University of São Paulo, Av. Bandeirantes, 3900, Ribeirão Preto, São Paulo 14049-900, Brazil. Electronic address: nccoimbr@fmrp.usp.br.Laboratory of Experimental and Physiological Psychology, Philipps-University of Marburg, Gutenbergstrasse 18, 35032 Marburg, Germany; Behavioural Neurosciences Institute (INeC), Av. do Café, 2450, Ribeirão Preto, 14050-220 São Paulo, Brazil; Department of Biosciences, Federal University of São Paulo (UNIFESP), Av. D. Ana Costa, 95, Vila Mathias, Santos, São Paulo 11060-001, Brazil. Electronic address: lianamel@gmail.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27595886

Citation

Medeiros, P, et al. "CB1 Cannabinoid Receptor-mediated Anandamide Signaling Mechanisms of the Inferior Colliculus Modulate the Haloperidol-induced Catalepsy." Neuroscience, vol. 337, 2016, pp. 17-26.
Medeiros P, de Freitas RL, Silva MO, et al. CB1 cannabinoid receptor-mediated anandamide signaling mechanisms of the inferior colliculus modulate the haloperidol-induced catalepsy. Neuroscience. 2016;337:17-26.
Medeiros, P., de Freitas, R. L., Silva, M. O., Coimbra, N. C., & Melo-Thomas, L. (2016). CB1 cannabinoid receptor-mediated anandamide signaling mechanisms of the inferior colliculus modulate the haloperidol-induced catalepsy. Neuroscience, 337, 17-26. https://doi.org/10.1016/j.neuroscience.2016.08.047
Medeiros P, et al. CB1 Cannabinoid Receptor-mediated Anandamide Signaling Mechanisms of the Inferior Colliculus Modulate the Haloperidol-induced Catalepsy. Neuroscience. 2016 Nov 19;337:17-26. PubMed PMID: 27595886.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - CB1 cannabinoid receptor-mediated anandamide signaling mechanisms of the inferior colliculus modulate the haloperidol-induced catalepsy. AU - Medeiros,P, AU - de Freitas,R L, AU - Silva,M O, AU - Coimbra,N C, AU - Melo-Thomas,L, Y1 - 2016/09/03/ PY - 2015/11/03/received PY - 2016/08/23/revised PY - 2016/08/28/accepted PY - 2016/10/25/pubmed PY - 2017/12/22/medline PY - 2016/9/7/entrez KW - AM251 KW - CB(1) cannabinoid receptor KW - anandamide KW - endocannabinoids KW - haloperidol catalepsy KW - inferior colliculus SP - 17 EP - 26 JF - Neuroscience JO - Neuroscience VL - 337 N2 - The 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 100pmol/0.2μl), the CB1 cannabinoid receptor antagonist AM251 at 50, 100 or 200pmol/0.2μl or vehicle, followed by intraperitoneal (IP) administration of either haloperidol at 0.5 or 1mg/kg or physiological saline. Systemic injection of haloperidol at both doses (0.5 or 1mg/kg, IP) produced a cataleptic state, compared to vehicle/physiological saline-treated group, lasting 30 and 50min after systemic administration of the dopaminergic receptors non-selective antagonist. The midbrain microinjection of AEA at 50pmol/0.2μl increased the latency for stepping down from the horizontal bar after systemic administration of haloperidol. Moreover, the intracollicular administration of AEA at 50pmol/0.2μl was able to increase the duration of catalepsy as compared to AEA at 100pmol/0.2-μl-treated group. Intracollicular pretreatment with AM251 at the intermediate concentration (100pmol/0.2μl) was able to decrease the duration of catalepsy after systemic administration of haloperidol. However, neither the intracollicular microinjection of AM251 at the lowest (50pmol/0.2μl) nor at the highest (200pmol/0.2μl) concentration was able to block the systemic haloperidol-induced catalepsy. Furthermore, the intracollicular administration of AM251 at 100pmol/0.2μl was able to decrease the duration of catalepsy as compared to AM251 at 50pmol/0.2μl- and AM251 at 200pmol/0.2-μl-treated group. The latency for stepping down from the horizontal bar - induced by haloperidol administration - was decreased when microinjection of AEA at 50pmol/0.2μl was preceded with blockade of CB1 receptor with AM251 (100pmol/0.2μl). 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. SN - 1873-7544 UR - https://www.unboundmedicine.com/medline/citation/27595886/CB1_cannabinoid_receptor_mediated_anandamide_signaling_mechanisms_of_the_inferior_colliculus_modulate_the_haloperidol_induced_catalepsy_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(16)30420-1 DB - PRIME DP - Unbound Medicine ER -