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Cannabinoid CB1 and cholecystokinin CCK2 receptors modulate, in an opposing way, electrically evoked [3H]GABA efflux from rat cerebral cortex cell cultures: possible relevance for cortical GABA transmission and anxiety.
J Pharmacol Exp Ther. 2009 May; 329(2):708-17.JP

Abstract

The effects of treatments with cannabinoid (CB)(1) and cholecystokinin (CCK)(2) receptor agonists and antagonists, as well as compounds that enhance endocannabinoid signaling by inhibiting degradation, e.g., the fatty acid amide hydrolase inhibitor 3'-carbamoyl-biphenyl-3-yl-cyclohexylcarbamate (URB597) or the endocannabinoid reuptake inhibitor (5Z,8Z,11Z,14Z)-N-(3-furanylmethyl)-5,8,11,14-eicosatetraenamide (UCM707), were studied both on spontaneous and electrically evoked [(3)H]GABA efflux from rat cerebral cortex cell cultures. The CCK(2) receptor agonist CCK-8S, the CB(1) receptor agonist (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone (WIN55,212-2), URB597, UCM707, the CB(1) receptor antagonist N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole-carboxamide (SR141716A), and the CCK(2) receptor antagonist 2-[2-(5-Br-1H-indol-3-yl)ethyl]-3-[3-(1-methylethoxy)phenyl]-4-(3H)-quinazolinone (LY225910) did not affect spontaneous [(3)H]GABA efflux. CCK-8S concentration-dependently increased electrically evoked [(3)H]GABA overflow, and this effect was prevented by LY225910. WIN55,212-2, URB597, and UCM707 induced a reduction of electrically evoked [(3)H]GABA overflow. This reduction was counteracted by SR141716A. When CCK-8S and one of cannabinoid-interfering compounds were simultaneously added, at concentrations by themselves ineffective, to the superfusion medium, an enhancement in electrically evoked [(3)H]GABA efflux was observed. This increase was counteracted by either SR141716A or LY225910 as well as by the inhibitor of protein kinase C, (1R)-2-[12-[(2R)-2-(benzoyloxy)propyl]-3,10-dihydro-4,9-dihydroxy-2,6,7,11-tetramethoxy-3,10-dioxo-1-perylenyl]-1-methylethylcarbonic acid 4-hydroxyphenyl ester (calphostin C). These results indicate that CB(1) and CCK(2) receptors modulate, in an opposing way, electrically evoked [(3)H]GABA efflux from rat cerebral cortex cell cultures. The existence of a CB(1)/CCK(2) receptor heteromer on cortical GABA terminals, with a possible relevance for cortical GABA transmission and anxiety, is postulated.

Authors+Show Affiliations

Department of Clinical and Experimental Medicine, University of Ferrara, Ferrara, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19197005

Citation

Antonelli, Tiziana, et al. "Cannabinoid CB1 and Cholecystokinin CCK2 Receptors Modulate, in an Opposing Way, Electrically Evoked [3H]GABA Efflux From Rat Cerebral Cortex Cell Cultures: Possible Relevance for Cortical GABA Transmission and Anxiety." The Journal of Pharmacology and Experimental Therapeutics, vol. 329, no. 2, 2009, pp. 708-17.
Antonelli T, Tomasini MC, Mazza R, et al. Cannabinoid CB1 and cholecystokinin CCK2 receptors modulate, in an opposing way, electrically evoked [3H]GABA efflux from rat cerebral cortex cell cultures: possible relevance for cortical GABA transmission and anxiety. J Pharmacol Exp Ther. 2009;329(2):708-17.
Antonelli, T., Tomasini, M. C., Mazza, R., Fuxe, K., Gaetani, S., Cuomo, V., Tanganelli, S., & Ferraro, L. (2009). Cannabinoid CB1 and cholecystokinin CCK2 receptors modulate, in an opposing way, electrically evoked [3H]GABA efflux from rat cerebral cortex cell cultures: possible relevance for cortical GABA transmission and anxiety. The Journal of Pharmacology and Experimental Therapeutics, 329(2), 708-17. https://doi.org/10.1124/jpet.109.150649
Antonelli T, et al. Cannabinoid CB1 and Cholecystokinin CCK2 Receptors Modulate, in an Opposing Way, Electrically Evoked [3H]GABA Efflux From Rat Cerebral Cortex Cell Cultures: Possible Relevance for Cortical GABA Transmission and Anxiety. J Pharmacol Exp Ther. 2009;329(2):708-17. PubMed PMID: 19197005.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cannabinoid CB1 and cholecystokinin CCK2 receptors modulate, in an opposing way, electrically evoked [3H]GABA efflux from rat cerebral cortex cell cultures: possible relevance for cortical GABA transmission and anxiety. AU - Antonelli,Tiziana, AU - Tomasini,Maria Cristina, AU - Mazza,Roberta, AU - Fuxe,Kjell, AU - Gaetani,Silvana, AU - Cuomo,Vincenzo, AU - Tanganelli,Sergio, AU - Ferraro,Luca, Y1 - 2009/02/05/ PY - 2009/2/7/entrez PY - 2009/2/7/pubmed PY - 2009/5/23/medline SP - 708 EP - 17 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 329 IS - 2 N2 - The effects of treatments with cannabinoid (CB)(1) and cholecystokinin (CCK)(2) receptor agonists and antagonists, as well as compounds that enhance endocannabinoid signaling by inhibiting degradation, e.g., the fatty acid amide hydrolase inhibitor 3'-carbamoyl-biphenyl-3-yl-cyclohexylcarbamate (URB597) or the endocannabinoid reuptake inhibitor (5Z,8Z,11Z,14Z)-N-(3-furanylmethyl)-5,8,11,14-eicosatetraenamide (UCM707), were studied both on spontaneous and electrically evoked [(3)H]GABA efflux from rat cerebral cortex cell cultures. The CCK(2) receptor agonist CCK-8S, the CB(1) receptor agonist (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone (WIN55,212-2), URB597, UCM707, the CB(1) receptor antagonist N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole-carboxamide (SR141716A), and the CCK(2) receptor antagonist 2-[2-(5-Br-1H-indol-3-yl)ethyl]-3-[3-(1-methylethoxy)phenyl]-4-(3H)-quinazolinone (LY225910) did not affect spontaneous [(3)H]GABA efflux. CCK-8S concentration-dependently increased electrically evoked [(3)H]GABA overflow, and this effect was prevented by LY225910. WIN55,212-2, URB597, and UCM707 induced a reduction of electrically evoked [(3)H]GABA overflow. This reduction was counteracted by SR141716A. When CCK-8S and one of cannabinoid-interfering compounds were simultaneously added, at concentrations by themselves ineffective, to the superfusion medium, an enhancement in electrically evoked [(3)H]GABA efflux was observed. This increase was counteracted by either SR141716A or LY225910 as well as by the inhibitor of protein kinase C, (1R)-2-[12-[(2R)-2-(benzoyloxy)propyl]-3,10-dihydro-4,9-dihydroxy-2,6,7,11-tetramethoxy-3,10-dioxo-1-perylenyl]-1-methylethylcarbonic acid 4-hydroxyphenyl ester (calphostin C). These results indicate that CB(1) and CCK(2) receptors modulate, in an opposing way, electrically evoked [(3)H]GABA efflux from rat cerebral cortex cell cultures. The existence of a CB(1)/CCK(2) receptor heteromer on cortical GABA terminals, with a possible relevance for cortical GABA transmission and anxiety, is postulated. SN - 1521-0103 UR - https://www.unboundmedicine.com/medline/citation/19197005/Cannabinoid_CB1_and_cholecystokinin_CCK2_receptors_modulate_in_an_opposing_way_electrically_evoked_[3H]GABA_efflux_from_rat_cerebral_cortex_cell_cultures:_possible_relevance_for_cortical_GABA_transmission_and_anxiety_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=19197005 DB - PRIME DP - Unbound Medicine ER -