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Presynaptic cannabinoid CB2 receptors modulate [ 3 H]-Glutamate release at subthalamo-nigral terminals of the rat

Presynaptic cannabinoid CB2 receptors modulate [ 3 H]-Glutamate release at subthalamo-nigral terminals of the rat

Rodolfo Sánchez-Zavaleta, Hernán Cortés, José Arturo Avalos-Fuentes, Ubaldo García, José Segovia Vila, David Erlij, Benjamín Florán

Synapse. 2018 Nov;72(11):e22061.

PMID: 30022523

Abstract:

Recent studies suggested the expression of CB2 receptors in neurons of the CNS, however, most of these studies have only explored one aspect of the receptors, i.e., expression of protein, messenger RNA, or functional response, and more complete studies appear to be needed to establish adequately their role in the neuronal function. Electron microscopy studies showed the presence of CB2r in asymmetric terminals of the substantia nigra pars reticulata (SNr), and its mRNA appeared is expressed in the subthalamic nucleus. Here, we explore the expression, source, and functional effects of such receptors by different experimental approaches. Through PCR and immunochemistry, we showed mRNA and protein for CB2rs in slices and primary neuronal cultures from subthalamus. GW833972A, GW405833, and JHW 133, three CB2r agonists dose-dependent inhibited K+ -induced [3 H]-Glutamate release in slices of SNr, and the two antagonist/inverse agonists, JTE-907 and AM630, but not AM281, a CB1r antagonist, prevented GW833972A effect. Subthalamus lesions with kainic acid prevented GW833972A inhibition on release and decreased CB2r protein in nigral synaptosomes, thus nigral CB2rs originate in subthalamus. Inhibition of [3 H]-Glutamate release was PTX- and gallein-sensitive, suggesting a Giβγ -mediated effect. P/Q Ca2+ -type channel blocker, ω-Agatoxin-TK, also inhibited the [3 H]-Glutamate release, this effect was occluded with GW833972A inhibition, indicating that the βγ subunit effect is exerted on Ca2+ channel activity. Finally, microinjections of GW833972A in SNr induced contralateral turning. Our data showed that presynaptic CB2rs inhibit [3 H]-Glutamate release in subthalamo-nigral terminals by P/Q-channels modulation through the Giβγ subunit and suggested their participation in motor behavior.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP1092502334	GW833972A		1092502-33-4	Price
AP158484425	ω-Agatoxin TK		158484-42-5	Price

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