Cannabinoid Receptor-Mediated Regulation Of Neuronal Activity In The Main Olfactory

[Truth Seeker]

Neurons in the main olfactory bulb (MOB) express cannabinoid receptor CB1R. In mouse brain slices we used patch-clamping to study the role of CB1R in regulating mitral and periglomerular cells. CB1R agonists evoked depolarization and increased firing; CB1R antagonists reduced firing of mitral cells. The CB1R effects on mitral cells were absent in subglomerular slices in which the olfactory nerve layer and glomerular layer were removed suggesting the glomerular layer as the site of action of CB1R. Periglomerular cells showed the inverse response pattern to CB1R activation. A CB1R agonist inhibited periglomerular cells whereas a CB1R antagonist activated periglomerular cells. Block of presynaptic inhibition in olfactory nerve afferents through blockade of GABAB and dopamine D2 receptors eliminated the CB1R effects on mitral cells. These findings suggest that CB1R indirectly regulates glutamate release from olfactory nerve terminals which in turn activates metabotropic glutamate receptors on mitral cells. Indeed, blockade of metabotropic glutamate receptor mGluR1 prevented CB1R-mediated firing increases and CB1R-mediated inhibition of mitral cells. We hypothesize that CB1R directly regulates periglomerular cells which in turn controls glutamate release by olfactory nerve afferents to regulate mitral cells.

Source: Cannabinoid receptor-mediated regulation of neuronal activity in the main olfactory bulb -- Heinbockel et al. 25 (1): 855.3 -- The FASEB Journal