Cannabinoid Receptor-Mediated Regulation of Neuronal Activity and Signaling in Glomeruli of the Main Olfactory Bulb

Abstract

Event Abstract Back to Event Cannabinoid Receptor-Mediated Regulation of Neuronal Activity and Signaling in Glomeruli of the Main Olfactory Bulb Thomas Heinbockel1*, Ze-Jun Wang1 and Liqin Sun1 1 Howard University College of Medicine, Dept. of Anatomy, United States Immunohistochemical and autoradiographic studies indicate that cannabinoid receptors, CB1R, are present in glomeruli of the main olfactory bulb (MOB). Furthermore, neurons in the glomerular layer are immunoreactive for enzymes that synthesize endocannabinoids. The cellular and network functions of CB1R and their endogenous activators, endocannabinoids, for glomerular signaling are unknown. Olfactory glomeruli contain at least three types of neurons: periglomerular (PG), external tufted (ET), and short-axon (SA) cells. PG cells are GABAergic, SA cells express both GABA and dopamine, and ET cells are glutamatergic. PG cells receive input from the olfactory nerve or dendrodendritic glutamatergic input from ET or mitral cells. PG cells presynaptically inhibit olfactory receptor neurons through GABAergic transmission. ET cells receive spontaneous bursts of IPSCs from PG cells at inhibitory GABAergic dendrodendritic synapses. ET cells can be a potential source of endocannabinoids in olfactory glomeruli. ET cells exhibit intrinsic, rhythmic bursting of action potentials at a frequency of 1 to 6 Hz. To determine the function of the endocanabinoid system in olfactory glomeruli, we used whole-cell patch-clamp recording in mouse brain slices and tested the effects of agonists and antagonists of CB1R on cellular and network activity. Specifically, we studied the role of CB1R in regulating PG and ET cells. PG cells are likely candidates for direct effects of endocannabinoids since CB1R is robustly expressed in the glomerular layer. Cannabinoids displayed strong, direct inhibitory effects on PG cells that persisted in the presence of blockers of fast synaptic transmission (NMDA, AMPA, and GABA-A receptor blockers). CB1R-regulated activity of PG cells may modulate transmitter release and synaptic transmission to ET cells. We tested the effects of CB1R drugs on the activity of ET cells and found weak effects on ET cells. Single depolarizing voltage steps applied to an ET cell in voltage-clamp mode evoked suppression of sIPSCs. A train of depolarizing voltage steps (>3) strengthened the inhibition of sIPSCs, suggesting that excitation of ET cells in the form of rhythmic bursting triggers the release of endocannabinoids and regulates glomerular activity. Our results suggest retrograde endocannabinoid signaling, namely, depolarization-induced suppression of inhibition (DSI) in ET cells. In DSI, a type of short-term synaptic plasticity, endocannabinoids are released from depolarized principal neurons and travel to presynaptic inhibitory interneurons to transiently reduce presynaptic firing and neurotransmitter (GABA) release. Our results support the hypothesis that burst firing of ET cells triggers the release of endocannabinoids which in turn directly inhibit PG cells and reduce GABA release from PG cells. Subsequently, this can result in a transient reduction of PG cell inhibitory input to ET cells. Bursting of neurons may modulate endocannabinoid release not only in the MOB but also in other brain systems. Support: Whitehall Foundation, U.S. PHS grants S06GM08016 (MBRS-SCORE, NIGMS/NIH), 8G12MD007597 (RCMI, NIH-NIMHD). Keywords: cannabinoid, glomerulus, neurotransmitter, Olfaction, patch-clamp electrophysiology, retrograde signaling, rhythmic bursting, Synaptic integration Conference: Tenth International Congress of Neuroethology, College Park. Maryland USA, United States, 5 Aug - 10 Aug, 2012. Presentation Type: Poster (but consider for Participant Symposium) Topic: Sensory: Olfaction and Taste Citation: Heinbockel T, Wang Z and Sun L (2012). Cannabinoid Receptor-Mediated Regulation of Neuronal Activity and Signaling in Glomeruli of the Main Olfactory Bulb. Conference Abstract: Tenth International Congress of Neuroethology. doi: 10.3389/conf.fnbeh.2012.27.00184 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 28 Apr 2012; Published Online: 07 Jul 2012. * Correspondence: Dr. Thomas Heinbockel, Howard University College of Medicine, Dept. of Anatomy, Washington, DC, 20059, United States, theinbockel@howard.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Thomas Heinbockel Ze-Jun Wang Liqin Sun Google Thomas Heinbockel Ze-Jun Wang Liqin Sun Google Scholar Thomas Heinbockel Ze-Jun Wang Liqin Sun PubMed Thomas Heinbockel Ze-Jun Wang Liqin Sun Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.