CB1 in the cortex (thanks to Gary)

J Neurophysiol 97: 2580-2589, 2007. First published January 31, 2007; doi:10.1152/jn.00603.2006 Free Article0022-3077/07 $8.00This ArticleFree upon publication Free ArticleRight arrow Full TextRight arrow Full Text (PDF)Right arrow All Versions of this Article:97/4/2580 most recent00603.2006v1Right arrow Alert me when this article is citedRight arrow Alert me if a correction is postedServicesRight arrow Email this article to a friendRight arrow Similar articles in this journalRight arrow Similar articles in PubMedRight arrow Alert me to new issues of the journalRight arrow Download to citation managerGoogle ScholarRight arrow Articles by Hill, E. L.Right arrow Articles by Lambolez, B.PubMedRight arrow PubMed CitationRight arrow Articles by Hill, E. L.Right arrow Articles by Lambolez, B.Functional CB1 Receptors Are Broadly Expressed in Neocortical GABAergic and Glutamatergic NeuronsElisa L. Hill1, Thierry Gallopin1, Isabelle Férézou1, Bruno Cauli1, Jean Rossier1, Paul Schweitzer2 and Bertrand Lambolez11Laboratoire de Neurobiologie et Diversité Cellulaire, Centre National de la Recherche Scientifique Unité Mixte de Recherche 7637, Ecole Supérieure de Physique et de Chimie Industrielles, Paris, France; and 2Molecular and Integrative Neurosciences Department, The Scripps Research Institute, La Jolla, CaliforniaSubmitted 9 June 2006; accepted in final form 31 January 2007The cannabinoid receptor CB1 is found in abundance in brain neurons, whereas CB2 is essentially expressed outside the brain. In the neocortex, CB1 is observed predominantly on large cholecystokinin (CCK)-expressing interneurons. However, physiological evidence suggests that functional CB1 are present on other neocortical neuronal types. We investigated the expression of CB1 and CB2 in identified neurons of rat neocortical slices using single-cell RT-PCR. We found that 63% of somatostatin (SST)-expressing and 69% of vasoactive intestinal polypeptide (VIP)-expressing interneurons co-expressed CB1. As much as 49% of pyramidal neurons expressed CB1. In contrast, CB2 was observed in a small proportion of neocortical neurons. We performed whole cell recordings of pyramidal neurons to corroborate our molecular findings. Inhibitory postsynaptic currents (IPSCs) induced by a mixed muscarinic/nicotinic cholinergic agonist showed depolarization-induced suppression of inhibition and were decreased by the CB1 agonist WIN-55212-2 (WIN-2), suggesting that interneurons excited by cholinergic agonists (mainly SST and VIP neurons) possess CB1. IPSCs elicited by a nicotinic receptor agonist were also reduced in the presence of WIN-2, suggesting that neurons excited by nicotinic agonists (mainly VIP neurons) indeed possess CB1. WIN-2 largely decreased excitatory postsynaptic currents evoked by intracortical electrical stimulation, pointing at the presence of CB1 on glutamatergic pyramidal neurons. All WIN-2 effects were strongly reduced by the CB1 antagonist AM 251. We conclude that CB1 is expressed in various neocortical neuronal populations, including glutamatergic neurons. Our combined molecular and physiological data suggest that CB1 widely mediates endocannabinoid effects on glutamatergic and GABAergic transmission to modulate cortical networks.

Functional CB1 Receptors Are Broadly Expressed in Neocortical GABAergic and Glutamatergic Neurons -- Hill et al. 97 (4): 2580 -- Journal of Neurophysiology

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