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Published online March 5, 2008, 10.1101/lm.741908
 LEARNING & MEMORY 15:143-152
©2008 by Cold Spring Harbor Laboratory Press; ISSN 1072-0502/08 $5.00
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Research
Activation of CB1 specifically located on GABAergic interneurons inhibits LTD in the lateral amygdala

Shahnaz Christina Azad1,2,6, Jörg Kurz1,3, Giovanni Marsicano4,5, Beat Lutz4, Walter Zieglgänsberger1, and Gerhard Rammes1,3

1 Max-Planck-Institute of Psychiatry, Clinical Neuropharmacology, 80804 Munich, Germany; 2 Department of Anaesthesiology, Ludwig-Maximilians-University, 81377 Munich, Germany; 3 Department of Anaesthesiology, University of Technology, 81675 Munich, Germany; 4 Johannes Gutenberg-University, Department of Physiological Chemistry, 55099 Mainz, Germany; 5 U862 INSERM NeuroCentre Magendie, Group AVENIR 4, Université Bordeaux 2, 33077 Bordeaux, France

Previously, we found that in the lateral amygdala (LA) of the mouse, WIN55,212-2 decreases both glutamatergic and GABAergic synaptic transmission via activation of the cannabinoid receptor type 1 (CB1), yet produces an overall reduction of neuronal excitability. This suggests that the effects on excitatory transmission override those on inhibitory transmission. Here we show that CB1 activation by WIN55,212-2 and {Delta}9-THC inhibits long-term depression (LTD) of basal synaptic transmission in the LA, induced by low-frequency stimulation (LFS; 900 pulses/1 Hz). The CB1 agonist WIN55,212-2 blocked LTD via Gi/o proteins, activation of inwardly rectifying K+ channels (Kirs), inhibition of the adenylate cyclase-protein kinase A (PKA) pathway, and PKA-dependent inhibition of voltage-gated N-type Ca2+ channels (N-type VGCCs). Interestingly, WIN55,212-2 effects on LTD were abolished in CB1 knock-out mice (CB1-KO), and in conditional mutants lacking CB1 expression only in GABAergic interneurons, but were still present in mutants lacking CB1 in principal forebrain neurons. LTD induction per se was unaffected by the CB1 antagonist SR141716A and was normally expressed in CB1-KO as well as in both conditional CB1 mutants. Our data demonstrate that activation of CB1 specifically located on GABAergic interneurons inhibits LTD in the LA. These findings suggest that CB1 expressed on either glutamatergic or GABAergic neurons play a differential role in the control of synaptic transmission and plasticity.

Received August 31, 2007; accepted in revised form January 14, 2008.

6 Corresponding author.

E-mail Shahnaz.Azad{at}med.uni-muenchen.de; fax 49-89-7095-4469.

Article is online at http://www.learnmem.org/cgi/doi/10.1101/lm.741908.


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