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Endocannabinoid-dependent plasticity at GABAergic and glutamatergic synapses in the striatum is regulated by synaptic activity.

Journal article
Authors Louise Adermark
Giuseppe Talani
David M Lovinger
Published in The European journal of neuroscience
Volume 29
Issue 1
Pages 32-41
ISSN 1460-9568
Publication year 2009
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 32-41
Language en
Keywords Action Potentials, drug effects, physiology, Animals, Arachidonic Acids, metabolism, pharmacology, Calcium Channel Agonists, pharmacology, Calcium Channels, L-Type, drug effects, metabolism, Endocannabinoids, metabolism, Female, Glutamic Acid, metabolism, secretion, Male, Neostriatum, cytology, drug effects, metabolism, Neuronal Plasticity, drug effects, physiology, Neurons, drug effects, metabolism, Organ Culture Techniques, Piperidines, pharmacology, Polyunsaturated Alkamides, metabolism, Pyrazoles, pharmacology, Pyrroles, pharmacology, Rats, Rats, Sprague-Dawley, Receptor, Cannabinoid, CB1, antagonists & inhibitors, metabolism, Synapses, drug effects, metabolism, Synaptic Transmission, drug effects, physiology, gamma-Aminobutyric Acid, metabolism, secretion
Subject categories Pharmacology


Long-term depression (LTD) at striatal synapses is mediated by postsynaptic endocannabinoid (eCB) release and presynaptic cannabinoid 1 receptor (CB(1)R) activation. Previous studies have indicated that eCB mobilization at excitatory synapses might be regulated by afferent activation. To further address the role of neuronal activity in synaptic plasticity we examined changes in synaptic strength induced by the L-type calcium channel activator 2,5-dimethyl-4-[2-(phenylmethyl)benzoyl]-1H-pyrrole-3-carboxylic acid methyl ester (FPL 64176, FPL) at glutamatergic and gamma-aminobutyric acid (GABA)ergic synapses in the striatum. We found that the basic mechanisms for FPL-mediated eCB signaling are the same at glutamatergic and GABAergic synapses. FPL-induced LTD (FPL-LTD) was blocked in slices treated with the CB(1)R antagonist AM251 (2 microm), but established depression was not reversed by AM251. FPL-LTD was temperature dependent, blocked by protein translation inhibitors and prevented by intracellular loading of the anandamide transporter inhibitor VDM11 (10 microm) at both glutamatergic and GABAergic synapses. FPL-LTD at glutamatergic synapses required paired-pulse afferent stimulation, while FPL-LTD at GABAergic synapses could be induced even in the absence of explicit afferent activation. By evaluating tetrodotoxin-insensitive spontaneous inhibitory postsynaptic currents we found that neuronal firing is vital for eCB release and LTD induction at GABAergic synapses, but not for short-term depression induced by CB(1)R agonist. The data presented here suggest that the level of neuronal firing regulates eCB signaling by modulating release from the postsynaptic cell, as well as interacting with presynaptic mechanisms to induce LTD at both glutamatergic and GABAergic synapses in the striatum.

Page Manager: Webmaster|Last update: 9/11/2012

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