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This Article Full Text Full Text (PDF) All Versions of this Article: 102/3/1358    most recent 00294.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Thörn Pérez, C. Articles by Grillner, S. PubMed PubMed Citation Articles by Thörn Pérez, C. Articles by Grillner, S.

Endocannabinoids Mediate Tachykinin-Induced Effects in the Lamprey Locomotor Network

Department of Neuroscience, Nobel Institute for Neurophysiology, Karolinska Institutet, Stockholm, Sweden

Submitted 2 April 2009; accepted in final form 28 June 2009

Abstract

The spinal network underlying locomotion in lamprey is composed of excitatory and inhibitory interneurons mediating fast ionotropic action. In addition, several modulator systems are activated as locomotion is initiated, including the tachykinin system and the metabotropic glutamate receptor 1 (mGluR1), the latter operating partially via the endocannabinoid system. The effects of mGluR1 agonists and tachykinins resemble each other. Like mGluR1 agonists, the tachykinin substance P accelerates the burst rate and reduces the crossed inhibition in an activity-dependent fashion. The present study therefore explores whether tachykinins also use the endocannabinoid system to modulate the locomotor frequency. By monitoring fictive locomotion, we were able to compare the facilitatory effects exerted by applying substance P (1 µM, 20 min), on the burst frequency before and during application of the endocannabinoid CB1 receptor antagonist AM251 (2–5 µM). By using two different lamprey species, we showed that the response to substance P on the burst frequency is significantly reduced during the application of AM251. To examine whether endocannabinoids are involved in the substance P–mediated modulation of reciprocal inhibition, the commissural axons were stimulated, while recording intracellularly from motoneurons. We compare the effect of substance P on the amplitude of the contralateral compound glycinergic inhibitory postsynaptic potential (IPSP) in control and in the presence of AM251. The blockade of CB1 receptors reduced the substance P–mediated decrease in the amplitude by 29%. The present findings suggest that the effects of substance P on the increase in the locomotor burst frequency and depression of IPSPs are mediated partially via release of endocannabinoids acting through CB1 receptors.