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Neurotensin reduces glutamatergic transmission in the dorsolateral striatum via retrograde endocannabinoid signaling.

Journal article
Authors Henry H Yin
Louise Adermark
David M Lovinger
Published in Neuropharmacology
Volume 54
Issue 1
Pages 79-86
ISSN 0028-3908
Publication year 2008
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 79-86
Language en
Keywords Animals, Animals, Newborn, Corpus Striatum, cytology, Dose-Response Relationship, Drug, Drug Interactions, Electric Stimulation, Endocannabinoids, antagonists & inhibitors, metabolism, Excitatory Postsynaptic Potentials, drug effects, Neurons, drug effects, Neurotensin, pharmacology, Patch-Clamp Techniques, methods, Piperidines, pharmacology, Pyrazoles, pharmacology, Quinolines, pharmacology, Rats, Rats, Sprague-Dawley, Signal Transduction, drug effects
Subject categories Physiology


Neurotensin is a peptide that has been suggested to mimic the actions of antipsychotics, but little is known about how it affects synaptic transmission in the striatum, the major input nucleus of the basal ganglia. In this study we measured the effects of neurotensin on EPSCs from medium spiny projection neurons in the sensorimotor striatum, a region implicated in habit formation and control of motor sequences. We found that bath-applied neurotensin reduced glutamate release from presynaptic terminals, and that this effect required retrograde endocannabinoid signaling, as it was prevented by the CB1 cannabinoid receptor antagonist AM251. Neurotensin-mediated inhibition of striatal EPSCs was also blocked by antagonists of D2-like dopamine receptors and group I metabotropic glutamate receptors, as well as by intracellular calcium chelation and phospholipase C inhibition. These results suggest that neurotensin can indirectly engage an endocannabinoid-mediated negative feedback signal to control glutamatergic input to the basal ganglia.

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