Research article summary (published 30 Mar 2009):

Endocannabinoid-mediated long-term depression in the avian midbrain expressed presynaptically and postsynaptically.

Full Abstract

Here, we examined long-term synaptic plasticity in the avian auditory midbrain, a region involved in experience-dependent learning. We found that coactivation of N-methyl-D-aspartate receptors (NMDAR) and type 1 cannabinoid receptors (CB1R) induces long-term depression (LTD) at the synapse between the central shell and the external portion of the inferior colliculus of the chicken. Although endocannabinoids are commonly thought of as presynaptic modulators, recent reports have suggested that they can also modulate the postsynaptic site. In the avian midbrain, we found that LTD is mediated by both presynaptic and postsynaptic changes. The presynaptic mechanism consists of a decrease in neurotransmitter release, whereas a depression of NMDAR-mediated current takes place on the postsynaptic side. Both the presynaptic and the postsynaptic effects depend on CB1R activation. The reduction of postsynaptic NMDAR currents represents a novel role of endocannabinoids in synaptic modulation.

Author information

Author/s: Penzo, Mario Alexander (MA); Peña, José Luis (JL);

Affiliation: Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

Grants: DC007690 (Agency:NIDCD NIH HHS) ; DC007690.S1 (Agency:NIDCD NIH HHS) ; R01 DC007690-04 (Agency:NIDCD NIH HHS)

Journal and publication information

Publication Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience (J Neurosci), published in United States. (Language: eng)

Reference: 2009-Apr; vol 29 (issue 13) : pp 4131-9

Dates: Created 2009/04/02; Completed 2009/04/23; Revised 2009/07/29;

PMID: 19339608, status: MEDLINE (last retrieval date: 8/20/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals Biophysics Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism Chelating Agents - pharmacology Chick Embryo Egtazic Acid - analogs & derivatives; pharmacology Electric Stimulation Endocannabinoids - antagonists & inhibitors; pharmacology Enzyme Inhibitors - pharmacology Excitatory Amino Acid Agents - pharmacology Guanosine Diphosphate - analogs & derivatives; pharmacology Intracellular Signaling Peptides and Proteins - pharmacology

Long-Term Synaptic Depression - drug effects Mesencephalon - cytology; drug effects; metabolism Methoxyhydroxyphenylglycol - analogs & derivatives; pharmacology Neurons - drug effects; physiology Patch-Clamp Techniques - methods Peptide Fragments - pharmacology Pertussis Toxin - pharmacology Piperidines - pharmacology Presynaptic Terminals - drug effects; physiology Pyrazoles - pharmacology Synapses - drug effects; physiology Thionucleotides - pharmacology

Associated Chemicals: AM 251 (0) ; Chelating Agents (0) ; Endocannabinoids (0) ; Enzyme Inhibitors (0) ; Excitatory Amino Acid Agents (0) ; Intracellular Signaling Peptides and Proteins (0) ; Peptide Fragments (0) ; Piperidines (0) ; Pyrazoles (0) ; Thionucleotides (0) ; protein kinase inhibitor (6-22) (0) ; Guanosine Diphosphate (146-91-8) ; dihydroxyphenylethylene glycol (3343-19-9) ; Methoxyhydroxyphenylglycol (534-82-7) ; Egtazic Acid (67-42-5) ; guanosine 5'-O-(2-thiodiphosphate) (71376-97-1) ; 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (85233-19-8) ; Pertussis Toxin (EC 2.4.2.31) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17)

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