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Input-specific plasticity at excitatory synapses mediated by endocannabinoids in the dentate gyrus.
Neuropharmacology. 2008 Jan; 54(1):68-78.N

Abstract

Endocannabinoids (eCBs) mediate transient and long-lasting synaptic plasticity in several brain structures. In the dentate gyrus, activation of the type 1 cannabinoid receptor (CB1R) by exogenous ligands reportedly depresses excitatory synaptic transmission. However, direct evidence of eCB signaling at excitatory synapses in this region has been lacking. Here, we demonstrate that eCB release can be induced by a brief postsynaptic depolarization of dentate granule cells (DGCs), which potently and transiently suppresses glutamatergic inputs from mossy cell interneurons (MCs) but not from entorhinal cortex via the lateral and medial perforant paths. This input-specific depolarization-induced suppression of excitation (DSE) is calcium-dependent and can be modulated by agonists of cholinergic and group I metabotropic glutamate receptors. Inhibiting the synthesis of 2-arachidonoyl glycerol (2-AG), one of the most abundant eCBs in the brain, by diacyglycerol lipase (DGL) does not abolish DSE. Moreover, preventing the breakdown of anandamide, the other main eCB, does not potentiate DSE. Thus, eCB signaling underlying DSE in the dentate does not require DGL activity and is unlikely to be mediated by anandamide. Finally, we find that manipulations known to induce eCB-LTD at other central synapses do not trigger LTD at MCF-DGC synapses.

Authors+Show Affiliations

Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17706254

Citation

Chiu, Chiayu Q., and Pablo E. Castillo. "Input-specific Plasticity at Excitatory Synapses Mediated By Endocannabinoids in the Dentate Gyrus." Neuropharmacology, vol. 54, no. 1, 2008, pp. 68-78.
Chiu CQ, Castillo PE. Input-specific plasticity at excitatory synapses mediated by endocannabinoids in the dentate gyrus. Neuropharmacology. 2008;54(1):68-78.
Chiu, C. Q., & Castillo, P. E. (2008). Input-specific plasticity at excitatory synapses mediated by endocannabinoids in the dentate gyrus. Neuropharmacology, 54(1), 68-78.
Chiu CQ, Castillo PE. Input-specific Plasticity at Excitatory Synapses Mediated By Endocannabinoids in the Dentate Gyrus. Neuropharmacology. 2008;54(1):68-78. PubMed PMID: 17706254.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Input-specific plasticity at excitatory synapses mediated by endocannabinoids in the dentate gyrus. AU - Chiu,Chiayu Q, AU - Castillo,Pablo E, Y1 - 2007/07/06/ PY - 2007/03/31/received PY - 2007/06/04/revised PY - 2007/06/21/accepted PY - 2007/8/21/pubmed PY - 2008/4/19/medline PY - 2007/8/21/entrez SP - 68 EP - 78 JF - Neuropharmacology JO - Neuropharmacology VL - 54 IS - 1 N2 - Endocannabinoids (eCBs) mediate transient and long-lasting synaptic plasticity in several brain structures. In the dentate gyrus, activation of the type 1 cannabinoid receptor (CB1R) by exogenous ligands reportedly depresses excitatory synaptic transmission. However, direct evidence of eCB signaling at excitatory synapses in this region has been lacking. Here, we demonstrate that eCB release can be induced by a brief postsynaptic depolarization of dentate granule cells (DGCs), which potently and transiently suppresses glutamatergic inputs from mossy cell interneurons (MCs) but not from entorhinal cortex via the lateral and medial perforant paths. This input-specific depolarization-induced suppression of excitation (DSE) is calcium-dependent and can be modulated by agonists of cholinergic and group I metabotropic glutamate receptors. Inhibiting the synthesis of 2-arachidonoyl glycerol (2-AG), one of the most abundant eCBs in the brain, by diacyglycerol lipase (DGL) does not abolish DSE. Moreover, preventing the breakdown of anandamide, the other main eCB, does not potentiate DSE. Thus, eCB signaling underlying DSE in the dentate does not require DGL activity and is unlikely to be mediated by anandamide. Finally, we find that manipulations known to induce eCB-LTD at other central synapses do not trigger LTD at MCF-DGC synapses. SN - 0028-3908 UR - https://www.unboundmedicine.com/medline/citation/17706254/Input_specific_plasticity_at_excitatory_synapses_mediated_by_endocannabinoids_in_the_dentate_gyrus_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(07)00192-X DB - PRIME DP - Unbound Medicine ER -