title: Developmental alterations of DHPG-induced long-term depression of corticostriatal synaptic transmission: switch from NMDA receptor-dependent towards CB1 receptor-dependent plasticity.
abstract: In animal models of early Parkinson's disease (PD), motor deficits are accompanied by excessive striatal glutamate release. Blockade of group I metabotropic glutamate receptors (mGluRs), endocannabinoid degradation and nitric oxide (NO) synthesis combats PD symptoms. Activation of group I mGluRs with the specific agonist 3,5-dihydroxyphenylglycine (DHPG) induces long-term depression of corticostriatal transmission (LTD(DHPG)) in the adult mouse striatum requiring NO synthesis downstream to cannabinoid CB1 receptor (CB1R) activation suggesting a dual role for LTD(DHPG): neuroprotective by down-regulation of glutamatergic transmission and, under certain circumstances, neurotoxic by release of NO. We report now that LTD(DHPG) undergoes a developmental switch from N-methyl-D-aspartate (NMDA)-receptor-dependent/CB1R-independent to NMDA receptor-independent/CB1R-dependent plasticity with NO playing an essential role for LTD(DHPG) at all developmental stages. The gain in function of CB1R is explained by their developmental up-regulation evaluated with real-time reverse transcription-polymerase chain reaction. These findings are relevant for the pathophysiology and therapy of PD as they link the activation of group I mGluRs, endocannabinoid release, and striatal NO production.
authors.affiliation: Department of Neurophysiology, Heinrich-Heine-University, Dusseldorf, 40001, Germany.
authors.forename: Aisa N
authors.initials: AN
authors.lastname: Chepkova
authors.forename: Wiebke
authors.initials: W
authors.lastname: Fleischer
authors.forename: Thomas
authors.initials: T
authors.lastname: Kazmierczak
authors.forename: Nanuli
authors.initials: N
authors.lastname: Doreulee
authors.forename: Helmut L
authors.initials: HL
authors.lastname: Haas
authors.forename: Olga A
authors.initials: OA
authors.lastname: Sergeeva
mesh_terms: D000818:Animals; D003342:Corpus Striatum / Q000254:growth & development* / Q000378:metabolism; D004594:Electrophysiology; D018683:Excitatory Amino Acid Agents / Q000494:pharmacology; D005998:Glycine / Q000031:analogs & derivatives / Q000494:pharmacology; D036881:Long-Term Synaptic Depression / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009473:Neuronal Plasticity / Q000502:physiology*; D043884:Receptor, Cannabinoid, CB1 / Q000378:metabolism*; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism*; D012118:Resorcinols / Q000494:pharmacology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D009435:Synaptic Transmission / Q000502:physiology*
chemical_list: D018683:Excitatory Amino Acid Agents; D043884:Receptor, Cannabinoid, CB1; D016194:Receptors, N-Methyl-D-Aspartate; D012118:Resorcinols; C079215:3,5-dihydroxyphenylglycine; D005998:Glycine
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