title: Bidirectional plasticity in striatonigral synapses: a switch to balance direct and indirect basal ganglia pathways.
abstract: There is no hypothesis to explain how direct and indirect basal ganglia (BG) pathways interact to reach a balance during the learning of motor procedures. Both pathways converge in the substantia nigra pars reticulata (SNr) carrying the result of striatal processing. Unfortunately, the mechanisms that regulate synaptic plasticity in striatonigral (direct pathway) synapses are not known. Here, we used electrophysiological techniques to describe dopamine D(1)-receptor-mediated facilitation in striatonigral synapses in the context of its interaction with glutamatergic inputs, probably coming from the subthalamic nucleus (STN) (indirect pathway) and describe a striatonigral cannabinoid-dependent long-term synaptic depression (LTD). It is shown that striatonigral afferents exhibit D(1)-receptor-mediated facilitation of synaptic transmission when NMDA receptors are inactive, a phenomenon that changes to cannabinoid-dependent LTD when NMDA receptors are active. This interaction makes SNr neurons become coincidence-detector switching ports: When inactive, NMDA receptors lead to a dopamine-dependent enhancement of direct pathway output, theoretically facilitating movement. When active, NMDA receptors result in LTD of the same synapses, thus decreasing movement. We propose that SNr neurons, working as logical gates, tune the motor system to establish a balance between both BG pathways, enabling the system to choose appropriate synergies for movement learning and postural support.
authors.affiliation: Instituto de Fisiologia Celular-Neurociencias, Universidad Nacional Autonoma de México (UNAM), México City, DF Mexico 04510.
authors.forename: Jose J
authors.initials: JJ
authors.lastname: Aceves
authors.forename: Pavel E
authors.initials: PE
authors.lastname: Rueda-Orozco
authors.forename: Ricardo
authors.initials: R
authors.lastname: Hernandez-Martinez
authors.forename: Elvira
authors.initials: E
authors.lastname: Galarraga
authors.forename: Jose
authors.initials: J
authors.lastname: Bargas
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D001479:Basal Ganglia; D001552:Benzazepines / Q000494:pharmacology; D048588:Benzoxazines / Q000494:pharmacology; D001703:Biophysics; D002186:Cannabinoids / Q000819:agonists; D002614:Chelating Agents / Q000494:pharmacology; D003342:Corpus Striatum / Q000166:cytology*; D018491:Dopamine Agonists / Q000494:pharmacology; D004347:Drug Interactions; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004558:Electric Stimulation; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D036881:Long-Term Synaptic Depression / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009025:Morpholines / Q000494:pharmacology; D009281:Naphthalenes / Q000494:pharmacology; D009434:Neural Pathways / Q000502:physiology; D010880:Piperidines / Q000494:pharmacology; D011720:Pyrazoles / Q000494:pharmacology; D051381:Rats; D013378:Substantia Nigra / Q000166:cytology*; D013569:Synapses; D009435:Synaptic Transmission / Q000502:physiology*; D013997:Time Factors; D014633:Valine / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D001552:Benzazepines; D048588:Benzoxazines; D002186:Cannabinoids; D002614:Chelating Agents; D018491:Dopamine Agonists; D018691:Excitatory Amino Acid Antagonists; D009025:Morpholines; D009281:Naphthalenes; D010880:Piperidines; D011720:Pyrazoles; C534628:SCH 23390; C103505:AM 251; D004533:Egtazic Acid; C070417:(3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanone; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; C056639:2-amino-5-phosphopentanoic acid; D014633:Valine; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid