Activation of subthalamic neurons produces NMDA receptor-mediated dendritic dopamine release in substantia nigra pars reticulata: a microdialysis study in the rat

Here we have studied whether the activation of the subthalamic neurons induces the release of dopamine (DA) from dopaminergic dendrites in the pars reticulata of the substantia nigra. Subthalamic neurons were activated by carbachol microinjected into the subthalamic nucleus. A microdialysis probe wa...

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Published inBrain research Vol. 645; no. 1; pp. 335 - 337
Main Authors Rosales, Manuel G., Flores, Gonzalo, Hernández, Salvador, Martínez-Fong, Daniel, Aceves, Jorge
Format Journal Article
LanguageEnglish
Published London Elsevier B.V 09.05.1994
Amsterdam Elsevier
New York, NY
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Abstract Here we have studied whether the activation of the subthalamic neurons induces the release of dopamine (DA) from dopaminergic dendrites in the pars reticulata of the substantia nigra. Subthalamic neurons were activated by carbachol microinjected into the subthalamic nucleus. A microdialysis probe was implanted in the medial aspect of the pars reticulata to collect samples of the perfusate. Carbachol (1 μg/0.25 μl saline) enhanced (58 ± 8% over basal values) nigral DA release. The enhancement was fully blocked by the NMDA antagonist AP5 added to the microdialysis medium perfusing the pars reticulata. Perfusion of the pars reticulata with NMDA also increased (125 ± 25% over basal) nigral DA release. Again, AP5 reversed the effect. These results suggest that activation of the glutamatergic subthalamonigral pathway enhances dendritic DA release by activating NMDA receptors present on dopaminergic dendrites.
AbstractList Here we have studied whether the activation of the subthalamic neurons induces the release of dopamine (DA) from dopaminergic dendrites in the pars reticulata of the substantia nigra. Subthalamic neurons were activated by carbachol microinjected into the subthalamic nucleus. A microdialysis probe was implanted in the medial aspect of the pars reticulata to collect samples of the perfusate. Carbachol (1 microgram/0.25 microliter saline) enhanced (58 +/- 8% over basal values) nigral DA release. The enhancement was fully blocked by the NMDA antagonist AP5 added to the microdialysis medium perfusing the pars reticulata. Perfusion of the pars reticulata with NMDA also increased (125 +/- 25% over basal) nigral DA release. Again, AP5 reversed the effect. These results suggest that activation of the glutamatergic subthalamonigral pathway enhances dendritic DA release by activating NMDA receptors present on dopaminergic dendrites.
Here we have studied whether the activation of the subthalamic neurons induces the release of dopamine (DA) from dopaminergic dendrites in the pars reticulata of the substantia nigra. Subthalamic neurons were activated by carbachol microinjected into the subthalamic nucleus. A microdialysis probe was implanted in the medial aspect of the pars reticulata to collect samples of the perfusate. Carbachol enhanced nigral DA release. The enhancement was fully blocked by the NMDA antagonist AP5 added to the microdialysis medium perfusing the pars reticulata. Perfusion of the pars reticulata with NMDA also increased nigral DA release. Again, AP5 reversed the effect. The results suggest that activation of the glutamatergic subthalamonigral pathway enhances dendritic DA release by activating NMDA receptors present on dopaminergic dendrites.
Here we have studied whether the activation of the subthalamic neurons induces the release of dopamine (DA) from dopaminergic dendrites in the pars reticulata of the substantia nigra. Subthalamic neurons were activated by carbachol microinjected into the subthalamic nucleus. A microdialysis probe was implanted in the medial aspect of the pars reticulata to collect samples of the perfusate. Carbachol (1 μg/0.25 μl saline) enhanced (58 ± 8% over basal values) nigral DA release. The enhancement was fully blocked by the NMDA antagonist AP5 added to the microdialysis medium perfusing the pars reticulata. Perfusion of the pars reticulata with NMDA also increased (125 ± 25% over basal) nigral DA release. Again, AP5 reversed the effect. These results suggest that activation of the glutamatergic subthalamonigral pathway enhances dendritic DA release by activating NMDA receptors present on dopaminergic dendrites.
Author Aceves, Jorge
Flores, Gonzalo
Martínez-Fong, Daniel
Hernández, Salvador
Rosales, Manuel G.
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  surname: Aceves
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Issue 1
Keywords Dopamine
Dopamine release
Substantia nigra
Glutamate receptor
Subthalamic nucleus
Brain microdialysis
Glutamate
NMDA receptor
Rat
Rodentia
Central nervous system
Catecholamine
Vertebrata
Mammalia
Locus niger
Microdialysis
Neurotransmitter
Release
Brain (vertebrata)
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Snippet Here we have studied whether the activation of the subthalamic neurons induces the release of dopamine (DA) from dopaminergic dendrites in the pars reticulata...
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SubjectTerms Animals
Biological and medical sciences
Brain microdialysis
Central nervous system
Central neurotransmission. Neuromudulation. Pathways and receptors
Dendrites - metabolism
Dopamine
Dopamine - metabolism
Dopamine release
Fundamental and applied biological sciences. Psychology
Glutamate
Glutamate receptor
Male
Microdialysis
NMDA receptor
Rats
Rats, Wistar
Receptors, N-Methyl-D-Aspartate - physiology
Substantia nigra
Substantia Nigra - metabolism
Subthalamic nucleus
Thalamic Nuclei - cytology
Thalamic Nuclei - physiology
Vertebrates: nervous system and sense organs
Title Activation of subthalamic neurons produces NMDA receptor-mediated dendritic dopamine release in substantia nigra pars reticulata: a microdialysis study in the rat
URI https://dx.doi.org/10.1016/0006-8993(94)91669-1
https://www.ncbi.nlm.nih.gov/pubmed/8062095
https://search.proquest.com/docview/16905783
https://search.proquest.com/docview/76662106
Volume 645
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