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Text
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URL Address
<a href="http://doi.org/10.1002/syn.10027" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/syn.10027</a>
Pages
112–117
Issue
2
Volume
43
Dublin Core
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Title
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Striatal dopamine output is compromised within +/- BDNF mice.
Publisher
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Synapse (New York, N.Y.)
Date
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2002
2002-02
Subject
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Animals; Brain-Derived Neurotrophic Factor/*deficiency/genetics; Dopamine/*metabolism; Drug Interactions/physiology; Extracellular Space/drug effects/metabolism; Female; Genotype; Inbred BALB C; Knockout; Male; Methamphetamine/pharmacology; Mice; Neostriatum/drug effects/*metabolism/physiopathology; Neural Pathways/drug effects/*metabolism/physiopathology; Neurons/drug effects/*metabolism; Parkinsonian Disorders/genetics/*metabolism/physiopathology; Perfusion/methods; Potassium/metabolism/pharmacology; Substantia Nigra/drug effects/*metabolism/physiopathology
Creator
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Dluzen Dean E; Anderson Linda I; McDermott Janet L; Kucera Jan; Walro Jon M
Description
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We reported previously that mice lacking one brain-derived neurotrophic factor (BDNF) allele demonstrate elevated striatal dopamine (DA) concentrations but impaired behavioral responses involving the nigrostriatal dopaminergic (NSDA) system. To test the hypothesis that these elevated striatal DA concentrations are associated with perturbed NSDA functioning, we compared striatal DA output between heterozygous mutant (+/-) and wild-type littermate control (+/+) BDNF mice under conditions of an intact NSDA system, as well as following methamphetamine (MA)-induced neurotoxicity. Basal DA output from superfused CS tissue fragments did not differ between +/+ and +/- BDNF mice. Potassium (K+) stimulated DA outputs from intact striatal fragments of +/+ mice were significantly greater than that of +/- BDNF mice. Following MA treatment, K+ stimulated DA output of +/+ mice was statistically equivalent to +/- BDNF mice. Striatal DA concentrations of +/- BDNF mice were elevated, albeit not significantly, in both intact and MA-treated mice relative to +/+ mice. Following MA treatment, striatal DA concentrations were significantly decreased for both genotypes; however, the degree of DA depletion was significantly greater in +/+ mice. Analyzed collectively, these data show the differential effects exerted by a BDNF mutation upon striatal DA concentrations and output. Notably, lower striatal DA concentrations of +/+ vs. +/- BDNF mice can be contrasted with the significantly greater K+ stimulated DA output from the former. This difference was abolished following MA treatment. These results suggest that processes involved with the dynamics of DA release within the NSDA system may be compromised in +/- BDNF mutant mice.
Identifier
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<a href="http://doi.org/10.1002/syn.10027" target="_blank" rel="noreferrer noopener">10.1002/syn.10027</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2002
Anderson Linda I
Animals
Brain-Derived Neurotrophic Factor/*deficiency/genetics
Dluzen Dean E
Dopamine/*metabolism
Drug Interactions/physiology
Extracellular Space/drug effects/metabolism
Female
Genotype
Inbred BALB C
Knockout
Kucera Jan
Male
McDermott Janet L
Methamphetamine/pharmacology
Mice
Neostriatum/drug effects/*metabolism/physiopathology
Neural Pathways/drug effects/*metabolism/physiopathology
Neurons/drug effects/*metabolism
Parkinsonian Disorders/genetics/*metabolism/physiopathology
Perfusion/methods
Potassium/metabolism/pharmacology
Substantia Nigra/drug effects/*metabolism/physiopathology
Synapse (New York, N.Y.)
Walro Jon M