1
40
2
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
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
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Striatal dopamine output is compromised within +/- BDNF mice.
Publisher
An entity responsible for making the resource available
Synapse (New York, N.Y.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2002
2002-02
Subject
The topic of the resource
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
An entity primarily responsible for making the resource
Dluzen Dean E; Anderson Linda I; McDermott Janet L; Kucera Jan; Walro Jon M
Description
An account of the resource
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
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/978-1-62703-505-7_19" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/978-1-62703-505-7_19</a>
Pages
325–342
Volume
1037
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Injury models to study cardiac remodeling in the mouse: myocardial infarction and ischemia-reperfusion.
Publisher
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Methods in molecular biology (Clifton, N.J.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
1905-07
Subject
The topic of the resource
*Ventricular Remodeling; Animal; Animals; Cardiovascular Surgical Procedures; Coronary Vessels/surgery; Disease Models; Ligation; Mice; Myocardial Infarction/*etiology/*pathology; Myocardial Reperfusion Injury/*etiology/*pathology; Perfusion/methods; Wound Healing
Creator
An entity primarily responsible for making the resource
Luther Daniel J; Thodeti Charles K; Meszaros J Gary
Description
An account of the resource
Deep tissue wound healing requires a complex sequence of several factors working in unison to repair the organ at risk. Myocardial infarction (MI) is particularly complex due to several local and systemic factors mediating the repair process within the heart. The wound healing process during this time is critical-the cardiac myocytes are at risk of apoptotic cell death, autophagy, and necrosis. During the early remodeling period, the fibroblasts and myofibroblasts play critical roles in infarct scar formation, a process that is greatly influenced by a robust inflammatory response. Construction of the infarct scar is a "necessary evil" that helps to limit expansion of the infarction; however, the collagen and matrix deposition will often spread to the healthy areas of the heart, causing reactive fibrosis in areas remote from the original damage. This chapter outlines in detail the procedures for two myocardial infarction injury models as well as how to quantify the size of the experimentally induced injury. These procedures are critical to the development of in vivo approaches to study myocardial injury, particularly for use in knockout and transgenic mice.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/978-1-62703-505-7_19" target="_blank" rel="noreferrer noopener">10.1007/978-1-62703-505-7_19</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Ventricular Remodeling
2013
Animal
Animals
Cardiovascular Surgical Procedures
Coronary Vessels/surgery
Department of Integrative Medical Sciences
Disease Models
Ligation
Luther Daniel J
Meszaros J Gary
Methods in molecular biology (Clifton, N.J.)
Mice
Myocardial Infarction/*etiology/*pathology
Myocardial Reperfusion Injury/*etiology/*pathology
NEOMED College of Medicine
Perfusion/methods
Thodeti Charles K
Wound Healing