Injury models to study cardiac remodeling in the mouse: myocardial infarction and ischemia-reperfusion.
*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
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.
Luther Daniel J; Thodeti Charles K; Meszaros J Gary
Methods in molecular biology (Clifton, N.J.)
2013
1905-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<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>
Striatal dopamine output is compromised within +/- BDNF mice.
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
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.
Dluzen Dean E; Anderson Linda I; McDermott Janet L; Kucera Jan; Walro Jon M
Synapse (New York, N.Y.)
2002
2002-02
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1002/syn.10027" target="_blank" rel="noreferrer noopener">10.1002/syn.10027</a>