Post-infarct cardiac sympathetic hyperactivity regulates galanin expression

• Published in: Neuroscience letters Vol. 436; no. 2; pp. 163 - 166
• Main Authors: Ewert, T. Jarred, Gritman, Kurt R., Bader, Michael, Habecker, Beth A.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 09.05.2008; Elsevier
• Subjects: Angiotensinogen - deficiency; Animals; Animals, Genetically Modified; Attention deficit disorders. Hyperactivity; Biological and medical sciences; Case-Control Studies; Child clinical studies; Enzyme-Linked Immunosorbent Assay - methods; Female; Fundamental and applied biological sciences. Psychology; Galanin; Galanin - genetics; Galanin - metabolism; Gene Expression Regulation - physiology; Male; Medical sciences; Myocardial infarction; Myocardial Infarction - physiopathology; Myocardial Reperfusion - methods; Myocardium - metabolism; Neuropeptide; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Rats; Rats, Sprague-Dawley; Stellate Ganglion - metabolism; Sympathetic; Sympathetic Nervous System - physiology; Vertebrates: nervous system and sense organs; Myocardial infarction; Galanin; Neuropeptide; Sympathetic; Sympathetic nervous system; Autonomic nervous system; Hyperactivity; Myocardial infarction,Galanin,Neuropeptide,Sympathetic
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2008.03.012

The neuropeptide galanin is elevated in the cardiac sympathetic innervation after myocardial infarction (MI). Galanin inhibits vagal transmission and may support the regeneration of sympathetic nerves, thereby contributing to the development of arrhythmia and sudden cardiac death after MI. The reason for increased galanin production in sympathetic neurons after myocardial infarction is not known. Cardiac sympathetic neurons are activated chronically after cardiac ischemia–reperfusion, and activation of sympathetic neurons in culture stimulates galanin expression. Therefore, we tested the hypothesis that increased sympathetic nerve activity stimulates galanin expression in cardiac sympathetic neurons after myocardial infarction. To test this hypothesis we used TGR(ASrAOGEN) transgenic rats, which lack brain angiotensinogen and do not exhibit post-infarct sympathetic hyperactivity. Hearts and stellate ganglia were collected 1 week after ischemia–reperfusion. Galanin mRNA was quantified by real-time PCR and peptide content was assayed by enzyme-linked immunosorbent assay. Galanin mRNA increased approximately 3-fold after MI in cardiac sympathetic neurons of both genotypes compared to unoperated and sham controls. Left ventricular galanin content, however, increased after MI only in Sprague–Dawley rats and not in AOGEN rats. These data suggest that post-infarct cardiac sympathetic hyperactivity stimulates galanin peptide production but is not required for increased galanin mRNA expression.