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Alterations of calcium channels and cell excitability in intracardiac and stellate ganglion neurons from chronic heart failure rats
Author(s) -
Liu Jinxu,
Tu Huiyin,
Zhang Dongze,
Li YuLong
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.928.1
Subject(s) - medicine , stellate ganglion , endocrinology , intracardiac injection , chemistry , acetylcholine , heart failure , cardiology , pathology , alternative medicine
Chronic heart failure (CHF) is characterized by increased cardiac sympathetic and decreased cardiac parasympathetic nerve activity. This autonomic imbalance increases the risk of arrhythmias and sudden death in CHF patients. As the final pathways for the autonomic control of the cardiac function, sympathetic postganglionic neurons from the stellate ganglia (SG) release norepinephrine and parasympathetic postganglionic neurons of the intracardiac ganglia (ICG) release acetylcholine upon neuronal excitation. In the present study, we measured the protein expression and current density of Ca 2+ channels in the SG and ICG neurons and investigated the role of Ca 2+ channels in neuronal excitability and also recorded the cardiac sympathetic nerve activity in sham and coronary artery ligation‐induced CHF rats. Immunofluorescent data showed that L, P/Q, N, and R types of Ca 2+ channels were expressed in the SG and ICG neurons, but only protein expression of N‐type Ca 2+ channels was decreased in the ICG neurons from CHF rats. Using whole‐cell patch clamp technique, we found that CHF significantly enhanced the Ca 2+ currents and cell excitability in SG neurons and reduced the Ca 2+ currents and cell excitability in ICG neurons. N‐type Ca 2+ channel blocker (1 μM ω‐Conotoxin GVIA) lowered the Ca 2+ currents and cell excitability to the same level in SG and ICG neurons from sham and CHF rats. In addition, the cardiac sympathetic nerve activity was augmented in CHF rats. Our results indicate that CHF caused changes of Ca 2+ channels and cell excitability in SG and ICG neurons may contribute to the cardiac autonomic imbalance in CHF.