Journal
AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
Volume 98, Issue 1-2, Pages 59-63Publisher
ELSEVIER
DOI: 10.1016/S1566-0702(02)00033-4
Keywords
mechanoelectrical transduction; amiloride; baroreceptors; vagal afferents; nodose ganglia; degenerin-epithelial Na+ channels
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Funding
- NHLBI NIH HHS [P01 HL14388] Funding Source: Medline
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Changes in arterial pressure and blood volume are sensed by baroreceptor and vagal afferent nerves innervating aorta and heart with soma in nodose ganglia. The inability to measure membrane potential at the nerve terminals has limited our understanding of mechanosensory transduction. Goals of the present study were to: (1) Characterize membrane potential and action potential responses to mechanical stimulation of isolated nodose sensory neurons in culture; and (2) Determine whether the degenerin/epithelial sodium channel (DEG/ENaC) blocker amiloride selectively blocks mechanically induced depolarization without suppressing membrane excitability. Membrane potential of isolated rat nodose neurons was measured with sharp microelectrodes. Mechanical stimulation with buffer ejected from a micropipette (5, 10, 20 psi) depolarized 6 of 10 nodose neurons (60%) in an intensity-dependent manner. The depolarization evoked action potentials in 4 of the 6 neurons. Amiloride (1 muM) essentially abolished mechanically induced depolarization (15 +/- 4 my during control vs. 1 +/- 2 mV during amiloride with 20-psi stimulation, n = 6) and action potential discharge. In contrast, amiloride did not inhibit the frequency of action potential discharge in response to depolarizing current injection (n = 6). In summary, mechanical stimulation depolarizes and triggers action potentials in a subpopulation of nodose sensory neurons in culture. The DEG/ENaC blocker amiloride at a concentration of 1 muM inhibits responses to mechanical stimulation without suppressing membrane excitability. The results support the hypothesis that DEGENaC subunits are components of mechanosensitive ion channels on vagal afferent and baroreceptor neurons. (C) 2002 Elsevier Science B.V. All rights reserved.
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