|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Received August 8, 2001
Accepted after revision January 29, 2002
1 The Neuroscience Program, University of Maryland, School of Medicine, 655 W. Baltimore Street, Baltimore, MD 21201-1559, USA
2 Department of Pharmacology and Experimental Therapeutics, University of Maryland, School of Medicine, 655 W. Baltimore Street, Baltimore, MD 21201-1559, USA
3 Department of Pharmacology and Experimental Therapeutics, University of Maryland, School of Medicine, Bressler Research Building, Room 4-002, 655 West Baltimore Street, Baltimore, MD 21201-1559, USA
* To whom correspondence should be addressed. E-mail: dweinrei{at}umaryland.edu.
Adult inferior vagal ganglion neurons (nodose ganglion neurons, NGNs) were acutely isolated 4-6 days after section of their peripheral axons (vagotomy) and examined with the whole-cell patch-clamp technique. A subset (~25 %) of vagotomized NGNs displayed depolarizing after-potentials (DAPs), not present in control NGNs. DAPs were inhibited by niflumic acid (125 µm) or cadmium (100 µm), and had a reversal potential near ECl, indicating that they were due to Ca2+-activated chloride current (ICl(Ca)). N-type, L-type, T-/R- and other types of voltage-dependent Ca2+ channels provided about 43, 2, 16 and 40 % of the trigger Ca2+ for DAP generation, respectively. Intracellular Ca2+ concentration ([Ca2+]i) was estimated using fura-2 fluorescence. Resting [Ca2+]i and peak [Ca2+]i elevation induced by activating Ca2+-induced Ca2+ release (CICR) stores with 10 mm caffeine were not significantly different among control NGNs, vagotomized NGNs with DAPs and vagotomized NGNs without DAPs, averaging 54 ± 7.9 (n = 19; P = 0.49) and 2022 ± 1059 nm (n = 19; P = 0.44), respectively. Blocking CICR with 10 µm ryanodine reduced DAP amplitude by ~37 %. Ca2+ influx induced by action potential waveforms was increased by over 250 % in vagotomized NGNs with DAPs (19.0 ± 2.1 pC) compared to control NGNs (5.0 ± 0.8 pC) or vagotomized NGNs without DAPs (7.0 ± 0.8 pC). L-type, N-type, T-/R-type and other types of Ca2+ influx were increased proportionately in vagotomized NGNs with DAPs. In conclusion, a subset of vagotomized NGNs have increased Ca2+ currents and express ICl(Ca). These NGNs respond electrically to increases in [Ca2+]i during regeneration.
This article has been cited by other articles:
![]() |
R. C. Rogers, M. J. Van Meter, and G. E. Hermann Tumor Necrosis Factor Potentiates Central Vagal Afferent Signaling by Modulating Ryanodine Channels J. Neurosci., December 6, 2006; 26(49): 12642 - 12646. [Abstract] [Full Text] [PDF] |
||||
![]() |
O. Sacchi, M. L. Rossi, R. Canella, and R. Fesce Synaptic and Somatic Effects of Axotomy in the Intact, Innervated Rat Sympathetic Neuron J Neurophysiol, May 1, 2006; 95(5): 2832 - 2844. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Verkhratsky Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons Physiol Rev, January 1, 2005; 85(1): 201 - 279. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. J. Oh and D. Weinreich Bradykinin decreases K+ and increases Cl- conductances in vagal afferent neurones of the guinea pig J. Physiol., July 15, 2004; 558(2): 513 - 526. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. E. Hoesch, D. Weinreich, and J. P. Y. Kao Localized IP3-Evoked Ca2+ Release Activates a K+ Current in Primary Vagal Sensory Neurons J Neurophysiol, May 1, 2004; 91(5): 2344 - 2352. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Andre, H. Boukhaddaoui, B. Campo, M. Al-Jumaily, V. Mayeux, D. Greuet, J. Valmier, and F. Scamps Axotomy-Induced Expression of Calcium-Activated Chloride Current in Subpopulations of Mouse Dorsal Root Ganglion Neurons J Neurophysiol, December 1, 2003; 90(6): 3764 - 3773. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |