|
|
||||||||
The Journal of Neurophysiology Vol. 85 No. 1 January 2001, pp. 247-253
Copyright ©2001 by the American Physiological Society
1The Neuroscience Program and 2Department of Pharmacology and Experimental Therapeutics, University of Maryland, School of Medicine, Baltimore, Maryland 21201-1559
Lancaster, Eric,
Eun Joo Oh, and
Daniel Weinreich.
Vagotomy Decreases Excitability in Primary Vagal Afferent Somata. J. Neurophysiol. 85: 247-253, 2001. Standard patch-clamp and intracellular recording techniques
were used to monitor membrane excitability changes in adult inferior vagal ganglion neurons (nodose ganglion neurons, NGNs) 5 days following
section of the vagus nerve (vagotomy). NGNs were maintained in vivo for
5 days following vagotomy, and then in vitro for 2-9 h prior to
recording. Vagotomy increased action potential (AP) threshold by over
200% (264 ± 19 pA, mean ± SE, n = 66) compared with control values (81 ± 20 pA, n = 68; P < 0.001). The number of APs evoked by a 3 times
threshold 750-ms depolarizing current decreased by >70% (from 8.3 to
2.3 APs, P < 0.001) and the number of APs evoked by a
standardized series of (0.1-0.9 nA, 750 ms) depolarizing current steps
decreased by over 80% (from 16.9 APs to 2.6 APs, P < 0.001) in vagotomized NGNs. Similar decreases in excitability were
observed in vagotomized NGNs in intact ganglia in vitro studied with
"sharp" microelectrode techniques. Baseline electrophysiological
properties and changes following vagotomy were similar in right and
left NGNs. A "sham" vagotomy procedure had no effect on NGN
properties at 5 days, indicating that changes were due to severing the
vagus nerve itself, not surrounding tissue damage. NGNs isolated after
being maintained 17 h in vivo following vagotomy revealed no
differences in excitability, suggesting that vagotomy-induced changes
occur some time from 1-5 days after injury. Decreased excitability was
still observed in NGNs isolated after 20-21 days in vivo following
vagotomy. These data indicate that, in contrast to many primary sensory
neurons that are thought to become hyperexcitable following section of
their axons, NGNs undergo a marked decrease in electrical excitability
following vagotomy.
This article has been cited by other articles:
![]() |
G. E. Hermann and R. C. Rogers TNF {alpha}: A Trigger of Autonomic Dysfunction Neuroscientist, February 1, 2008; 14(1): 53 - 67. [Abstract] [PDF] |
||||
![]() |
J. H. Peters, S. M. Simasko, and R. C. Ritter Leptin Analog Antagonizes Leptin Effects on Food Intake and Body Weight but Mimics Leptin-Induced Vagal Afferent Activation Endocrinology, June 1, 2007; 148(6): 2878 - 2885. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. R. Gillespie, G. A. Burns, and R. C. Ritter NMDA channels control meal size via central vagal afferent terminals Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2005; 289(5): R1504 - R1511. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. H. Peters, A. B. Karpiel, R. C. Ritter, and S. M. Simasko Cooperative Activation of Cultured Vagal Afferent Neurons by Leptin and Cholecystokinin Endocrinology, August 1, 2004; 145(8): 3652 - 3657. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. J. Undem, E. J. Oh, E. Lancaster, and D. Weinreich Effect of Extracellular Calcium on Excitability of Guinea Pig Airway Vagal Afferent Nerves J Neurophysiol, March 1, 2003; 89(3): 1196 - 1204. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. M. Simasko, J. Wiens, A. Karpiel, M. Covasa, and R. C. Ritter Cholecystokinin increases cytosolic calcium in a subpopulation of cultured vagal afferent neurons Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2002; 283(6): R1303 - R1313. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Lancaster, E. J. Oh, T. Gover, and D. Weinreich Calcium and calcium-activated currents in vagotomized rat primary vagal afferent neurons J. Physiol., April 15, 2002; 540(2): 543 - 556. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |