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The Journal of Neurophysiology Vol. 88 No. 3 September 2002, pp. 1512-1522
Copyright ©2002 by the American Physiological Society
Departments of 1Oral and Craniofacial Biological Sciences, 2Anatomy and Neurobiology, and 3Program and Neuroscience, University of Maryland, Baltimore, Maryland 21201
Gold, Michael S.,
Lei Zhang,
Dena L. Wrigley, and
Richard J. Traub.
Prostaglandin E2 Modulates TTX-R
INa in Rat Colonic Sensory Neurons. J. Neurophysiol. 88: 1512-1522, 2002. This study was performed to determine the
impact of the inflammatory mediator prostaglandin
E2 (PGE2) on the
biophysical properties of tetrodotoxin resistant voltage-gated
Na+ currents (TTX-R
INa) in colonic dorsal root ganglion
(DRG) neurons. TTX-R INa was studied
in DRG neurons from thoracolumbar (TL:
T13-L2) and lumbosacral
(LS: L6-S2) DRG
retrogradely labeled following the injection of
DiIC18 (DiI) into the wall of the descending colon of adult male rats. TTX-R INa in
colonic DRG neurons had a high threshold for activation
[V0.5 of conductance-voltage
(G-V) curve = 
3.1 ± 1.0 (SE) mV] and
steady-state availability (V0.5 for
H-infinity curve = 18.4 ± 1.4 mV), was slowly inactivating (10.6 ± 1.4 ms at 0 mV), and recovered rapidly from inactivation (83.5 ± 5.0% of the current recovered with a time constant of 1.3 ± 0.1 ms at 80 mV). TTX-R
INa was present in every colonic DRG
neuron studied (n = 62). PGE2
induced a rapid (<15 s) increase in TTX-R
INa that was associated with a
hyperpolarizing shift in the G-V curve (3.4 ± 0.7 mV),
an increase in the rate of inactivation (4.21 ± 0.7 ms at 0 mV),
and no change in steady-state availability. There was no statistically
significant difference (P > 0.05) between TL and LS
colonic DRG neurons with respect to the biophysical properties of TTX-R
INa, the current density or the
magnitude of PGE2-induced changes in the current.
However, both the proportion of TL and LS neurons in which TTX-R
INa was modulated by
PGE2 (16 of 16 TL neurons and 12 of 14 LS
neurons) as well as the magnitude of PGE2-induced
changes in the current were significantly larger in colonic DRG neurons
than in the total population of DRG neurons. These results suggest that
changes in nociceptive processing associated with inflammation of the
colon does not reflect differences between TL and LS neurons with
respect to the properties of TTX-R INa, distribution of current, or magnitude of inflammatory mediator-induced changes in the current. However, these results do suggest modulation of
TTX-R INa in colonic afferents is an
underlying mechanism of hyperalgesia and pain associated with
inflammation of the colon and that this current constitutes a novel
target for therapeutic relief of visceral inflammatory pain.
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