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J Neurophysiol (March 1, 2003). 10.1152/jn.00834.2002
Submitted on Submitted 19 September 2002; accepted in final form 1 November 2002
1Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73190; and 2Oklahoma Foundation for Digestive Research, Basic Science Laboratories, V. A. Medical Center, Oklahoma City, Oklahoma 73104
Qin, Chao,
Beverley Greenwood-Van Meerveld,
Dean A. Myers, and
Robert D. Foreman.
Corticosterone Acts Directly at the Amygdala to Alter Spinal
Neuronal Activity in Response to Colorectal Distension. J. Neurophysiol. 89: 1343-1352, 2003. Administration
of glucocorticoids to the amygdaloid nucleus facilitates visceromotor
responses to colorectal distension in rats. The aim of this study was
to determine if colorectal hypersensitivity develops through central
modulation of spinal neuronal activity. Stereotaxic delivery of
corticosterone (n = 10) or cholesterol (control,
n = 10) onto the dorsal margin of the amygdala was
performed on male Fischer-344 rats. Seven days later, extracellular
potentials of single L6-S1
spinal neurons were examined for responses to colorectal distension
(CRD, 20-80 mmHg, 20 s) in sodium pentobarbital anesthetized and paralyzed animals. The proportions of neurons that
responded to noxious CRD in corticosterone-implanted (62/186, 33%) and
cholesterol-implanted (55/163, 34%) animals were virtually identical.
However, the mean excitatory response of spinal neurons to CRD in
corticosterone-treated rats was significantly greater (26.7 ± 2.2 vs. 16.4 ± 1.8 imp/s, P < 0.01) and the duration
was longer (37.0 ± 3.9 vs. 25.8 ± 1.5 s,
P < 0.05) than in the control group. No significant
differences were found in neural responses to nonnoxious and noxious
mechanical stimulation of somatic fields between
corticosterone-implanted and control groups. In conclusion, our data
support the hypothesis that central stimulation of the amygdala by
corticosterone sensitizes the lumbosacral spinal neurons that mediate
visceromotor reflexes to CRD.
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