Corticosterone acts directly at the amygdala to alter spinal neuronal activity in response to colorectal distension.

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 L(6)-S(1) 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.