J. Lu et Da. Bereiter, ACUTE INJECTION OF ADRENAL-STEROIDS REDUCES CORNEA-EVOKED EXPRESSION OF C-FOS WITHIN THE SPINAL TRIGEMINAL NUCLEUS OF ADRENALECTOMIZED RATS, Neuroscience, 66(4), 1995, pp. 933-941
The influence of transient increases in adrenal steroid hormones on th
e number of Fos-positive neurons after nociceptor activation was asses
sed in adrenalectomized rats. Fos protein, the product of the immediat
e early gene, c-fos, was detected immunocytochemically within the spin
al trigeminal nucleus 2 h after noxious thermal stimulation of the cor
nea. Adrenalectomized rats displayed an enhanced number of Fos-positiv
e neurons within the caudal-most portions of trigeminal subnucleus cau
dalis compared to that seen in adrenal-intact animals, an effect rever
sed by a single acute injection of corticosterone (1 mg/kg, i.p.) give
n 5 min prior to stimulation. Acute injection of the selective mineral
ocorticoid receptor agonist, aldosterone, or the selective glucocortic
oid receptor agonist, RU28362, also reduced the number of Fos-positive
neurons. Aldosterone and RU28362 had an additive effect on Fos when g
iven concurrently. In contrast, adrenal status or acute injections of
adrenal steroid receptor agonists had no effect on the number of Fos-p
ositive neurons after corneal stimulation located within the ventrolat
eral pole of the spinal trigeminal nucleus at the level of the subnucl
eus interpolaris/caudalis junction. Acute administration of adrenal st
eroids to adrenalectomized rats greatly attenuated the number of Fos-p
ositive neurons seen after corneal stimulation within select portions
of trigeminal subnucleus caudalis. The contribution of both glucocorti
coid and mineralocorticoid receptor subtypes in reducing Fos suggested
a central site of action rather than an anti-inflammatory effect on p
eripheral tissue. These results are consistent with the hypothesis tha
t transient increases in adrenal steroids, such as occur after injury,
are sufficient to modify the production of Fos protein in central neu
rons that process nociceptive information.