In the present paper we demonstrate the effect of immobilization stress on c-fos-like immunoreactivity (Fos-LI) in the rat amygdaloid complex. Furthermore, since the subnuclei of the amygdaloid complex contain numerous glucocorticoid receptor-immunoreactive (GR-IR) neurons, we also studied the possible colocalization of GR- and Fos-LI ie. Fos-LIs and the action of a synthetic glucocorticoid, dexamethasone, and an anti-glucocorticoid, RU 38486, on Fos-LI. Immobilization stress caused a remarkable increase in the number of the Fos-IR neurons in all the subnuclei of the amygdaloid complex except in the lateral nucleus. The majority of Fos-IR neurons also contained GR-LI, with the highest colocalization in the central amygdaloid nucleus. A similar induction of Fos-LI after immobilization was seen in the hypothalamic paraventricular nucleus and almost all the Fos-IR neurons in this nucleus also exhibited GR-LI. Treatments with dexamethasone or RU 38486 prior to stress did not have any marked effect on Fos-LI when compared to stress alone. The present findings suggest that Fos may function as a transcriptional regulator in the amygdaloid complex after stress and affect the synthesis of neurotransmitters and receptors in the amygdaloid neurons. Since we did not observe any effect of dexamethasone or RU 38486 on Fos-LI, it is likely that glucocorticoids do not directly regulate the expression of the c-fos gene or the formation of Fos protein. In view of the fact that Fos is capable of forming a stabile complex with GR and repress the transactivational capacity of GR, Fos may inhibit the negative feedback effect of circulating glucocorticoids and thus maintain elevated plasma glucocorticoid levels in stress.
