A. Chiba et al., A POSSIBLE ROLE OF THE PINEAL-GLAND IN ACUTE IMMOBILIZATION-RELATED SUPPRESSION OF NALOXONE-INDUCED LH-RELEASE IN OVARIECTOMIZED ESTROGEN-PRIMED RATS, Journal of neuroendocrinology, 10(2), 1998, pp. 79-84
It has been recently reported that acute immobilization stress almost
completely suppresses the luteinizing hormone (LH) release induced by
naloxone, a mu-opioid antagonist, in ovariectomized estrogen-primed ra
ts. The present study examined the possible involvement of the pineal
gland in the acute immobilization-related suppression of the naloxone-
induced LH release. An intraventricular (ICV) injection of 15 mu g nal
oxone produced an abrupt increase in circulating LH concentrations in
non-stressed rats. The naloxone-induced LH release was completely elim
inated when tested 60 min after the end of a 30 min session of acute i
mmobilization. The same stress conditions did not affect LH-releasing
hormone (LHRH)-induced LH release, suggesting that the stress-related
suppression of the naloxone-induced LH release was a suprapituitary ev
ent. In chronically-pinealectomized rats, but not in sham-pinealectomi
zed rats, naloxone injected 60 min after the end of the stress session
evoked a significant increase in serum LH concentrations. However, na
loxone injected ICV during the acute immobilization did not elicit LH
release in either pinealectomized or sham-operated rats. Under non-str
essed conditions, the LH secretory response to naloxone was similar in
pinealectomized and sham-operated animals. The same stress (30 min im
mobilization) significantly increased pineal melatonin content as well
as plasma melatonin concentrations in rats bearing intact pineal glan
ds, indicating that stress actually affected the pineal function. Thes
e results provide evidence for a role of the pineal in the suppression
of the LH response to naloxone after stress, but not during stress.