No abstract

Diurnal variations in splenic ornithine decarboxylase and tyrosine hydroxylase activities were examined in rats subjected to pinealectomy, bilateral superior cervical ganglionectomy, or their respective sham operations. Rats were treated with Freund's complete adjuvant or its vehicle 2 days before sacrifice. After immunization, splenic ornithine decarboxylase activity was augmented 5-6-fold. In both immunized and nonimmunized sham-operated rats, significant diurnal variations in ornithine decarboxylase activity were detectable, with a maximum at early morning, acrophases after Cosinor analysis varying from 0845 to 1048h. In pinealectomized or superior cervical ganglionectomized, immunized rats, ornithine decarboxylase activity attained values 22-27% lower than those of immunized sham-operated controls, while amplitude decreased significantly by 27-30%. Administration of melatonin (30 microg/animal s.c. at late evening for 11 days in immunized rats) significantly augmented mesor levels of splenic ornithine decarboxylase activity and increased the amplitude of the diurnal rhythm both in pinealectomized and in superior cervical ganglionectomized rats. Melatonin treatment also augmented rhythm mesor in immunized, sham-ganglionectomized rats, as well as rhythm amplitude in immunized and nonimmunized, sham-ganglionectomized rats. Splenic tyrosine hydroxylase activity attained its maximum at late afternoon and early night, with acrophases varying from 1800 to 2023h. Immunization significantly increased mesor values of splenic tyrosine hydroxylase activity, whereas neither pinealectomy nor superior cervical ganglionectomy affected circadian rhythm parameters. Melatonin treatment augmented mesor values of tyrosine hydroxylase rhythm and increased its amplitude in pinealectomized, ganglionectomized, or sham-operated rats. The results are compatible with the view that the pineal gland plays a role in circadian changes of immune responsiveness in rat spleen via an immunopotentiating effect of melatonin on splenic cell proliferation.

No abstract

Male rats were grafted an anterior pituitary within breast muscles or received a sham operation on day 5 of life. At the 60th day of life, the sympathetic denervation of rat submaxillary lymph nodes was achieved by a bilateral sympathetic superior cervical ganglionectomy (SCGx; at 15.00 h). Rats were killed either 18 h later (acute SCGx) or after 12 days (chronic SCGx) to measure lipopolysaccharide (LPS)- and concanavalin A (ConA)-induced cell proliferation in submaxillary lymph nodes, submaxillary lymph node cellularity and serum prolactin levels. In control rats, acute SCGx significantly augmented LPS or ConA activity on lymph cells while chronic SCGx had no effect. In pituitary-grafted rats, acute SCGx depressed the mitogenic effect of LPS or ConA whereas chronic SCGx augmented it. A global inhibitory effect of surgical stress on submaxillary lymph node cellularity was found in rats subjected to SCGx or its sham operation 18 h earlier. Serum prolactin levels increased significantly in pituitary-grafted rats, particularly in those subjected to chronic SCGx. In pituitary-grafted rats, a significant effect of acute SCGx was apparent, with serum prolactin levels augmenting about twice in sham-SCGx rats, and to a significantly less extent in acute SCGx rats. The results provide further evidence of the immunomodulatory role of local sympathetic nerves in submaxillary lymph nodes.

The objective of this study was to evaluate the involvement of the pineal gland in modulation of parathyroid hormone (PTH) and calcitonin release found in rats after changes in activity of cervical sympathetic nerves. The response of serum PTH to a hypocalcemia produced by EDTA injection, and of serum calcitonin to a hypercalcemia produced by administering calcium chloride, were studied in rats at the time of the wallerian degeneration of regional sympathetic nerves (i.e., 16 hr after superior cervical ganglionectomy, SCGx). Rats received a pinealectomy or its sham-operation 4 days before SCGx. During wallerian degeneration of nerves after SCGx, a higher hypocalcemia and a lower PTH response were found as compared to sham-SCGx rats, regardless of whether the pineal gland was present or not. When the response of calcitonin to a bolus injection of calcium chloride was assessed, rats subjected to SCGx 16 hr earlier showed a depressed calcitonin release, which was also unaffected after pinealectomy. To a similar extent in pinealectomized and sham-pinealectomized rats, a mild stress given by the subcutaneous injection of turpentine oil brought about a greater hypocalcemia after EDTA, concomitantly with a higher PTH secretory response. In turpentine oil-injected rats, the rise of serum calcitonin was significantly greater than that of vehicle-treated rats, regardless of pineal presence. The results further indicate that cervical autonomic nerves constitute a pathway through which the brain modulates calcium homeostasis and do not support the participation of the pineal gland in short term changes of PTH or calcitonin release.