Cell receptors to sulphated polysaccharides in the acute and chronically inflamed synovial joint.

Receptors to sulphated polysaccharides have recently been discovered on "free" joint fluid cells and synovial membrane cells in the normal joint. A search for these receptors on cells was made in rabbits with acute and chronic adjuvant inflammatory arthritis in an attempt to further elucidate their role in joint homeostasis. These experiments demonstrated a significant increase in cell numbers within the joint. Receptor activity was most marked on macrophages found free within the synovial fluid. It is postulated that exogenous cells may be important in the process of joint destruction and are outside the control of the normal joint regulatory mechanisms. The endogenous cell population, which exhibits receptor activity, may be responding to the process of joint destruction by proliferation as a secondary phenomenon.

Dopaminergic and serotonergic involvement in opiate-induced prolactin release in monkeys.

The present experiments were performed to determine the site of action (hypothalamic or hypophyseal) and the mechanism (dopaminergic or serotonergic) by which morphine increases PRL in monkeys (Macaca mulatta and Macaca nemestrina). To determine the site of action, 9 mg morphine were injected iv to four intact and four pituitary stalk-sectioned monkeys. PRL concentrations rose significantly (P less than 0.01) from less than 5 ng/ml to an average maximum value of 208 +/- 20 ng/ml at 15 min in intact animals, but remained unchanged in pituitary stalk-sectioned animals. There was a significant reduction (P less than 0.01) of this response in intact monkeys that received 5 mg L-dopa, iv, 5 min before the morphine stimulus. In these animals, PRL only rose to 100 +/- 46 ng/ml. In contrast, the PRL response in four monkeys pretreated with 5 or 20 mg methysergide, iv (a serotonin receptor blocker), 5 min before the opiate stimulus was not different from in controls. Likewise, the daily administration of 100 mg p-chlorophenylalanine, sc (a serotonin synthesis blocker), for 6 days failed to alter the PRL response to morphine. These data suggest that opiates increase PRL via a neural site of action and that the mechanism may involve dopaminergic but not serotonergic pathways.