Identification of G-protein coupled receptor subunits in normal human dental pulp.

To respond appropriately to their environment, dental pulp cells must integrate informational input from multiple ligands, such as neuropeptides, growth factors, and vasoactive amines. These ligands act through multiple intracellular signaling pathways. G-protein coupled receptor subunits play a major role in this process, providing a mechanism for coordinated regulation of both messengers and effectors. Increasing number of neuropeptides have been found in pulpal tissue. However, there is no data about molecular identification of G-protein subunits in human dental pulp. To identify the postreceptor mechanism involved in dental pulp cell signal transduction, we performed a Western blot analysis of different G-protein subunits. Biopsy specimens of human dental pulp were prepared and subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis, followed by analysis with appropriate antibodies. We detected G alpha q/alpha 11, short and long forms of G alpha s, beta common, Gio-3, and Gil-2 antigens with a molecular weight approximately 42 kDa, 42 and 45 kDa, 36 kDa, 40 kDa, and 40 kDa, respectively. These results indicate that human pulp cells possess the cellular machinery to respond to sensory neuropeptides when they are released from the peptidergic nerve fibers. On this basis, the relationships of postdevelopmental, age-dependent, and pathophysiological disorders of G-proteins subunits in dental pulp could be studied.

Physiological concentrations of melatonin inhibit the norepinephrine-induced activation of prostaglandin E2 and cyclic AMP production in rat hypothalamus: a mechanism involving inhibiton of nitric oxide synthase.

In this paper, we summarize the results of in vitro studies showing that physiological concentrations of melatonin inhibit the norepinephrine-induced activation of prostaglandin E2 (PGE2) and cyclic AMP production in rat medial basal hypothalamus (MBH). Interestingly, a concentration of melatonin as low as 1 nM, which is roughly equivalent to the nocturnal serum physiological concentration of the hormone in the rat, significantly inhibit PGE2 and cyclic AMP production in the MBH. The suppressive effect of melatonin may be mediated by an inhibition of nitric oxide synthase (NOS) activity, since the stimulatory effect of sodium nitroprusside (SNP), a spontaneous generator of NO, was not prevented by melatonin. Melatonin also inhibited NOS activity in rat MBH in a dose-dependent manner. The results suggest the existence of a new or an ancillary means by which melatonin may regulate the physiology of the hypothalamus-pituitary unit.

Melatonin reduces nitric oxide synthase activity in rat hypothalamus.

In this report, rat hypothalamic nitric oxide synthase (NOS) activity is shown to be partially inhibited by physiological concentrations of the pineal hormone melatonin. In vitro studies demonstrate that 1 nM melatonin, which approximates the physiological concentration of the hormone at night, significantly inhibited NOS activity. In vivo studies show that administering melatonin or collecting the hypothalamus from animals at night, when endogenous melatonin levels are elevated, results in a significant decrease of NOS activity. Results also show that calmodulin may be involved in this process since its presence in the incubation medium prevents the inhibitory effect of melatonin on NOS activity.