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At least 127 records · Page 7Linked to original sources
PubMed1991

Evidence for direct non-genomic effects of triiodothyronine on bone rudiments in rats: stimulation of the inositol phosphate second messenger system.

Thyroid hormones increase cytosolic free calcium by binding to plasma membrane receptors in several tissues. This calcium increase appears to initiate extranuclear effects in these tissues. Increases in cytosolic calcium are often a consequence of stimulation of inositol phosphate second messenger pathway. Several calcemic hormones act via this signal transduction route. Therefore we investigated the effects of the metabolically active T3 and the inactive analogues 3,5-diiodotyrosine and rT3 on the inositol phosphate pathway in fetal rat limb bone cultures prelabeled with [3H]myoinositol. Labelled inositol and inositol phosphates were separated by HPLC. There was a significant increase in the radioactivity in inositol bis- and trisphosphates after 1 min of exposure to 10(-7) mol/l T3. Stimulation was also observed at 10(-6) mol/l T3, but not at 10(-5) mol/l. Time course studies demonstrated a rapid effect of T3 on inositol phosphates within 30 seconds that lasted through 5 min. After 20 min incubation with T3, no increase was observed in inositol mono- and bisphosphates, and a decrease was seen in inositol trisphosphate. Pretreatment with indomethacin prevented these effects of T3. 3,5-diiodotyrosine and rT3 did not affect inositol phosphate metabolism. These results suggest the existence of plasma membrane-associated receptors for T3 in bone, in addition to the nuclear receptors demonstrated previously. The role of these receptors in the effects of thyroid hormones on bone remains to be established.

Animals↗
PubMed1989

The second-messenger system for peptide hormones.

There are three major hormone classes--peptide, steroid, and the newly defined growth factors--each with its own system for signal transduction in the cell. Two interdependent theses are proposed for the peptide hormone: that incoming signal transduction requires coupling to a G protein in a second-messenger pathway, and that second-messenger redundancy assures checks and balances in cell regulation.

Adult↗
PubMedDate not supplied

Evaluation of the role of second messenger systems in tumor necrosis factor-stimulated resorption of fetal rat limb bones.

Tumor necrosis factor (TNF) actions in target tissues are mediated by various signalling pathways. The effect of TNF to stimulate resorption in fetal rat limb bones is not inhibited by indomethacin. The current studies were designed to assess the role of cyclic AMP (cAMP) and calcium as second messengers in this prostaglandin-independent action of TNF on bone resorption. TNF alone failed to increase cyclic AMP in fetal rat limb bones after either brief (15 min) or long-term (72 h) treatment. TNF-stimulated resorption in fetal rat limb bones was enhanced by the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX). In short term incubations, the combination of TNF + IBMX did not elicit increases in cAMP in the limb bones. In 72 h cultures, addition of IBMX revealed a dose-dependent effect of TNF to increase cAMP. TNF produced a significant increase in inositol phosphate turnover in limb bones, with a greater response at 5 min than at 1 or 20 min. The calcium channel blocker nitrendipine inhibited TNF-stimulated resorption in the fetal rat limb bones. TNF-stimulated resorption was attenuated by pretreatment with pertussis toxin (PTx). PTx did not inhibit the effect of TNF to increase inositol phosphate turnover. TNF did not increase cAMP, intracellular calcium, or inositol phosphates in the UMR-106 cells.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1994

Roles of second-messenger systems and neuronal activity in the regulation of lordosis by neurotransmitters, neuropeptides, and estrogen: a review.

Many neurotransmitters and neuropeptides can affect the rodent feminine sexual behavior, lordosis, when administered in the ventromedial hypothalamus (VMH), midbrain central gray (MCG), or other brain regions. A survey of the electrophysiological and biochemical actions of these neural agents revealed that there is a very consistent association between lordosis facilitation with both the activation of the phosphoinositide (PI) pathway and the excitation of VMH and MCG neurons. In contrast, lordosis inhibition is associated, less consistently, with alterations of the adenylate cyclase (AC) system and the inhibition of neuronal activity. The findings that lordosis could be facilitated by going beyond membrane receptors and directly activating the PI pathway, suggest that this second-messenger pathway is a common mediator for the lordosis-facilitating agents. Furthermore, as in the case of stimulating membrane receptors, direct activation of this common mediator also requires estrogen priming for lordosis facilitation. Therefore, it is likely that the PI pathway is modulated by estrogen in the permissive action of estrogen priming. Indeed, a literature review shows that estrogen can affect selective isozymes of key enzyme families of the PI pathway at various levels. Such selective modulations, at several levels, could easily alter the course of a PI cascade; thence, the eventual functional outcome. These findings prompt us to propose that estrogen enables lordosis to be facilitated by a selective modulation of the PI pathway.

Animals↗
PubMed1990

Selective cross-activation/inhibition of second messenger systems and the reduction of age-related deficits in the muscarinic control of dopamine release from perifused rat striata.

Possible alterations in muscarinic cholinergic (mACh) signal transduction in senescence were studied in rat neostriata. Acetylcholine (ACh) activation of striatal muscarinic heteroreceptors by carbachol or oxotremorine enhances K(+)-evoked release of dopamine from perifused striata of 6- but not 24-month-old rats. Present experiments determined the effects of simultaneous activation or activation/inhibition of more than one second messenger on K(+)-evoked release of DA from perifused striatal slices from these age groups. Combinations of carbachol (500 microns), which stimulates inositol-1,4,5-bisphosphate (IP3) production and inhibits cyclic AMP production, with oxotremorine (500 microns), which inhibits cyclic AMP production, in the presence of 30 mM KCl (in a modified Krebs-Ringer medium) reduced the age-related reduction in mAChR enhancement of DA release (analyzed by HPLC coupled to electrochemical detection; 5 min fractions were collected on ice in perchloric acid; flow rate 120 microliters/min). Combinations of these agonists with the putative second messenger arachidonic acid (10 microM), also enhanced K(+)-evoked release of DA in the striatal tissue from the 24-month group. IP3 activation was lower in the striatal tissue from old animals than those from young under all conditions, but cross-activation/inhibition actually may have lowered the IP3 threshold necessary for enhanced DA release to occur. In a subsequent experiment, pre-loading striatal tissue from young animals with either carbachol or oxotremorine under basal release conditions reduced the responding when the basal release medium was switched to one containing 30 mM KCl and combinations of the agonists.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗