[Regulation of receptors and mechanism of action of growth hormone].

The initial step in the action of growth hormone (GH) is interaction with specific sites localized in target cell membranes. Growth hormone receptors have been demonstrated in different tissues and have been extensively studied in the liver. 125I-human growth hormone injected IV in the intact male rat is internalized in the hepatocytes by a receptor-mediated process; the radioactive material is sequentially associated with plasma membranes, endocytic structures and lysosomes.

Fate of injected human growth hormone in the female rat liver in vivo.

[125I]Iodohuman GH ([125I]iodo-hGH) was injected iv to female rats, and its subcellular distribution was studied with time using fractionation techniques. Uptake in the total particulate fraction was maximal by 15 min after injections; at that time, 7% of the radioactivity injected was recovered per g liver. Liver uptake of [125I]iodo-hGH was markedly inhibited by coinjection of native hGH.

[Growth hormone receptors in liver membranes of rats with renal insufficiency].

Binding sites for human growth hormone (hGH) were studied in liver membranes of rats with chronic renal insufficiency (CRI) associated with a marked growth defect. A subtotal nephrectomy was performed in young female rats. One month after surgery, the rats with a plasma creatinine greater than or equal to 3 times that of controls were killed.

[Analysis of the circadian rhythm of motor activity in white rats by using several pharmacologic agents which act on cerebral monoamines].

Three pharmacological agents, (disulfiram, imipramine and reserpine) influencing the brain monoamine transmitters have been studied to explain the mechanism involved in the motor circadian rhythm. The new results corroborate our previous ones : the norepinephrine transmitter responsible for the paradoxical sleep is unable to explain the depressed metabolic phase of the circadian rhythm; the negative results obtained with disulfiram and imipramine corroborate the previous results with nialamide. On the contrary, the agents which reduce the serotonine transmitter mechanisms (p-chlorophenylalanine) decrease the difference between active and sleep phases by their action involved in the non-activated sleep.

The circadian rhythm of rat motor activity and the effect of brain monoamine inhibitors (PCPA and nialamide).

The study of the circadian motor rhythm in free-running conditions of 500 g rats during 6 successive days shows that the endogenous period of the rhythm in these conditions is 23.40 hrs. The two poisons studied (PCPA in 40 mg/100 g dose and nialamide 5 and 10 mg/100 g doses) have both a deep effect on the functioning of the endogenous rhythm.

[Brain monoamines and circadian rhythm of spontaneous motor activity of rats].

The effect of three drugs, parachlorophenylalanine, nialamide and disulfiram, drugs known by their action on the two sleep phases, slow wave sleep and I-REM-sleep, have been studied and tested by their effect on the motor circadian rhythm : PCPA and disulfiram reduce the amplitude of the rhythm by two opposed mechanisms : PCPA increases the motor activity, especially the day-time activity, disulfiram reduces the motor activity, especially the night-time activity. The former reduces the serotonine content, the latter the noradrenaline content of the central nervous system. Nialamide (5 or 10 mg/1000 g) is without any action of the rhythm.