Plasticity in the human central nervous system.

Long-term potentiation (LTP) is a well-characterized form of synaptic plasticity that fulfils many of the criteria for a neural correlate of memory. LTP has been studied in a variety of animal models and, in rodents in particular, there is now a strong body of evidence demonstrating common underlying molecular mechanisms in LTP and memory. Results are beginning to emerge from studies of neural plasticity in humans. This review will summarize findings demonstrating that synaptic LTP can be induced in human CNS tissue and that rodent and human LTP probably share similar molecular mechanisms. We will also discuss the application of non-invasive stimulation techniques to awake human subjects to induce LTP-like long-lasting changes in localized neural activity. These techniques have potential therapeutic application in manipulating neural plasticity to treat a variety of conditions, including depression, Parkinson's disease, epilepsy and neuropathic pain.

The effect of aminophylline on renin release from human chorio-decidua.

The effect of aminophylline on renin release from human chorion was investigated by perfusing the tissue with various concentrations of the drug. Buffer containing aminophylline (2 X 10(-6) mol/l) doubled the rate of active and total renin secretion, but a more concentrated solution (10(-5) mol/l) released proportionately less active and total renin although the result was statistically significant. Renin secretion was not altered by aminophylline (5 X 10(-5) mol/l). The pattern of renin release was modulated by concentrations of aminophylline which were at least a 100-fold lower than those required to inhibit cyclic adenosine 3',5'-monophosphate phosphodiesterase. However, as the methylxanthines are potent adenosine receptor antagonists, we suggest that in the human chorion adenosine is a mediator of renin release.

Osmolarity changes can enhance the release of renin from human chorion.

Sections of human chorion were perfused with an aerated buffer for 5 hours. Samples were collected every 20 minutes and the concentration of active and total renin in the perfusate was measured. Substitution of the initial bicarbonate buffer (281 mosm/L) with a buffer of 251 mosm/L doubled the rate at which active and inactive renin were released into the perfusate. When the osmolarity of the solution was reduced by 60 mosm/L, a threefold rise in the concentration of active renin and a sixfold rise in that of total renin was seen. However, these effects were transient, and renin secretion decreased before osmolarity was raised to the previous value.

A study of angiotensin II binding sites in human placenta, chorion, and amnion.

The binding of tritiated angiotensin II to 20,000 x g particulate tractions of human placenta, chorion, and amnion was investigated. Binding to particles from the three tissues reached equilibrium within 10 minutes at 29 degrees C and was displaced by the addition of 1,000-fold excess of unlabeled angiotensin II. Scatchard analysis of the data showed that two classes of binding sites were present in the placental preparation. For the high-affinity site, values of 9 x 10(-9) M and 300 fmoles/mg of protein were obtained for the dissociation constant and the binding capacity, respectively. There was little specific binding in chorion and amnion.