Influence of oxytocin on human memory processes: Validation by a control study

An earlier report (1) of an adverse effect of high doses of oxytocin on human memory included results of studies on women receiving oxytocin as part of the treatment to induce 2nd trimester therapeutic abortion. These women served as their own controls. We have now been able to study a group of women who have been treated in all ways like the original group, with the exception that they did not receive oxytocin. The results from this external control corroborate the finding that oxytocin affected memory.     

Protective reaction of the myocardium in poisoning

Intensive synthesis of collagen-like substance was revealed in the rabbit myocardium during experimental diphtheria intoxication. It was more marked in the right ventricle 24 hours after the injection of diphtheria toxin. Since similar changes (the substance was mainly formed around blood vessels) have been observed in other cases of toxic myocardial alterations (i.e. ethanol intoxication, injection of pharmacological agents, etc.), it can be assumed that it is a standard protective reaction of the altered heart to the penetration of toxic agents from the blood into the myocardial tissue.     

Effects of EEG of the osmotic opening of the blood-brain barrier in rats

EEG activity was recorded in rats submitted to osmotic opening of the BBB by intracarotid mannitol infusion.This procedure produced an immediate short-lasting depression of the EEG and a tardive paroxysmal EEG activity. Both these phenomena were more relevant on the ipsilateral hemisphere. In some instances a tonico-clonic seizure was recorded.Pre-treatment with diazepam abolished the occurrence of the tardive EEG and behavioral modifications.In accord with previous findings, focal seizure activity is likely to be responsible for the metabolic abnormalities associated with osmotic opening of the BBB. This preparation therefore produces in the brain unphysiological states in respect to local metabolism and electrical function.     

Penetration of analogues of H2O and CO2 in proteins studied by room temperature phosphorescence of tryptophan.

The influence of the protein matrix on the reactivity of external molecules with a species buried within the protein interior is considered in two general ways: (1) there may be structural fluctuations that allow for the diffusive penetration of the small molecules and/or (2) the external molecule may react over a distance. As a means to study the protein matrix, a reactive species within the protein can be formed by exciting tryptophan to the triplet state, and then the reaction of the triplet-state molecule with an external molecule can be monitored by a decrease in phosphorescence. In this work, the quenching ability (i.e., reactivity) was examined for H2S, CS2, and NO2- acting on tryptophan phosphorescence in parvalbumin, azurin, horse liver alcohol dehydrogenase, and alkaline phosphatase. A comparison of charged versus uncharged quenchers (H2S vs SH- and CS2 vs NO2-) reveals that the uncharged molecules are much more effective than charged species in quenching the phosphorescence of fully buried tryptophan, whereas the quenching for exposed tryptophan is relatively independent of the charge of the quencher. This is consistent with the view that uncharged triatomic molecules can penetrate the protein matrix to some extent. The energies of activation of the quenching reaction are low for the charged quenchers and higher for the uncharged CS2. A model is presented in which the quenchability of a buried tryptophan is inversely related to the distance from the surface when diffusion through the protein is the rate-limiting step.(ABSTRACT TRUNCATED AT 250 WORDS)     

Beta 2-receptors in the rat anterior pituitary mediate adrenergic stimulation of prolactin release

As previously shown, the beta-adrenergic agonists isoproterenol, epinephrine and norepinephrine stimulate prolactin (PRL) release from superfused rat anterior pituitary cell aggregates. In order to further characterize the beta-adrenergic response in this tissue preparation, the effects of various beta-adrenergic agents were investigated. The beta 2-agonist, zinterol, stimulated PRL release at concentrations more than 4 orders of magnitude lower than prenalterol, a beta 1-agonist with high potency in rat heart. The order of potency of the antagonists IPS 339 (beta 2), ICI 118.551 (beta 2), propranolol, sotalol, practolol (beta 1), metoprolol (beta 1) and H 35/25 for inhibition of beta-agonist-stimulated PRL release provided additional support for a beta 2-stimulatory effect. beta-Agonists were also capable of stimulating PRL release from superfused intact pituitaries. The beta-adrenergic response desensitized rapidly during prolonged exposure of the aggregates to beta-agonists.