Role of the serotoninergic raphe-hippocampus system for the antinocifensive effect of morphine

As revealed in earlier studies, the antinocifensive effect of morphine is brought about, among other things, with involvement of serotoninergic transmission mechanisms. In this context the role of the serotoninergic raphe-hippocampus system has been studied in this paper. Topical microinjections of serotonin into the dorsal hippocampus increased morphine analgesia in a dose-dependent fashion, while application into the striatum had no effect. Morphine injections into the median raphe nucleus in relatively low doses exert an antinocifensive effect which is inhibitable by methysergide. Lysergic acid diethylamide administered into the median raphe nucleus also abolished the effect of morphine in a dose-dependent manner. The results in connection with literature data lend support to the presumed integrative function of the serotoninergic raphe-hippocampus system in the mechanism of antinocifensive action of morphine.     

The redox state of pyridine nucleotides controls permeability of uncoupled mitochondria to K+

Heart mitochondria respiring in the presence of P_i release endogenous K⁺ to a sucrose medium when an uncoupler is added. The uncoupled mitochondria retain K⁺, however, if the oxidation of NAD(P)H is prevented by the addition of rotenone or antimycin. Addition of rotenone, once the uncoupler-dependent K⁺-efflux has been initiated, results in a rapid reduction of NAD(P) and a simultaneous decrease in permeability to K⁺. These changes are independent of respiration. The results suggest that a latent pathway for K⁺-permeability is present in the membrane, that it can be opened and closed reversibly, and that it reflects, either directly or indirectly, the redox status of mitochondrial pyridine nucleotides. The possible relationship of this putative pathway to those available for Ca²⁺ uptake and release is considered.     

Reduction in postprandial energy expenditure during pregnancy.

Energy expenditure was measured during pregnancy in seven primigravid women at 12-15, 25-28, and 34-36 weeks and after the cessation of lactation. On each occasion the resting metabolic rate and the increase in metabolic rate after ingestion of a liquid test meal were measured by indirect calorimetry. In absolute terms the resting metabolic rate increased steadily during pregnancy but when expressed per unit of body weight no change was found. The energetic response to a mixed constituent meal was significantly reduced by 28% in the middle trimester of pregnancy. These findings suggest a possible maternal adaptation to increase energetic efficiency at a time when the energy demands of the fetus are high.