Neuronal localization of dopamine and 5-Hydroxytryptamine in some mollusca

Summary The localization of biogenic monoamines in ganglionic tissues from Anodonta piscinalis, Helix pomatia, and Buccinum undatum has been studied by means of the histochemical fluorescence method of Falck and Hillarp.In cerebral, visceral, and pedal ganglia (besides nonfluorescent nerve cells) neurons emitting a green or yellow fluorescence were found. No other cell systems exhibiting a specific fluorescence were observed. An abundance of monoaminergic terminals were found in the central parts of these ganglia. Spectrophotofluorimetric determinations showed that there are large quantities of dopamine and 5-hydroxytryptamine in the tissues investigated. The amounts of dopamine and 5-hydroxytryptamine agree well with the distribution of green and yellow fluorescence, respectively, in the ganglia.There are many similarities between the vertebrate and the molluscan monoaminergic neurons. The morphology of the neurons is the same, the intraneuronal distribution of the monoamines is identical, depletion experiments with reserpine and denervation experiments give the same results, and the synaptic arrangement of monoaminergic fibres on non-adrenergic neurons has the same appearance. Apparently, however, dopamine and 5-hydroxytryptamine are the only monoamines acting as neuronal transmitters in the species investigated.The research reported in this document has been sponsored by the Air Force Office of Scientific Research under Grant AF EOAR 64-5 through the European Office of Aerospace Research (OAR), United States Air Force and by the Swedish Natural Science Research Council.     

Dietary and species influence on potential of plasma to stimulate differentiation and lipid accumulation in cultured adipocyte precursors

Sera and plasma from different species and from rats of various dietary statuses were compared with regard to effects on proliferation, glycerophosphate dehydrogenase (GPDH) activity, and lipid-filing of rat adipocyte precursors converting to adipocytes in primary cell culture. All of the tested sera and plasma samples were comparably supportive of cell multiplication, but their effects on elevation of GPDH activity (a key event in adipocyte differentiation) and lipid-filling varied greatly. Plasma supported a much greater increase in GPDH activity than serum, while serum from cats supported a much lower increase than serum from humans, calves, goats, or rats. Dietary status of rats did not affect the potential of plasma to support GPDH activity, but did affect plasma support of lipid-filing. A higher than normal degree of lipid-filling was promoted by plasma from rats fed a high-fat, high-sugar diet, while a lower than normal degree was promoted by plasma from fasted rats. Lipid-filling was also found to vary in response to changes in content of very low density lipoprotein (VLDL) in human plasma. This suggests that the influence of diet on the potential of plasma to promote adipocyte lipid-filling may be mediated by the effect of diet on plasma VLDL. The absence of a diet-dependent effect of plasma either on multiplication of adipocyte precursors or on degree of elevation of GPDH activity leaves unresolved the mechanism by which diet affects adipocyte production in animals.     

Effects of volatile anesthetics on elastic stiffness in isometrically contracting ferret ventricular myocardium.

The effects of halothane, isoflurane, and sevoflurane on elastic stiffness, which reflects the degree of cross-bridge attachment, were studied in intact cardiac muscle. Electrically stimulated (0.25 Hz, 25 degrees C), isometrically twitching right ventricular ferret papillary muscles (n = 15) at optimal length (L(max)) were subjected to sinusoidal length oscillations (40 Hz, 0.25- 0.50% of L(max) peak to peak). The amplitude and phase relationship with the resulting force oscillations was decomposed into elastic and viscous components of total stiffness in real time. Increasing extracellular Ca(2+) concentration in the presence of anesthetics to produce peak force equal to control increased elastic stiffness during relaxation, which suggests a direct effect of halothane and sevoflurane on cross bridges.