Gelsolin inhibition of fast axonal transport indicates a requirement for actin microfilaments

The actions of actin-based microfilaments in cell motility suggest a possible role in the mechanism of fast axonal transport, but the pharmacological data evaluating their role in this process are equivocal. Moreover, microfilaments are difficult to preserve and identify in ultrastructural studies, so the organization and function of axonal actin has remained uncertain. We have now evaluated the role of actin microfilaments in intracellular transport of membranous organelles using video-enhanced contrast microscopy and gelsolin to analyse fast axonal transport directly in isolated axoplasm from the squid giant axon. With this preparation it is possible to perfuse axoplasm with large molecules that do not cross the plasmalemma, while controlling cation levels. The 90,000-molecular weight protein gelsolin depolymerizes actin microfilaments in micromolar Ca2+, but not in the absence of Ca2+. Axonal transport of membranous organelles has previously been shown to be unaffected by levels of Ca2+ up to 10 microM. In the presence of EGTA, gelsolin has no effect on the movement of membranous organelles, but in the presence of 10 microM Ca2+ it completely blocks transport of all membranous organelles. No changes in the organization of the axoplasm were detected. These results and results using other probes for actin are consistent with the hypothesis that actin-based microfilaments are involved in the movement of membranous organelles in the axon.     

Sclerotization and coloration of the insect cuticle

Summary Evidence indicating linkage between the processes of cuticle hardening and coloration are reviewed. Data and observations for the mutants black and ebony inDrosophila melanogaster are used to construct a possible model for the relationship between these developmental events.     

Influence of pinealectomy on corticotropin (ACTH)

Summary Sensory deprivation produced by removing the eyes and olfactory bulbs in male rats allowed pinealectomy to markedly augment the post-adrenalectomy elevation of ACTH levels. Pineal removal or sensory deprivation separately did not have this effect. Thus, intact sensory input and an intact pineal gland are independently capable of restricting the post-adrenalectomy rise in ACTH levels.This work was supported in part by NIH Grant No. P30 HD 10202. We thank F. Lynd and R.J. Reiter for advice, P. Starr and J. Sackman for technical assistance, and Bess Mitchell for typing.     

Colour mixing and colour preferences in neonate gulls

Zusammenfassung Junggeschlüpfte Silber- und Heringsmöven zeigen beim Picken von kleinflächigen, beweglichen Reizen Spektralfarbbevorzugungen. Drei theoretische Modelle sind vorgeschlagen worden, die diese Bevorzugungen erklären sollen. Die Voraussagen dieser Modelle bezüglich der Bevorzugung von Mischfarben wurden experimentell geprüft und als nicht zutreffend befunden. Vielmehr legen die Ergebnisse die Vermutung nahe, dass die Bevorzugung nicht, wie bisher angenommen, auf einem afferenten sensorischen Filtermechanismus beruht, sondern auf einen mehr zentralen, postperzeptualen Prozess zurückzuführen ist.     

Superoxide dismutase activity during the plasmodial life cycle ofPhysarum polycephalum

Summary Superoxide dismutase activity was slow throughout the cell cycle of surface cultures ofPhysarum polycephalum. This activity increased markedly when the organism was induced to spherulate. Glutathione (GSH) and hydrogen peroxide (H₂O₂) concentrations changed very little during the cell cycle. During spherulation GSH decreased; H₂O₂ and the cyanide-resistant respiration of plasmodial homogenates increased.     

Cholinergic-rich brain transplants reverse alcohol-induced memory deficits

Alcohol-induced memory impairment in man has been attributed to deficiencies in subcortical noradrenergic and cholinergic systems, as well as to damage in midbrain structures. Korsakoff's psychosis, a disease in which alcohol poisoning causes apparently irreversible memory defects, is characterized by lesions in cholinergic and noradrenergic nuclei and by a decrease in the activity of choline acetyltransferase (ChAT) and the content of noradrenaline (NA) in forebrain areas such as cerebral cortex and hippocampus, innervated by these nuclei. Prolonged intake of ethanol in rodents similarly produces signs of noradrenergic and cholinergic deafferentation in the cortex and hippocampus, as well as persistent memory deficits. To test whether alcohol-induced memory impairments depend on cholinergic deafferentation, we transplanted cholinergic-rich fetal basal forebrain cell suspensions into the cortex and hippocampus of alcohol-treated rats. The substantial and persistent memory losses produced in our rats by ethanol intake were associated with an impairment of cholinergic function, and were reversed by cholinergic-rich transplants into cortex and hippocampus.