The effect produced by veratrine on transmembrane potential was investigated in five distinct regions of the isolated rat diaphragm blocked with eitherd-tubocurarine or α-bungarotoxin. It was found that small (0.4μg/ml) and large (2.0μg/ml) doses of veratrine depolarize only two or three of these regions. With the use of a very large (10.0μg/ml) dose depolarization occured in all five regions of the diaphragm but the effect was much larger in those areas of the muscle fibre membrane which were selectively depolarized by the smaller ones. These results clearly indicate either an unequal distribution of sodium channels activated by veratrine or differences in sodium channel density in distinct areas of the muscle fibre membrane. Supersensitivity of veratrinized muscles to potassium was confirmed. However, the sensitiveness to the depolarizing action of potassium was only increased in the regions of the diaphragm partially depolarized by veratrine. This suggests that partial depolarization of the muscle fibre membrane was actually the cause of the supersensitivity. The possible involvement of potassium and of the unequal depolarization of the muscle fibre membrane in the veratrine response is considered.

We have used genomic DNA from human or mouse cells as a calcium phosphate precipitate to transfect three different respiration-deficient Chinese hamster mutant cell lines with defects in complex I of the electron transport chain. Transformants were selected in DMEM containing galactose, a medium in which respiration-deficient cells do not grow. Evidence for the DNA-mediated transformation of these respiration-deficient cells with a putative complex I gene includes: (1) the clones are respiration-positive and respire at rates comparable to those of wild-type human, hamster, or mouse cells; (2) the clones have rotenone-sensitive NADH oxidase activities, indicating a functional complex I of the electron transport chain; and (3) the clones appear to be true transformants, as demonstrated by hybridization and Southern blot analyses. These experiments provide the basis for the isolation and subsequent characterization of several of the genes involved with complex I of the mammalian electron transport chain.

Probably the most striking example of uniformity in the neuronal fabric of the brain is that present in the cerebellar cortex. Its connectivity and neuronal circuitry have an almost crystal-like structural organization. An example of the former is the precise distribution of the synaptic inputs onto the soma and dendrites of the cerebellar cortical neurons at the most superficial stratum, the molecular layer (cf. Palay and Chan-Palay 1974). At the neuronal circuit level the parallel fibers course in parallel to the cerebellar surface, the basket cell axons run orthogonally with respect to the direction of the parallel fibers, and all dendrites in the molecular layer run radially towards the surface of the cortex. This organization gives the cerebellar cortex a tridimensional matrix structure. As observed from the surface, the x axis is the direction of the parallel fibers, the y axis the direction of the basket cell axons, and the z axis the direction of the Purkinje cell dendrites (Ramón y Cajal 1911). In addition, since the descriptions by Ramón y Cajal (1888) it has been well known that the Purkinje cell dendrites are close to isoplanar and that the dendritic plane is oriented orthogonally with respect to the parallel fibers (Fig. 1).

Summary

Three recent wild-type H1N1 influenza virus isolates (A/USSR/90/77, A/Fiji/15899/83 and A/Firenze/13/83) replicated poorly in organ cultures of ferret bronchial tissue compared with the replication of an H3N2 wild-type virus (A/England/939/69). All four viruses replicated well in nasal turbinate tissue. Examination of one H1N1 virus (A/USSR/90/77)in vivo showed heavy infection in the upper respiratory tract of ferrets but little in the lower respiratory tract. These results raise the possibility that the mildness of human influenza arising from the H1N1 strains may be due to lack of capacity to attack the lower respiratory tract as well as the presence of antibody in previously exposed persons.

The body’s cells require a stable internal environment in which to carry out their functions despite variations in the external environment to which the body is exposed. The maintenance of a stable internal environment is accomplished by complex regulatory devices involving the endocrine system and the autonomic subdivision of the nervous system. Not only do these systems function to maintain homeostasis, but they also permit the individual to respond quickly to the requirements for increased energy use when the situation demands mobilization of the body’s resources.

A stable, temperature-sensitive, nonfusing variant of the L₆ rat myoblast cell line has been isolated following mild EMS-induced mutagenesis. At the permissive temperature (37° C), the growth characteristics and developmental pattern of the tsA1 variant are essentially identical to those of the parental L₆D₀ line at either 37° C or 40° C. At the nonpermissive temperature (40° C), the tsA1 variant grows normally but does not align, fuse, or synthesize detectable amounts of β-tropomyosin or myosin LC₂. A peptide corresponding to myosin LC_lemb is barely detectable. The temperature-sensitive period spans the interval from 4 to 72 h postplating with a midpoint at approximately 40 h. Under standard culture conditions, commitment to terminal differentiation occurs between days 3 and 4, and alignment and fusion begin on days 4 and 5, respectively. Thus, the temperature-sensitive event occurs very early in the L₆ developmental program. A spontaneous revertant of the temperature-sensitive phenotype (tsA1[R3]) exhibits recovery of the capacities to align, fuse, and synthesize the repertoire of muscle-specific proteins, suggesting that a single pleiotropic mutation in the tsA1 variant may regulate several stages in L₆ myogenesis.

Marek’s disease (MD) is one of the most commonly occurring neoplastic diseases of chickens and is endemic in almost all poultry-producing areas of the world. Highly successful vaccination programmes have dramatically reduced natural outbreaks of MD in commercial chickens. However, vaccination has not eradicated MD and outbreaks continue to occur sporadically, hence the need for proper diagnosis of the disease.