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Biomedical subjects

F Collins

Publications and source records attributed to F Collins.

At least 109 records · Page 6Linked to original sources

The spatial control of ganglionic neurite growth by the substrate-associated material from conditioned medium: an experimental model of haptotaxis.

Techniques are described for forming on the culture substrate a narrow pathway of material derived from medium conditioned by embryonic non-neuronal cells. There is a precise correlation between the known location of the pathway and the spatial distribution of neurites extended from whole ciliary ganglia or dissociated neurons grown on the patterned substrate. When individual growth cones moving on the pathway contact one of its edges, they turn sharply so as to remain on the pathway. This turning response is not simply due to a physical barrier to movement across the edge, since growth cones can cross onto the pathway when entering from the adjacent untreated substrate. The strong preference for neurites to maintain contact with the pathway also is not simply a result of their inability to survive or elongate outside of the pathway, since neurites from whole ganglia elongate readily on other regions of the substrate, although their growth is then undirected. Direct contact with the pathway is required for these directive effects, and there is no indication that the material bound to the substrate diffuses off and exerts its effects at a distance. The neurite-guiding activity is found in partially purified fractions of conditioned medium which also contain a substrate-bound inducer of neurite outgrowth. It is possible that both activities may be due to the same components of conditioned medium. These results suggest that ciliary ganglion growth cones are able to detect specific components of conditioned medium on the substrate and respond to their presence by changing their direction of movement so as to remain in contact with these components.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

An effect of nerve growth factor on the parasympathetic ciliary ganglion.

Mouse submaxillary nerve growth factor (NGF) increases the length and density of neurites extended from embryonic chick ciliary ganglia in vitro. The effect is not as pronounced as with dorsal root ganglia, but it occurs at the same low concentrations of NGF. This effect was observed on polyornithine substrata with or without pretreatment of the substratum with conditioned medium. NGF did not significantly increase the length or density of neurites extended from spinal cord or neural retina explants in the same culture conditions. Stimulation of ciliary ganglion neurite outgrowth did not occur when NGF was replaced with cytochrome c or epidermal growth factor, whereas insulin had an effect comparable to that of NGF when present at much higher concentrations. Four different purified preparations of NGF gave identical results. The purity of two of these preparations was determined after radioiodination; greater than 98% of the radioactivity migrated as a single band on polyacrylamide gels, and greater than 94% of the radioactivity was bound by affinity purified anti-NGF antibody. The effect of NGF on neurite growth could be separated from its effect on neuronal survival. NGF failed to promote the survival of ciliary ganglion neurites even at concentrations 1000-fold higher than those which significantly stimulated neurite growth.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

An effect of nerve growth factor on parasympathetic neurite outgrowth.

Addition of nerve growth factor (NGF) to dissociated parasympathetic ciliary ganglion neurons resulted, within 60 min of its addition, in a 2-fold increase in average neurite length and an accompanying enlargement and spreading of neuronal growth cones. These effects occurred over a concentration range of NGF of 0.1-10 ng/ml and were blocked by affinity-purified antibody to NGF. Epidermal growth factor, fibroblast growth factor, and angiotensin did not have these effects, although insulin at high concentrations was able to induce a response similar to that of NGF. Dissociated sympathetic chain neurons also responded to NGF with increased neurite lengths, and, in addition, NGF considerably extended the survival time of these neurons in culture. However, the effect of NGF on ciliary ganglion neurons was limited to neurite outgrowth, and NGF did not promote the survival of these parasympathetic neurons.

Animals↗

In vitro Evidence for two distinct hippocampal growth factors: basis of neuronal plasticity?

The rat hippocampal formation was tested for the presence of factors that would accelerate neurite extension from chick parasympathetic (ciliary ganglion) or sympathetic (lumbar chain) neurons in vitro. Two growth factors were identified in extracts of this brain region. One accelerated neurite extension from sympathetic neurons and was blocked by antiserum to nerve growth factor. The other accelerated neurite extension from parasympathetic neurons but was not affected by the antiserum. These results suggest that specific growth factors account for the specificity of neuronal sprouting.

Animals↗

Reversible developmental change in the ability of ciliary ganglion neurons to extend neurites in culture.

From stages 35 to 40 in the chicken embryo, ciliary ganglion neurons undergo a developmental change which is detected in our assay system as a marked decline in the ability to extend neurites when placed in culture. This developmental loss is observed when the neurons are placed in culture as single, dissociated cells or as undissociated ganglion explants. The loss of the ability to extend neurites in culture is not a transitory phenomenon, for no recovery of this ability is observed during the rest of embryonic development or posthatching. There is a close temporal correlation between the embryonic period during which the ability of ciliary ganglion neurons to extend neurites declines and the period (stages 35 to 40) when these neurons form functional peripheral synapses in the embryo. The ability to extend neurites rapidly is not recovered during normal development as long as the ganglion and its connections within the organism remain intact. However, if the ciliary ganglia are removed from a stage 40 embryo and cultured for 3 to 4 days before being dissociated, the neurons have largely recovered their ability to initiate neurite outgrowth rapidly. This recovery after removal from the embryo is also presumably responsible for the eventual dense outgrowth of neurites from stage 40 ganglion explants after a 3- to 4-day delay in culture. Our results, in conjunction with similar results from other systems, suggest a cause and effect relationship between the establishment or disruption of peripheral connections and the loss or recovery, respectively, of the ability to extend neurites rapidly.

Animals↗

Conditioned medium increases the rate of neurite elongation: separation of this activity from the substratum-bound inducer of neurite outgrowth.

Heart cell-conditioned medium supports extensive neurite outgrowth from dissociated parasympathetic neurons of the chicken embryo ciliary ganglion. We have shown previously that neurite outgrowth in this system depends on the deposition of a substratum-conditioning factor from conditioned medium onto the polyornithine culture substratum. However, in the presence of only the substratum-bound material, neurite outgrowth is never as extensive as in whole conditioned medium. The present report demonstrates that a different and soluble component of conditioned medium is required to achieve the rates of neurite elongation normally observed in whole conditioned medium. This second component, while unable by itself to support neurite outgrowth, is able to increase the rate of neurite elongation approximately 3-fold within 30 to 60 min of its addition. This conclusion is based on direct time-lapse observations of the rate of elongation of individual neurites before and after the addition of fractions of conditioned medium previously depleted of the substratum-conditioning factor. Correlated with the effect of such fractions of conditioned medium on the rate of neurite elongation is a change in the morphology of the growth cones, which become larger and more spread. The activity of the soluble, elongation-promoting component of conditioned medium is nondialyzable and is sensitive to treatments known to affect proteins, such as repeated freeze-thawing, heating, and trypsinization. Fractions of conditioned medium which contain the elongation-promoting activity also contain all of the survival factor for parasympathetic neurons previously shown to be present in heart cell-conditioned medium. The methods described here represent a convenient new assay which we have used recently to demonstrate elongation-promoting factors with neuronal specificity in extracts of rat hippocampus.

Animals↗

The effect of electrode placement on frontalis EMG measurement in headache patients.

Comparisons were made between frontalis EMG surface recordings concurrently taken from horizontal, right vertical, and left vertical electrode placement configurations. Six migraine and seven tension headache patients were used as subjects. Results showed that, in general, a positive correlation existed between recordings from the three placements for both migraine and tension subjects as a group. However, marked individual differences were noted. It was concluded that electrode placement can be quite important in measuring changes in frontalis muscle tension for headache patients.

Action Potentials↗

Elongating nerve fibers are guided by a pathway of material released from embryonic nonneuronal cells.

Dissociated parasympathetic neurons rapidly initiate neurite outgrowth when exposed to culture medium previously conditioned by the growth of embryonic heart cells. The inducer of neurite outgrowth in the conditioned medium is a substratum-conditioning factor; that is, it does not act in a soluble form, but acts only when bound to the nerve cell culture substratum. When a sharp border is created between a region of the substratum coated with this factor and a region coated with unconditioned medium, neurites fail to cross this border; rather, they change their direction of outgrowth so as to remain on the conditioned substratum. Thus, long after the initiation of outgrowthhas been induced, elongating neurites continue to respond to the substratum-conditioning factor in a manner that allows their outgrowth to be channeled along a pathway of this neurotropic substratum-associated material.

Animals↗

Structure of and alterations to defective murine sarcoma virus particles lacking envelope proteins and core polyprotein cleavage.

HTG2 hamster cells produce a defective murine sarcoma virus lacking gp70 and, consequently, viral surface projections (knobs), but the lack of knobs appears to have no effect on intramembrane particle distribution. In addition, it has been noted that the core of the virus remains in the "immature" form as a result of the failure of the polyprotein precursor (p65) to undergo cleavage. However, incubation of HTG2 virus with avian myoblastosis virus was found to yield specific cleavage products of p65.

Animals↗

Mixed malignant tumour of the lung.

A mixed malignant tumour of the lung intermediate in type between pulmonary blastoma and carcinosarcoma is described. The epithelial component consisted of squamous carcinoma, undifferentiated carcinoma, and clefts lined by bland epithelial cells. The supporting stroma was composed of pleomorphic sarcoma, fibrosarcoma, chondrosarcoma, osteosarcoma, and indeterminate mesenchymal tissue. The tumour was removed surgically, but the patient died postoperatively with rapidly developing multiple bony and soft tissue metastases. Subcutaneous metastases showed the appearnce of poorly differentiated pleomorphic sarcoma. Published reports of mixed malignant lung tumours are reviewed.

Adenocarcinoma↗

Induction of neurite outgrowth by a conditioned-medium factor bound to the culture substratum.

Heart-cell conditioned medium (HCM) induces rapid neurite outgrowth from isolated neurons in culture. The following evidence indicates that this action of HCM is due to a trypsin-sensitive factor which attaches to the polyornithinecoated culture substratum: (i) Pretreatment of the culture substratum with HCM allows rapid neurite outgrowth to occur even in unconditioned media. The active factor remains bound to the substratum during the period of neurite outgrowth. (ii) The substratum-bound activity is destroyed by trypsin treatment, but is insensitive to collagenase, RNase, and DNase. (iii) The factor that binds to the substratum is essential for neurite outgrowth, because HCM is no longer active when the material that binds to the polyornithine substratum has been removed by passage of the HCM over a series of culture dishes. However, this "depleted" HCM is still able to support the growth of nonneuronal cells. (iv) Most significantly, when neurons are cultured in whole HCM, the extent of neurite outgrowth is proportional to the amount of substratum-bound activity and not to the amount in solution, indicating that the substratum-bound form of the factor is more active. Previous observations [Collins, F. (1978) Dev. Biol. 65, 50-57] suggest that HCM promotes neurite outgrowth by increasing the adhesion between nerve cell surface extensions and the polyornithine-coated culture substratum. It is possible, therefore, that the factor in HCM that binds to the substratum possesses sites to which nerve cell surface components adhere.

Axons↗