PubMed Health⌕ Search

Biomedical subjects

D Mayor

Publications and source records attributed to D Mayor.

At least 19 recordsLinked to original sources

Axonal regeneration through a peripheral nerve implanted into a brain cavity.

A cavity was prepared in the rat parietal cortex by suction, filled with gel foam and left for 3 weeks during which time it became highly vascularised. Into this 3-week-old capillary bed a 5 mm length of autologous common peroneal nerve was implanted. Animals were killed at various time intervals up to 7 months after implantation of the nerve segment. The ultrastructural features of the vascular bed before and after implantation of the nerve segment were compared. In the absence of a peripheral nerve implant no axons were found within the cavity. However, at 5 weeks after implantation numerous axon-like profiles and capillaries containing fenestrations were observed within the implant. Eight weeks after implantation of the peripheral nerve both myelinated and non-myelinated axons were observed within the implant and in the surrounding capillary bed. No obvious increase in the number of axons was observed with increasing time periods. To investigate the origin of the axons within the vascular bed and/or implant the fluorochrome true blue was injected into the cavity 7 months after implantation of the nerve. Three days later selected areas of the brain, the trigeminal, superior cervical and otic ganglia were examined for retrogradely labelled fluorescent cells. Labelled cells were found adjacent to the cavity and in the ipsilateral trigeminal and superior cervical ganglia. The significance of these results in relation to the enhancement of axonal regeneration from the damaged central nervous system (CNS) is discussed.

Animals↗

The permeability of the capsule of autonomic ganglia to horseradish peroxidase.

Horseradish peroxidase (HRP) was applied to the capsules of various autonomic ganglia in vivo. The capsules of the inferior mesenteric ganglion and superior cervical ganglion of guinea-pigs and the inferior mesenteric ganglion of mice were readily penetrated by the enzyme. The capsule of the mouse superior cervical ganglion was apparently impermeable to HRP, while that of the guinea-pig lumbar sympathetic trunk was intermediate in permeability, being most readily penetrated by HRP around the blood vessels entering or leaving the ganglia. The results of retrograde transport experiments from the guinea-pig inferior mesenteric ganglion to spinal ganglia are considered in the light of the ready permeability of its capsule.

Animals↗

The uptake and retrograde transport of horseradish peroxidase--polylysine conjugate by ligated postganglionic sympathetic nerves in vitro.

The uptake and retrograde transport of horseradish peroxidase (HRP) and horseradish peroxidase-poly-L-lysine conjugate (HRP-PL) were compared using a system comprising the guinea-pig inferior mesenteric ganglion (IMG) and ligated hypogastric hypogastric nerves maintained in vitro in a twin chamber apparatus. 0.5 mg of HRP-PL applied to the ligated nerves produced stronger retrograde labelling of neurons within the IMG than did 10 mg of HRP. This may have been due to the greater uptake of HRP-PL in a vesicular form by the axons immediately proximal to the ligation. The possible roles of large rounded vesicles and elongated cisternae in retrograde axoplasmic transport are discussed.

Animals↗

A morphological study of the uptake and orthograde axoplasmic transport of horseradish peroxidase by damaged autonomic neurons in vitro.

A preparation comprising the guinea-pig inferior mesenteric ganglion (IMG) and ligated hypogastric nerves was maintained in vitro in a twin-chamber apparatus. Horseradish peroxidase (HRP), added to the ganglion compartment, was taken up via coated pinocytotic vesicles into the neuronal perikarya, and subsequently accumulated in many polymorphic cytoplasmic organelles, but it did not enter the Golgi complex. After 24 h incubation, HRP was also localized in membrane-bounded organelles in the nonmyelinated axons of the hypogastric nerves in the ligated nerve compartment. HRP-labelled organelles accumulated in swollen nonmyelinated axons immediately proximal to the ligation along with other organelles known to undergo fast axoplasmic transport. It is suggested that HRP taken up by the neuronal perikarya subsequently underwent fast axoplasmic transport without passing through the Golgi complex. The organelles in which HRP was transported in an orthograde direction were very similar to those in which the enzyme is known to be transported retrogradely in the same neuronal system. The advantages of this in vitro system for studying the orthograde transport of exogenous protein are discussed.

Animals↗

On the mechanism of the uptake of horseradish peroxidase into the retrograde transport system of ligated postganglionic sympathetic nerves in vitro.

The mechanism of the uptake of horseradish peroxidase (HRP) by damaged post-ganglionic sympathetic axons was studied in vitro. HRP was applied to the damaged axons at the time of nerve injury or after a 3 hours or 17 hours delay. An interval of 3 hours or 17 hours between nerve injury and exposure to HRP had no effect on the localisation of the HRP in the damaged axons or on its retrograde transport to their perikarya. Evidence was found for the pinocytotic uptake of the enzyme by the damaged axons and its accumulation within those axons in elongated cisternae and larger rounded vesicles. In further experiments the damaged axons were treated with HRP at 0 degrees C and then washed in HRP-free medium. The tracer entered the axons in a diffuse form under these conditions but no pinocytotic uptake was observed. However, following 24 hours further incubation at 37 degrees C, HRP could not be found in the perikarya. Treatment at 0 degrees C did not produce any lasting damage to the retrograde transport mechanism. The results of these experiments are compatible with the involvement of pinocytosis in the uptake of HRP in a form suitable for retrograde transport.

Animals↗

The uptake of horseradish peroxidase by neuronal elements within the guinea-pig distal colon and its subsequent retrograde transport to the inferior mesenteric ganglion: an in vitro study using an intact neuronal system.

An in vitro guinea-pig preparation comprising the inferior mesenteric ganglion (IMG), the colonic nerves, and a segment of the distal colon was used to study the uptake and retrograde transport of horseradish peroxidase by intact neurons. Peroxidase rapidly penetrated the colonic wall from the lumen and was taken into autonomic nerves by pinocytotic vesicles, usually of the coated variety. The peroxidase subsequently appeared in long vesicles within the axons, and, 24 hours later, could be detected in many neuronal perikarya throughout the IMG. The similarities between the modes of uptake of peroxidase by damaged and intact axons are discussed.

Animals↗

The uptake of intravenous horseradish peroxidase by the guinea-pig inferior mesenteric ganglion.

The uptake of intravenously injected horseradish peroxidase (HRP) by the neuronal perikarya and SIF cells has been studied in the guinea-pig inferior mesenteric ganglion (IMG). The HRP rapidly penetrated the walls of the blood vessels within the ganglion and was taken up by neurons and SIF cells by means of coated pinocytotic vesicles. HRP reaction product was subsequently found within larger vesicles which were most prominent 6--9 hours after injection. Thirty hours after injection all the neurons and SIF cells within the IMG were free of peroxidase reaction product. The implications of these findings were considered in relation to retrograde axonal transport studies in autonomic neurons.

Animals↗

The uptake of horseradish peroxidase by damaged autonomic nerves in vitro.

The uptake of horseradish peroxidase by damaged autonomic nerves was studied in vitro. Large amounts of the enzyme penetrated the axons in a diffuse (nonvesicular) form. This occurred within 90 minutes of application of the enzyme. Twenty four hours after application of the enzyme diffuse peroxidase was still present in the axoplasm, but it was 'diluted' as a result of great axonal swelling. Pinocytotic uptake of the enzyme was observed both 90 minutes and 24 hours after application of the enzyme. The swollen axons close to the point of ligation showed most evidence of pinocytotic uptake, largely into coated vesicles, and much membrane-bound peroxidase reaction product was present. The uptake of peroxidase in a membrane-bound form may be of particular significance for the subsequent retrograde transport of the enzyme.

Animals↗

The role of calcium ions in the synthesis and transport of noradrenaline carrier vesicles in guinea-pig sympathetic neurons in vitro.

Guinea-pig inferior mesenteric ganglia (IMG)/hypogastric nerve preparations were incubated in tissue culture media containing ethylene glycol-bis-(beta-aminoethyl ether)N,N'tetra-acetic acid (EGTA) or colchicine and examined either by fluorescence microscopy or by transmission electron microscopy. Two millimolar EGTA inhibited the accumulation of noradrenaline (NA) fluophore proximal to a crush, but did not produce an increase in the fluorescent intensity of, or the number of dense-cored vesicles (DCVs) within the neuronal perikarya. Calcium ions, but not magnesium ions, were able to block this effect of EGTA. Preparations incubated in the presence of colchicine (2.5 microgram/ml) showed a reduction in the amount of fluorescent material accumulating proximal to a crush, but an increase in both the fluorescent intensity and the number of DCVs within the neuronal perikarya. The suggestion that calcium ions are required for the synthesis of some part of the NA-containing vesicle rather than for their loading onto the axoplasmic transport mechanism is discussed.

Animals↗

The effect of tetrabenazine on the accumulation of noradrenaline in constricted postganglionic sympathetic nerves in vitro.

The accumulation of noradrenaline proximal to a constriction applied to cat hypogastric nerves in vitro has been studied in preparations treated with tetrabenazine. The accumulation of amine was almost completely abolished by the drug. Evidence is presented which suggests that tetrabenazine exerts a direct noradrenaline-depleting effect on the intraneuronal storage vesicles. Recovery of noradrenaline levels after the removal of the drug was rapid and was effected by the biosynthesis of new noradrenaline within the axon.

Animals↗

Effects of low temperatures on microtubules in the non-myelinated axons of post-ganglionic sympathetic nerves.

The effect of temperature changes on the number of microtubules in non-myelinated axons has been studied in cat inferior mesenteric ganglion/hypogastric nerve preparations incubated at various temperatures in Eagles minimal essential tissue culture medium in vitro. At 37 degrees C the non-myelinated axons contained 28.4 plus or minus 0.8 S.E.M. (54) microtubules per axon. After incubation at 0 degrees C for 4 h this number fell to 2.3 plus or minus 0.1 S.E.M. (41) but returned to normal levels when the nerves were rewarmed. This loss of microtubules on cooling the nerves and their reappearance on rewarming was a rapid process; it was independent of the influence of the nueronal cell body and of protein synthesis within the axon. The preservation of the microtubules was improved when D2O was present in the incubation medium. Reformed microtubules appeared to function normally with respect to their possible role in the transport of noradrenaline storage vesicles along the axons.

Animals↗

Metabolic aspects of the synthesis and intra-axonal transport of noradrenaline storage vesicles.

1. Constricted cat hypogastric nerve/inferior mesenteric ganglion preparations have been maintained for 24 hr in vitro, in either test-tubes or a two compartment box, and used to study the roles of energy metabolism, protein synthesis and calcium ions in the synthesis and transport of noradrenaline storage vesicles in sympathetic neurones.2. When preparations were incubated so that the nerve trunks but not the ganglia were made anoxic, dense-cored vesicles lost their store of noradrenaline and did not accumulate above the ligature. This was accompanied by profound ultrastructural damage to the nerves.3. When in contact with the ligated nerve trunks, sodium fluoride inhibited the intra-axonal movement of dense-cord vesicles but did not deplete them of their stored noradrenaline. When sodium fluoride and pyruvate were present in the medium bathing the nerve trunks the movement of noradrenaline storage vesicles was unaffected.4. Whilst a reduction of the calcium ion concentration in the incubation medium and the inhibition of protein synthesis by cycloheximide prevented the synthesis of dense-cored vesicles in the neuronal perikaryon they had no effect on the movement of preformed dense-cored vesicles along non-myelinated axons.

Animals↗