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Biomedical subjects

E R Feringa

Publications and source records attributed to E R Feringa.

At least 19 recordsLinked to original sources
PubMed1992

Ventral horn motoneurons 10, 20 and 52 weeks after T-9 spinal cord transection.

To determine if transneuronal degeneration occurs in ventral horn motoneurons caudal to a spinal cord transection, we completely transected the spinal cord at T-9 in seven-week-old female rats. Ten, 20 or 52 weeks later, the motoneurons of the right sciatic nerve of transected and control rats were retrogradely labeled with Fluoro-Gold. There were no differences between control and transected rats in numbers or rostrocaudal distribution of labeled motoneurons at either 10, 20 or 52 weeks. At 20 weeks, there was no significant difference between control and transected rats in mean cross-sectional area of labeled neurons. We conclude that transneuronal degeneration did not occur.

Animals↗
PubMed1991

Fluoro-Gold's toxicity makes it inferior to True Blue for long-term studies of dorsal root ganglion neurons and motoneurons.

We studied the long-term effects of two retrogradely transported fluorescent dyes on survival of dorsal root ganglion neurons (DRGNs) and motoneurons (MNs). In adult female rats, we labeled DRGNs and MNs by soaking the cut sciatic nerve in Fluoro-Gold or True Blue. With True Blue, we found no difference in the number of labeled MNs or DRGNs in rats surviving 4 days or 20 weeks after nerve soak. With Fluoro-Gold, labeled DRGNs and MNs were decreased at 20 weeks compared with 4 days. Since there was no offsetting increase in unlabeled DRGNs at 20 weeks, Fluoro-Gold caused cell death.

Animals↗
PubMed1990

Retrograde transport of fluoro-gold in corticospinal and rubrospinal neurons 10 and 20 weeks after T-9 spinal cord transection.

Retrograde labeling with horseradish peroxidase is greatly diminished in corticospinal and rubrospinal neurons axotomized by complete T-9 spinal cord transection. We found, 10 or 20 weeks after a complete T-9 cord transection, that the number of corticospinal and rubrospinal neurons retrogradely labeled after Fluoro-Gold insertion into a new transection at T-1 did not differ from that of controls. While transection alters uptake, transport, and/or intracellular metabolism of some transportable substances, it does not affect the ability of the neurons to be retrogradely labeled with Fluoro-Gold.

Animals↗
PubMed1989

Prelabeled red nucleus and sensorimotor cortex neurons of the rat survive 10 and 20 weeks after spinal cord transection.

To demonstrate definitively the fate of the somata of rubrospinal and corticospinal neurons axotomized by a complete spinal cord transection at T-9, in young adult rats we prelabeled the neurons by injection into the lumbar enlargement of a retrogradely transported fluorescent dye, Fluoro-Gold, and four days later transected the cord. We found no loss in cell number ten or 20 weeks after axotomy. The average size of the neurons in each case is slightly but significantly reduced. These findings unequivocally demonstrate that the somata of long tract neurons of the rubrospinal and corticospinal systems persist in an atrophic and presumably inactive state for at least 20 weeks, and raise the possibility that treatment of spinal cord injury may normalize cell activity and allow long tract regeneration.

Animals↗
PubMed1988

The fate of prelabeled Clarke's column neurons after axotomy.

We studied Clarke's Column of the L-1 spinal cord segment of young adult female rats after first prelabeling its neurons by the intracerebellar injection of Fluoro-Gold or true blue and subsequently axotomizing the labeled cells by a complete spinal cord transection at T-9. In control rats, the number of labeled neurons at 1, 5, 10, and 20 weeks showed a progressive decrease, probably due to leakage of dye from the cells. A much greater loss of labeled neurons was found in T-9 spinal cord-transected rats than in their matched controls. At 5 weeks after transection, loss of large neurons was somewhat offset by an increase in small neurons; neuron shrinkage was a likely cause of this increase, because small, very intensely labeled neurons were found in transected rats but not in control rats. By 10 and 20 weeks post-transection, the number of all prelabeled neurons in transected rats had sharply decreased. In transected rats, but not in controls, very significant increases in labeled astroglia and microglia and other labeled small cells were found at 5 weeks. At 10 weeks, the identifiable labeled astroglia had decreased but marked increases in microglia and other labeled small cells persisted. We conclude that, following a complete T-9 spinal cord transection, axotomized Clarke's column neurons first shrink in size and then die. Labeled reactive astrocytes, which are most evident 5 weeks after injury, probably indicate phagocytosis of axotomized neurons.

Animals↗
PubMed1988

Loss of neurons in the red nucleus after spinal cord transection.

Red nucleus neurons, particularly those of the caudal one-half of the nucleus, die or severely atrophy following complete spinal cord transection at T9. The size of residual horseradish peroxidase-labeled cells was smaller at 10 and 15 weeks, but those survivors which could be labeled at 25 weeks were normal in size. Hematoxylin and eosin-stained sections of the red nucleus at 52 weeks postoperative showed loss of cells from all size groups.

Animals↗
PubMed1988

Corticospinal axons persist in cervical and high thoracic regions 10 weeks after a T-9 spinal cord transection.

Ten weeks after complete spinal cord transection at T-9, there was a decrease in the volume of the rat corticospinal tract but no loss in the number of axons contained in the cervical (C-2) or high thoracic (T-1) corticospinal tract. The mean area of the myelinated axon profile decreased in spinal cord-transected rats, with fewer axons found in the largest size groups and more in the smaller size groups. The survival of corticospinal axons in the cervical and thoracic cord 10 weeks after cord transection at T-9 indicates that the corticospinal neurons survive at least 10 weeks after cord transection. The fate of axotomized neurons after longer survival times remains to be determined.

Animals↗
PubMed1987

Changes in number and size of Clarke's column neurons after cord transection.

The number of large neurons in Clarke's column of the L-1 segment of the spinal cord of the rat decreases five or more weeks after a T-9 spinal cord transection. Analysis of cells at 1, 2, 3, 5, 7, 9, 12, and 15 weeks (wk) postoperatively demonstrates a loss of large neurons at each time interval beyond five wk postoperatively. Comparison of cell sizes found in the anatomic region of Clarke's column at two or three wk postoperatively with the cells found at 15 wk after transection and their respective control groups, shows a decrease in total cells found in operated rats 15 wk postoperative with a profound decrease in larger neurons in these rats. We did not detect a significant offsetting increase in smaller neurons. We believe the observed changes are due to death of large neurons and can find no evidence to support the contention that axotomized cells persist in a shrunken, atrophic state.

Animals↗
PubMed1986

Long-term effects of spinal cord transection on fast and slow rat skeletal muscle. I. Contractile properties.

Contractile properties of rat soleus and extensor digitorum longus muscles were studied 1 year after complete thoracic spinal cord transection (spinal cord level T9). Force-generating capacity and contraction speed were unchanged in the extensor digitorum longus 1 year after transection. However, the rate of contraction and relaxation increased in the soleus as reflected by a decrease in time-to-peak tension and increase in fusion frequency. Additionally, the soleus muscle cross-sectional area decreased significantly (50%) while generating the same absolute tension. Thus, a large increase in soleus specific tension (force per unit area) was observed. These data, in conjunction with the increase in contractile speeds, suggest soleus slow-to-fast fiber type conversion secondary to cordotomy. Discriminant analysis of the contractile properties yields fusion frequency as the best discriminator between muscle groups. Thus, following cordotomy, predominantly slow muscles are affected to a greater extent than fast muscles.

Analysis of Variance↗
PubMed1986

Long-term effects of spinal cord transection on fast and slow rat skeletal muscle. II. Morphometric properties.

Morphometric properties of rat soleus and extensor digitorum longus muscles were studied 1 year following complete thoracic spinal cord transection (spinal cord level T9). Both muscles demonstrated almost complete type 1 to type 2 muscle fiber type conversion after 1 year. Muscle fiber atrophy was observed in both muscles. Type 2 fiber atrophy occurred to about the same extent in both muscles. Atrophy was most severe for the soleus type 1 fibers (50% decrease in size). Calculations based on the fiber type and size changes observed indicate that the percentage of the muscle cross-sectional area occupied by each fiber type was almost the same for both muscles 1 year after transection. Discriminant analysis of the data indicated that the percentage of type 2 fibers present in the muscle was the best discriminator between the various groups. These morphometric data provided a basis for understanding the contractile results presented in the previous study as well as insights into the mechanism of transformation in skeletal muscle. Furthermore, inherent differences between type 1 and type 2 fibers were demonstrated between predominantly slow and predominantly fast muscles. Thus, after almost one-half a lifetime of transection, rat muscles are almost completely transformed to fast muscle, and, regardless of initial conditions, have nearly identical properties.

Adenosine Triphosphatases↗
PubMed1986

Corticospinal neurons 25 weeks after right hind limb amputation.

Neuronal cell death in embryos and adult animals is seen after removal of target tissue. Transsynaptic cell death has been described in the mammalian visual system and suggested as a possible mechanism for loss of upper motor neurons in amyotrophic lateral sclerosis. We previously demonstrated that amputation of a hind limb decreased the number of motor neurons in the rat spinal cord. Careful counts of corticospinal neurons in these rats 25 weeks after amputation failed to demonstrate any loss of corticospinal neurons. Although amputation caused a loss of ventral horn neurons, no subsequent loss of upper motor neurons was detected at 25 weeks.

Amputation, Surgical↗
PubMed1985

Labeled corticospinal neurons one year after spinal cord transection.

One year after a T9 spinal cord transection, horseradish peroxidase was inserted into the spinal cord at T3-T4. Only about 7% of the number of corticospinal neurons labeled in control rats were labeled in exactly matched transected rats. This long-term loss of labeled neurons makes cell death the most likely explanation for the failure to identify corticospinal neurons in spinal-cord-transected rats.

Animals↗
PubMed1985

Basal lamina at the site of spinal cord injury in normal, immunotolerant and immunosuppressed rats.

The cut ends of a rat spinal cord are capped with basal lamina (BL) within 20 days. This BL may block regenerating axons. BL at the transection site in rats made immunologically unresponsive to central nervous system antigens is not significantly different from that of control rats, but rats treated with cyclophosphamide show a less complete BL cap during the first 25 days. This may account for the increased axonal regeneration found in cyclophosphamide-treated rats.

Animals↗
PubMed1985

Cell death in the adult rat dorsal root ganglion after hind limb amputation, spinal cord transection, or both operations.

Cell death of embryonic neurons which are unable to attain a proper target is well established. A delayed cell death of adult neurons permanently separated from their target tissue has been demonstrated for several cell groups. Cells of the dorsal root ganglia (DRG) are unique in that a single T-shape neurite has a peripheral branch which extends (for root L5) to the hind limb and a central branch extending into the spinal cord. We found a significant loss of L5 DRG neurons 25 weeks after hind limb amputation. This finding is consistent with the hypothesis that neuron survival is dependent on connection with a suitable target. We were unable to detect cell death in the DRG of L5 after complete spinal cord transection at T9. Separation of DRG cells from their central target is unimportant to neuronal survival.

Amputation, Surgical↗
PubMed1985

Cell death in Clarke's column after spinal cord transection.

The death of embryonic central nervous system (CNS) neurons deprived of a target is well established. In adult rats, similar cell death of corticospinal and rubrospinal motor neurons occurs as a delayed response to spinal cord transection. We document the loss of neurons in Clarke's column, secondary ascending spinocerebellar neurons in adult rats, after complete spinal cord transection at T-9. Twenty-five weeks after spinal cord transection, horseradish peroxidase (HRP) studies showed a dramatic loss of labeled cells in rats with transected spinal cords as compared to matched control rats. Cresyl echt violet-stained sections failed to support the hypothesis that unlabeled cells persist in a shrunken, inactive state; instead we found far fewer identifiable neurons in Clarke's column. Although we saw little gliosis in the area of cell loss, gliosis was evident in the adjacent corticospinal tract which was severed in the original surgical injury. Amputation of the right hind limb resulted in a paradoxical increase in labeled Clarke's column cells on the right. Total cells stained with cresyl echt violet in amputated animals were not different from right to left. The increase in labeled cells on the amputated side may have been caused by an increase in metabolic activity of these deafferentated neurons which resulted in more effective axoplasmic transport of the HRP label.

Animals↗
PubMed1984

Basal lamina at the site of spinal cord transection in the rat: an ultrastructural study.

This electron microscopic study confirms that basal lamina (BL) begins to cap the cut end of the spinal cord 15 days after spinal cord transection. BL is first seen immediately adjacent to reactive glial cells but only when there is collagen in the nearby interstitial space. This finding suggests that collagen may provide a trigger to initiate the production of BL by reactive glia. We found no direct evidence that BL in this injury area impeded the outgrowth of regenerating neurites.

Animals↗
PubMed1984

The orthograde flow of tritiated proline in corticospinal neurons at various ages and after spinal cord injury.

The amount of radioactive proline which reaches the cervical cord by axoplasmic flow after intracortical injection of label is higher in rapidly growing 3 to 6 week old rats but becomes relatively constant in unoperated control rats beyond age 10 weeks. In adult rats with spinal cord transection at T-8, however, the amount of tritiated proline detected in the cervical cord above the site of transection is markedly increased five weeks after surgery, falls to more normal levels by 14 weeks after surgery, and is significantly below normal at 25 weeks after surgery. These findings are consistent with abortive attempts to regenerate axons at five weeks after injury. Twenty-five weeks after injury neuronal death and loss of both cells and axons which would normally project to the caudal cord through the site of spinal cord transection result in a decrease in the axon label found in the cervical region. Recognition of this variability in the amount of radioactivity that reaches the cervical region after spinal cord injury forced a reconsideration of previously reported evidence for regeneration in spinal cord transected animals receiving no specific postoperative therapy. There is no evidence for regeneration in such untreated transected rats.

Animals↗