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D J Stelzner

Publications and source records attributed to D J Stelzner.

At least 19 recordsLinked to original sources
PubMed1996

Attempts to facilitate dorsal column axonal regeneration in a neonatal spinal environment.

The response to injury of ascending collaterals of dorsal root axons within the dorsal column (DC) was studied after neonatal spinal overhemisection (OH) made at different levels of the spinal cord. The transganglionic tracer, cholera toxin conjugated to horseradish peroxidase, and the anterograde tracer, biotinylated dextran amine, were used to label dorsal root ganglion cells with peripheral axons contributing to the sciatic nerve. There was no indication of a regenerative attempt by DC axons at acute survival times (3 days and later) after cervical injury, replicating previous work done at chronic survival periods (Lahr and Stelzner [1990] J. Comp. Neurol. 293:377-398). There was also no evidence of DC regeneration after lumbar OH injury even though immunohistochemical studies using the oligodendrocyte markers Rip and myelin basic protein showed few oligodendrocytes in the gracile fasciculus at lumbar levels at birth. Therefore, the lack of myelin in the dorsal funiculus at lumbar levels does not enhance the growth of neonatally axotomized DC axons. In addition, DC axons did not regenerate when presented with fetal spinal tissue implanted into thoracic OH lesions, even though positive control experiments showed that segmental dorsal root axons containing calcition gene-related peptide and corticospinal axons grew into these implants, replicating previous work of others. When a thoracic OH lesion, with or without a fetal spinal implant, was combined with sciatic nerve injury to attempt to stimulate an intracellular regenerative response of DRG neurons, again, no evidence of DC axonal regeneration was detected. Quantitative studies of the L4 and L5 dorsal root ganglia (DRG) showed that OH injury did not result in DRG neuronal loss. However, sciatic nerve injury did result in significant post-axotomy retrograde cell loss of DRG neurons, even in groups receiving thoracic embryonic spinal implants, and is one explanation for the minimal effect of sciatic nerve injury on DC regeneration. Although fetal tissue did not appear to rescue a significant number of DRG neurons, the quantitative analysis showed an enlargement of the largest class of DRG neuron, the class that contributes to the DC projection, in all groups receiving fetal tissue implants. This apparent trophic effect did not affect DC regeneration or neuronal survival after peripheral axotomy. Further studies are needed to determine why DC axons do not regenerate in a neonatal spinal environment or within fetal tissue implants, especially because previous work by others in both the developing and adult spinal cord shows that dorsal root axons will grow within the same type of fetal spinal implant.

Animals↗
PubMed1995

NMDA antagonism during development extends sparing of hindlimb function to older spinally transected rats.

Hindlimb weight support and bipedal stepping occur after spinal cord transection in neonatal rats (birth to 12 days of age) while the same lesion in 15-day and older animals results in permanent loss of these responses. Some compensatory change in lumbar spinal circuitry must occur after spinal transection in young animals subserving these hindlimb behaviors. In contrast, animals just a few days older are incapable of such compensatory responses. We have examined the hypothesis that neural activity leads to the postnatal loss of plasticity in spinal circuitry. We find that antagonism of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor with MK-801 in young animals extends the sparing of hindlimb function after spinal transection to older animals. This effect is not due to a non-specific depression of all exciatory drive to motor neurons since Ia to motor neurons synaptic transmission through non-NMDA receptors is preserved during MK-801 treatment. Acute administration of MK-801 at the time of spinal transection or chronic administration of MK-801 after postnatal day 17 has no effect on recovery of hindlimb function after spinal transection. These results highlight the importance of NMDA receptor activation in spinal circuit maturation.

Aging↗
PubMed1993

Corticospinal tract plasticity and astroglial reactivity after cervical spinal injury in the postnatal rat.

We have investigated corticospinal (CS) axon growth around cervical spinal injury in the neonatal rat and related this growth to the astroglial reaction occurring at the lesion site. Rats received a high cervical overhemisection (left dorsal funiculotomy, right spinal hemisection) and a right cortical ablation on Postnatal Days (PNDs) 0, 3, 6, 12, and 21 to 24 (weanlings). In chronic operates the remaining CS projection from the left sensorimotor cortex was then assayed using wheat germ agglutinin-horseradish peroxidase as an anterograde tracer. In other operates the formation of the astroglial scar at the spinal lesion site was studied using a monoclonal antibody to glial fibrillary acidic protein. In PNDs 0-6 operates labeled axons extend through the intact left hemicord to bypass the lesion. The labeled axons travel to the edge of the lesion, cross the midline, and pass lateral to the lesion within the dorsal and intermediate gray and dorsal lateral white matter. Axons project bilaterally to normal areas of CS termination in PND 0 operates for a distance of 2.5 to 4 spinal segments caudal to the lesion which decreases to 1.5 to 2 segments in PND 6 operates. In PND 12 and weanling operates labeled fibers do not grow around the lesion but instead are retracted rostrally. There is an astrocytic reaction to injury at all ages by 3 days postoperatively (p.o.) that becomes greater with age and p.o. survival time. A more complicated cystic scar forms in 6-day and older operates. These data show that there is an age-related change in the ability of CS axons to grow around spinal injury which ends near the time CS elongation and gliogenesis is complete in the spinal cord.

Aging↗
PubMed1993

Extension and regeneration of corticospinal axons after early spinal injury and the maintenance of corticospinal topography.

It has been established that neonatal corticospinal (CS) axons are able to grow around lesions of the spinal cord early in neonacy (Bernstein and Stelzner, J. Comp. Neurol. 221:382-400; Firkins, Bates, and Stelzner, Exp. Neurol., 120:1-15). To determine if these corticospinal axons include regenerating as well as late developing axons a double-labeling paradigm is used in which CS neurons are retrogradely labeled from the cervical spinal cord by injections of fast blue (FB) on Postnatal Day (PND) 2, 4, or 10. Two days later, the FB is aspirated along with the left dorsal funiculus and the right hemicord (CHR). As adults, the animals receive an injection of diamidino yellow (DY) or rhodamine into the spinal cord caudal to the lesion site. Thus, FB neurons are those that originally projected to the spinal cord before the lesion and which survived axotomy, DY neurons are those whose axons reached the spinal cord after the lesion, and double-labeled neurons (FB/DY) are cells which projected to the spinal cord prior to the lesion and regenerated a spinal axon postlesion. Animals FB injected on PND 2 have a widespread distribution of FB-labeled neurons in cortex, including areas outside of sensorimotor cortex. These animals also had both DY- and FB/DY-labeled cells within sensorimotor cortex, indicating that the population of axons growing caudal to neonatal spinal lesions consists of both late growing and regenerating axons. In animals FB injected on PND 10, the FB neurons were all located in sensorimotor cortex. Very few DY and no FB/DY neurons were present. We have also looked at the topography of the CS neurons which project caudal to early spinal lesions. Rat pups received a CHR on PND 0, 3, 6, or 12. As adults, horseradish peroxidase was injected into the cervical or lumbar enlargement of the spinal cord and the distribution of labeled cells in the cerebral cortex was plotted and compared to normal and lesioned adult controls. In all experimental animals, the distribution of retrogradely labeled cells was restricted to the area containing CS projection neurons in the normal animal. This is despite the fact that the number of CS projection neurons is greatly reduced from normal and the normal pathway for CS axonal outgrowth has been completely disrupted by the neonatal lesion.

Amidines↗
PubMed1991

Do propriospinal projections contribute to hindlimb recovery when all long tracts are cut in neonatal or weanling rats?

Lateral hemisection lesions separated by 1 to 3 spinal segments were made on opposite sides of the mithoracic spinal cord in 1-month-old (N = 15; weanling operates) and newborn albino rats (N = 16; neonatal operates). Hindlimb behavior was assessed between 1 and 6 months p.o. for both groups of operates using a protocol and rating system that have previously proved effective in differentiating behavioral recovery of the hindlimbs as a function of age of spinal transection. In addition, at the conclusion of behavioral testing, operates received spinal injections of [3H]proline and HRP caudal to the spinal lesions to determine if lesions were complete and if neurons within the region between the two lesions (interlesion zone) projected into the caudal spinal cord. In both groups of operates, neurons were retrogradely labeled within the interlesion zone bilaterally, primarily in laminae VII-VIII. When both lesions were complete lateral hemisections in weanling operates, little behavioral recovery was observed, similar to complete spinal cord transection (N = 3). However, much greater behavioral recovery was seen, including supporting reactions and locomotor responses, when one or both lesions spared axons along the ventrolateral rim of the white matter. Neurons were retrogradely labeled in the brain stem reticular formation (N = 12) in these cases. All lesions were complete lateral hemisections in neonatal operates but much greater behavioral recovery was seen than in weanling operates with the same lesions, including supporting, placing, and locomotor responses. In an additional group of eight neonatal operates, the spinal cord rostral to the spinal hemisections was transected at 1 month of age. Supportive, placing, and locomotor responses were seen immediately after recovery from anesthesia and responses returned to pretransection levels in six of eight operates over the 10-day survival period. Fink-Heimer impregnation showed that degeneration argyrophilia from the transection bilaterally filled the interlesion zone but little argyrophilia was seen caudal to this region. Our results indicate that an intact propriospinal circuit remains in both neonatal and weanling operates but does not appear to contribute to hindlimb response development or recovery. The greater behavioral recovery in neonatal operates appears due to intrinsic connections (doral root, interneuronal) continuing to be able to drive the spinal circuitry underlying the spared behaviors.

Aging↗
PubMed1991

Frog tectal efferent axons fail to regenerate within the CNS but grow within peripheral nerve implants.

Tectal efferent axons, located adjacent to the optic tract, fail to regenerate past diencephalic lesions in Rana pipiens even though optic axons regenerate after the same injury (M. J. Lyon and D. J. Stelzner, J. Comp. Neurol. 255: 511-525). We tested the possibility that tectal efferent axons can regenerate within peripheral nerve implants. A 6- to 8-mm segment of autologous sciatic nerve was implanted into the anterolateral (N = 23) or centrolateral (N = 22) portion of the dorsal surface of the tectum. Frogs survived for 6 (N = 16) or 12 weeks (N = 29) before the free end of the nerve was recut and HRP applied. A control group had the nerve crushed prior to the HRP application. Neurons within the tectum, near and medial to the implant site, were retrogradely labeled from the nerve graft in most experimental operates but no neurons were labeled in controls. In addition, neurons were also labeled in nuclei which projected to the tectum in a number of cases. Three times as many neurons were labeled in 12-week operates (42 +/- 46) as in 6-week operates (15 +/- 12). The morphology and location of labeled neurons in the tectum was similar to tectal efferent neurons except that the somal area of neurons labeled from the graft was significantly larger (41%) than normal tectal efferent neurons. The basic finding is similar to experiments using the same paradigm in the mammalian central nervous system (CNS). One difference is the minimal glial reaction at the graft insertion site.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Anatomical studies of dorsal column axons and dorsal root ganglion cells after spinal cord injury in the newborn rat.

The response of dorsal column axons was studied after neonatal spinal overhemisection injury (right hemicord and left doral funiculus). Rat pups (N = 11) received this spinal lesion at the C2 level within 30 hours after birth. The cauda equina was exposed 3 months later in one group of chronic operates (N = 5) and in a group of normal adults (N = 2), and all spinal roots from L5 caudally were cut bilaterally; 4 days later the spinal cord and medulla were processed for Fink-Heimer impregnation of degenerating axons and terminals. In a second group of chronic operates (N = 6) and normal adult controls (N = 4) the left sciatic nerve was injected with a cholera toxin-HRP conjugate (C-HRP), followed by a 2-3 day transganglionic transport period, and then the spinal cord and medulla were processed with tetramethylbenzidine histochemistry. Both control groups have a consistent dense projection in topographically adjacent regions of the dorsal funiculus and gracile nucleus. However, there is no sign of axonal growth around the lesion in either group of chronic experimental operates. Instead, there is a decreased density of projection within the dorsal funiculus near the lesion site. Many remaining C-HRP labeled axons in the experimental operates have abnormal, thick varicosities and swollen axonal endings (5-10 microns x 10-30 microns) within the dorsal funiculus through several spinal segments caudal to the lesion. Ultrastructural analysis of the dorsal funiculus in three other chronic experimental operates reveals the presence of numerous vesicle filled axonal profiles and reactive endings which appear similar to the C-HRP labeled structures. Transganglionic labeling after C-HRP sciatic nerve injections (N = 4) and retrograde labeling of L4, L5 dorsal root ganglion neurons after fast blue injections of the gracile nucleus (N = 6) both suggest that all dorsal column axons project to the gracile nucleus in the newborn rat. Dorsal root ganglion (DRG) cell survival following the neonatal overhemisection injury was also examined in the L4 and L5 DRG. DRG neurons that project to the gracile nucleus were prelabeled by injecting fast blue into this nucleus at birth two days prior to the cervical overhemisection spinal injury. Both normal littermates (N = 9) and spinally injured animals (N = 12) were examined after postinjection survival periods of 10 or 22 days.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Laminin distribution during corticospinal tract development and after spinal cord injury.

The glycoprotein laminin is a prominent constituent of basal laminae and has been suggested to play an important role in axonal growth. We have tested this hypothesis, by examining the temporal and spatial distribution of laminin in the rat spinal cord, relative to elongating corticospinal tract (CST) axons, during normal development and after newborn and adult spinal lesions. The distribution of laminin was demonstrated in spinal cord sections from animals ranging in age from 14 days embryonic to adult using immunocytochemistry. Anti-laminin immunolabeling was seen around blood vessels and meninges in all the animals examined. However, within the grey and white matter its distribution was age-dependent. In the normal cord, immunostaining appeared in small amounts in early embryos, but was absent from all postnatal animals even at ages when the CST was growing down the cord. Following injury, intense immunostaining was associated with lesions in both newborn and adult operates at all postoperative periods examined. Within the matrix of the lesion laminin immunostaining was especially prominent. In the intact cord it was prominent only around blood vessels near the lesion site. Our results indicate that the distribution of laminin does not closely correlate with axonal growth of the CST either during normal development or after spinal injury.

Animals↗
PubMed1988

Effect of spinal cord transection in the newborn, weanling, and adult rat on the morphology of thoracic motoneurons.

The midthoracic spinal cord was transected in neonatal (N = 12), weanling (N = 9), and adult (N = 9) rats and sections were prepared at various postoperative survival periods (2 to 106 days p.o.) using a modified Golgi-Cox stain. The morphology of large lamina IX "motoneurons" was examined 0 to 5 mm rostral to the lesion border and compared with the morphology of similar cells from this region in developing and adult rats. Motoneurons examined in neonatal operates underwent the same temporal sequence of morphologic changes seen during normal development. Motoneurons in weanling operates underwent rapid morphologic changes which were most marked at the earliest period studied (2 days p.o.). These changes included a decrease in perikaryal diameter, dendritic loss, and the appearance of perikaryal and dendritic spines and varicose swellings. At the longest p.o. survival period analyzed (60 days p.o.), neurons had partially recovered but still retained somatic and dendritic spines and a reduced dendritic arbor. Motoneurons stained in adult operates showed no morphologic changes at 15 days p.o. but by 90 days p.o. somatic and dentritic spines were apparent, more similar to the morphology normally seen in the early postnatal period. We interpret these data to indicate that motoneurons surviving spinal transection are relatively unaffected by this lesion during the synaptogenic period and most severely affected when denervated near the end of this time. The more gradual appearance of regressive morphologic changes seen in adult motoneurons may indicate the continued partial denervation of these cells.

Animals↗
PubMed1988

Increase in ganglion cell size after optic nerve regeneration in the frog, Rana pipiens.

Even though optic regeneration is successful in the frog, Rana pipiens, at completion considerable ganglion cell loss has occurred. To determine whether ganglion cell loss affects the size of the remaining ganglion cells, these cells were back-filled with horseradish peroxidase. The size of one class of ganglion cell 6 months to 1 year following nerve crush injury (N = 4) was compared to that of normal cells of this class (N = 4). The average area of the perikaryon was 35% larger than normal (less than 0.01). This change is interpreted to reflect the increased metabolic needs of the neuron required to maintain a larger than normal axonal arbor.

Animals↗
PubMed1987

Tests of the regenerative capacity of tectal efferent axons in the frog, Rana pipiens.

Experiments were designed to determine if neurons of the ranid optic tectum, a major target of the optic nerve, possess the same regenerative potential as optic axons. Normal tectal efferent (TE) projections were reexamined by using the anterograde transport of 3H-proline and autoradiography (n = 18), bulk-filling damaged TE axons with horseradish peroxidase (HRP; n = 18) and anterogradely transporting wheat germ agglutinin-HRP (n = 8) to label TE axons. Results were similar to reports that used degeneration methods (Rubinson: Brain Behav. Evol. 1:529-561, '68; Lazar: Acta. Biol. Hung. 20:171-183, '69). Following a brainstem hemisection just caudal to the nucleus isthmi (1-20 weeks), the ipsilateral descending TE pathway was autoradiographically examined (n = 20). While all other TE projections appeared normal, there was no detectable ipsilateral descending projection beyond the lesion site. Ascending TE axons were cut at the anterior tectal border by hemisecting the left diencephalon (LDH)--a lesion that also cuts optic axons projecting to the left tectum. There was no indication of TE axonal regeneration with the aid of autoradiography or HRP histochemistry 1-30 weeks postlesion (n = 48) even when the medial diencephalon was intentionally left intact (n = 4). However, in all four cases examined, optic axons regenerated following the same LDH where TE axonal regeneration failed (also see Stelzner, Lyon, and Strauss: Anat. Rec. 205:191A-192A, '83). Local effects of LDH should be similar for both the cut optic and cut TE axons. Other factors were tested that may contribute to the lack of TE axonal regeneration. Our results indicate that optic regeneration itself (n = 8), postaxotomy retrograde cell death of TE neurons (n = 6), deafferentation of the tectum of optic axons, and potential sprouting within tectal targets by intact contralateral TE axons (n = 10) are not critical factors aborting TE axonal regeneration. TE axons filled with HRP at chronic periods after LDH (n = 4) terminate anomalously near the LDH border. Many of these endings are similar to reactive endings or terminal clubs seen after axonal injury in the mammalian CNS. Our results suggest that this disparity in regenerative ability of optic and TE axons may be related to a difference in the responsive ability of these cell types to initiate or maintain axonal elongation after axotomy within the amphibian CNS environment.

Afferent Pathways↗
PubMed1986

A quantitative analysis of frog optic nerve regeneration: is retrograde ganglion cell death or collateral axonal loss related to selective reinnervation?

The present study was designed to assess whether axon collateral formation and loss or retrograde cell death contribute to selective reinnervation during optic nerve regeneration in the frog, Rana pipiens. The right optic nerve was crushed in 18 frogs, and samples were taken near the optic disc (retinal segment) and near the optic chiasm (brain segment). These samples were studied quantitatively with the electron microscope at various postoperative survival times (1, 2, 3, 4, 6, 12 weeks, 6 months, 1 year; N = 2). The number and size of axons in each segment were estimated from a series of electron micrographs taken at intervals across the transverse extent of each nerve and compared with normal nerves (N = 4). Results show that there are 5.3 +/- 1.8 X 10(5) (S.D.) unmyelinated and 2.3 +/- .5 X 10(4) myelinated axons in the normal nerve. One week post-crush (p.c.) there is a 27% decrease in the number of axons in the retinal segment (4.1 +/- 1.4 X 10(5)), indicating early retrograde axonal loss. As expected, there is a greater loss of axons at this time in the brain segment (3.0 +/- 1.3 X 10(5)). Between 2 and 6 weeks p.c. the number of axons increases in the retinal segment to over twice the normal number of axons increases in the retinal segment to over twice the normal number (12.3 +/- 3.8 X 10(5)) and to over four times this number in the brain segment (20.0 +/- 3.0 X 10(5)), showing collateral axon formation results from this injury. A large loss in the number of axons occurs in both nerve segments between 6 and 12 weeks p.c. (4.3 +/- 1.5 X 10(5)) and an additional loss at 20 weeks p.c. (2.2 +/- .98 X 10(5)). Subsequently, the number remains constant, approximately 40% of normal. Visual recovery was seen in the two frogs tested one year after optic nerve crush that were used for optic axon counts. Autoradiography in these same animals showed the optic nerve projections normally seen after regeneration. Besides axonal loss, our results also indicate that the size of both myelinated and unmyelinated axons is significantly above normal at chronic postoperative periods. This increase in axonal size is interpreted to be related to the increased territory each remaining optic axon must fill to restore the optic projections.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Regeneration of the frog optic nerve. Comparisons with development.

Developing and regenerating frog optic axons grow within optic pathways and form connections only with optic targets. However, unlike normal development, many regenerating optic axons in the adult frog are misrouted within optic pathways, including axons that grow into the opposite retina. Many of the axons misrouted during regeneration appear to be collaterals of axons that grow in normal directions. Ganglion cell loss of up to 60% occurs after optic nerve damage, beginning prior to reinnervation of optic targets. Massive axonal collateralization also takes place near the point of nerve damage, causing the normal order found within the nerve to be lost. Collaterals are eliminated as selective reinnervation is completed, and the smaller complement of optic cell axons remaining after regeneration form an expanded projection within optic targets. Evidence is reviewed that suggests that factors involved in axonal guidance and target recognition during development remain intact in the adult frog brain. Additional conditions resulting from nerve injury causes axonal guidance to be less successful during regeneration.

Animals↗
PubMed1986

Ascending tract neurons survive spinal cord transection in the neonatal rat.

Retrograde axonal transport was used to determine which ascending nerve tracts from the lumbosacral spinal cord are present in the cervical spinal cord of the newborn rat and if their cell bodies survive axotomy. A pledget of true blue was applied to a low cervical spinal transection in the newborn rat (N = 4). After a 5-day survival period, neurons were labeled in the laminae of origin of all ascending nerve tracts throughout the lumbosacral spinal cord. Neurons labeled in the same way survived for at least 1 month postoperatively when the spinal cord was transected at a midthoracic level at 5 days of age (N = 4). No neurons in the lumbosacral spinal cord were labeled if the midthoracic spinal cord was transected at the same time as application of the dye to cervical spinal cord (N = 2). Therefore, neurons labeled with true blue from cervical spinal cord during the neonatal period are likely to have been axotomized by thoracic injury made at 5 days of age. Three months after midthoracic spinal transection of newborn rats, HRP was injected or a pledget was applied to the first spinal segment caudal to this lesion (N = 8). The same population of neurons was labeled as in adult rats receiving application of HRP to an acute midthoracic spinal transection (N = 4). Neurons were seldom labeled in adult rats in which HRP was injected and ascending nerve tract axons not damaged (N = 4). These results suggest that most ascending nerve tract axons are present in cervical spinal cord during the neonatal period (by 4 to 5 days of age).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Prenatal and postnatal development of lamina IX neurons in the rat thoracic spinal cord.

The maturation of lamina IX neurons in the thoracic spinal cord of the rat was studied from day 13 of gestation until adulthood using a modified Golgi-Cox stain. The large multipolar neurons developed in an orderly and progressive manner. At day G-13, the round or stellate perikarya were smooth. Primary and secondary dendrites were adult in number with numerous irregular expansions and growth cones. Tertiary dendrites were beginning to form. Between day G-18 and postnatal day 5 the irregular surface of the perikarya and all portions of the dendrites had numerous long spines and filopodia. Growth cones were present at the end of terminal dendrites and also along the shafts of secondary and tertiary dendrites. By postnatal day 11 there was a decrease in the number of spines on the perikarya and proximal dendrites but spines remained prominent on secondary and tertiary dendrites. Between postnatal days 18 and 31 the adult morphology was attained. The perikarya and dendrites of adult neurons were devoid of spines except for occasional spines on the distal half of the dendritic tree. Elongated smooth varcosities were present except for the distal half of terminal dendrites where these expansions were more beaded. Although these morphologic changes were, in certain respects, the reciprocal of the regressive changes seen in these neurons after spinal hemisection in the adult rat (3), a major difference was the apparent absence of a "spiny stage" in the denervated lamina IX neurons of the adult.

Animals↗
PubMed1983

Plasticity of the corticospinal tract following midthoracic spinal injury in the postnatal rat.

Rats received a midthoracic spinal cord "overhemisection" including right hemicord and left dorsal funiculus at birth (neonatal operates, N = 15) or 21 days of age (weanling operates, N = 14). In a second experiment neonatal (N = 6), 6-day (N = 3), and 12-day (N = 7) rats sustained a right sensorimotor cortex (SmI) ablation to destroy the left corticospinal tract (CST) at the same time as the spinal injury (double lesion operates). Later (3-12 months) injections of 3H-proline and autoradiography were used to label the left or right CST. The results of the first experiment showed that most right CST axons failed to grow around the spinal lesion in neonatal operates (N = 9). There was an increase in the density of label, mainly to CST projection areas, in a 1-mm zone rostral to the lesion. However, left CST axons bypassed the lesion by growing through the intact tissue in neonatal operates (N = 6). These displaced axons were consistently located within the dorsal portion of the lateral funiculus (dLF) and remained within that location caudal to the lesion, an area normally containing only a few CST axons. In spite of this abnormal position, these axons terminated bilaterally throughout the remainder of the cord in normal CST sites. In weanling operates, CST axons severed by the lesion did not regenerate around the lesion site. An increased density of label over the few spared axons within the left dLF and in CST projection zones immediately caudal to the lesion site suggested axonal sprouting by these axons. The results of the second experiment showed that the lack of growth of right CST axons around this injury in neonatal operates was, at least partially, due to an interaction with left CST axons. In neonatal double lesion operates, right CST axons grew around the spinal injury for a varying distance within the left dLF and distributed bilaterally to normal CST sites. The number of right CST axons bypassing the lesion was related to the configuration of the lesion site. A smaller number of right CST axons bypassed the lesion in 6-day double lesion operates and most terminated within 2-3 mm of the lesion site. Right CST axons failed to grow around this injury in 12-day double lesion operates.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1981

Neocortical projections of the rat anterior commissure.

The posterior limb of the rat anterior commissure (ACp) was studied in order to better define a temporal cortex in this species. Two methods were used: (1) the anterior commissure (AC) was destroyed on one side of the midline, and the resulting anterograde degeneration was traced with the Fink-Heimer stain; and (2) the corpus callosum and hippocampal commissure were severed, but the AC was left intact. [3H]-Leucine and proline were injected into one hemisphere, and the transported label was traced into the contralateral hemisphere with autoradiography. ACp was found to project to the contralateral cortex along the rhinal sulcus. The pyriform cortex received a projection along the entire length of the sulcus. There was also a distinct projection to neocortex on the lateral surface above the rhinal sulcus which appears to be analogous to the temporal cortex projection of ACp in other species. This finding of a neocortical projection of the ACp in the rat is consistent with observations that have been made on other mammals.

Animals↗