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PubMed1986

The precision of pathway selection by developing peripheral axons in the axolotl.

At the time of hindlimb development in the axolotl there is a well-established but still developing trunk innervation. The trunk innervation is primarily composed of the segmental nerves, each of which consists of a dorsal and a ventral ramus and its branches. At a few segmental levels in the region of the hindlimb a large number of additional axons arise to innervate the limb. To reach the limb, they must grow via the ventral rather than the dorsal rami. The precision with which this pathway is selected was determined by counting axons in the dorsal and ventral rami at limb segmental levels, prior to and during the period of maximum axon proliferation. If outgrowth is highly directed rather than random, then the ratio of ventral/dorsal ramus axons should increase significantly during the period when large numbers of additional axons are produced. In addition, since the dorsal trunk varies little in size between limb segments and immediately caudal 'non-limb' segments, the number of axons in the dorsal rami can be compared at the two levels. Mistaken projections should result in inordinately large axon numbers in dorsal rami at limb compared to non-limb levels. The results show that there is approximately a tenfold increase in the ratio of ventral/dorsal ramus axons at the time of maximum outgrowth to the limb, thus the mode of distribution at the ventral-dorsal branch point is significantly altered in favour of growth toward the limb, and outgrowth appears to be highly directed rather than random. Moreover at this time there is no discernible increase in the number of dorsal ramus axons at limb levels while those at non-limb levels increase fourfold. The apparent growth of all axons into the ventral ramus suggests the presence of a strong, non-specific attraction.

Ambystoma mexicanum↗
PubMed1986

Determinants of directional specificity in the regeneration of lamprey spinal axons.

The projection patterns of regenerating spinal axons in the larval sea lamprey (Petromyzon marinus) were determined by intracellular injection of HRP. Four hundred and eighty-six of 562 stained axons and axon-like neurites (87%) arising from Muller and Mauthner axons, giant interneurons, and dorsal cells terminated in an orientation similar to that of their counterpart control cells. Therefore, lamprey spinal axons regenerate selectively along their normal projection paths. During the first 4 weeks of recovery, i.e., before any had regenerated beyond the transection site, 91 of 114 axons and long neurites (80%) projected in the proper direction. Thus, the correctness of the final projection patterns did not result from selective retraction of randomly directed long neurites. When the cords were doubly transected 1 cm apart, orientation of regenerating neurites remained normal both within the 1 cm island and in the adjacent spinal cord. This suggests that the directional specificity of axonal regeneration was determined neither by the location of the scar nor by the availability of channels formed by the degenerating fibers. Finally, removing 1 cm of spinal cord eliminated potential synaptic targets for regenerating axons on either side of the lesion, but did not affect the direction of axonal growth. These findings are consistent with the hypothesis that the regeneration of lamprey spinal axons is guided by local chemical cues that persist long after the pathways are formed early in development.

Animals↗
PubMed1986

Pathways of regenerated retinotectal axons in goldfish. I. Optic nerve, tract and tectal fascicle layer.

This study investigates the order of regenerating retinal axons in the goldfish. The spatiotemporal pattern of axon regrowth was assessed by applying horseradish peroxidase (HRP) to regenerating axons in the optic tract at various times after optic nerve section and by analysing the distribution of retrogradely labelled ganglion cells in retina. At all regeneration stages labelled ganglion cells were widely distributed over the retina. There was no hint that axons from central (older) ganglion cells might regrow earlier, and peripheral (younger) ganglion cells later, as occurs in normal development. The absence of an age-related ordering in the regenerated optic nerve was demonstrated by labelling a few axon bundles intraorbitally with HRP (Easter, Rusoff & Kish, 1981) caudal to the previous cut. The retrogradely labelled cells in retina were randomly distributed in regenerates and not clustered in annuli as in normals. Tracing regenerating axons which were stained anterogradely from intraretinal HRP applications or retrogradely from single labelled tectal fascicles illustrated the fact that the regenerating axons coursed in abnormal routes in the optic nerve and tract. On the surface of the tectum regenerated fibres re-established a fascicle fan. The retinal origin of tectal fascicles was assessed by labelling individual peripheral, intermediate and rostral fascicles with HRP. The retrogradely labelled ganglion cells in the retina were often more widely distributed than in normals, but were mostly found in peripheral, intermediate and central retina, respectively. The order of fibre departure from each tectal fascicle was revealed by placing HRP either on the fascicle's proximal or on its distal half. With proximal labelling sites labelled ganglion cells were found in the temporal and nasal retina, and with distal labelling sites labelled ganglion cells were confined to nasal retina only. Further, the axonal trajectories of anterogradely labelled dorsotemporal retinal ganglion cells were compared to those of dorsonasal retinal ganglion cells in tectal whole mounts. Dorsotemporal axons were confined to the rostral tectal half, whereas dorsonasal axons followed fascicular routes into the fascicle's distal end and reached into caudal tectum. This suggests that the fibres exited along their fascicle's course in a temporonasal sequence. Thus in the tectum, fibres in fascicles restore a gross spatial and age-related order and tend to follow their normal temporonasal sequence of exit.

Animals↗
PubMed1979

Organophosphorous neuropathy. I. A teased-fiber study of the spatio-temporal spread of axonal degeneraion.

The spatio-temporal spread of axonal degeneration in organophosphorous neuropathy has been studied by means of the teased-fiber technique. Young adult cats were given a single intraperitoneal injection of di-isopropylfluorophosphate (DFP) and were killed 14, 18, 20, 21, and 28 days later by intracardiac perfusion with aldehydes. The cats developed clinical signs of delayed neurotoxicity 16 to 18 days after DFP injection. A histologic survey of the central and peripheral nervous systems revealed that the topographic distribution of axonal degeneration was characteristic of a dying-back neuropathy. In teased-fiber preparations from the left recurrent laryngeal nerve, we found that the axonal degeneration was initially focal and nonterminal but that the axonal degeneration subsequently spread in a somatofugal direction to involve the entire distal axon. Nerve fibre varicosities and paranodal demyelination preceded the axonal degeneration. It is concluded that neurotoxic organophosphates induce a focal, distal but not terminal axonal degeneration. This "chemical transection" of the axon then precipitates wallerian degeneration of the more distal axon. Thus, the traditional hypothesis that dying-back neuropathies evolve from a retrograde axonal degeneration is not valid for organophosphorous neuropathy.

Animals↗
PubMed1981

Development of a sensory afferent projection in the grasshopper embryo. I. Growth of peripheral pioneer axons within the central nervous system.

The grasshopper's cercal nerve is established early in embryogenesis by an identified pair of peripheral neurons called the cercal pioneers. Like the peripheral pioneer neurons in other insect appendages, these two cells send their axons from the periphery to the rudimentary CNS and thus lay the foundation for a nerve that will later be followed by a large number of sensory axons. In this paper, cobalt fills of the primordial cercal nerve were used to characterize the disposition of these peripheral pioneer axons within the embryonic CNS. The pioneer axons stained by this technique terminate in ellipsoidal growth cones which have filopodia radiating from the leading edge and a single long terminal filament pointing along the path the axon is taking. The growing axons also bear filopodia along their sides, but these structures disappear as the cells mature. The pioneer axons of the cercal nerve make an abrupt turn where they first enter the ganglion rudiment and join the axons of the primary longitudinal tract. The pioneers then grow along this tract for several hundred microns without forming secondary growth cones or branches. This prolonged absence of central arborization distinguishes the peripheral pioneer axons from the axons of later-arising epidermal sensory neurons.

Animals↗
PubMed1983

Sprouting and regeneration of sensory axons after destruction of ensheathing glial cells in the leech central nervous system.

To test the importance of glia during regeneration of mechanosensory neuron axons in the leech central nervous system, individual glial cells that ensheathed the axons were destroyed by intracellular protease injection. Recordings with intracellular microelectrodes showed that glial-desheathed axons re-established synaptic connections with their appropriate target cell, a motor neuron, as frequently and as selectively as control, glial-ensheathed axons. Intracellular staining with horseradish peroxidase showed that desheathed regenerating axons sprouted more than controls, and loss of the glial cell in some cases caused uninjured (intact) axons to sprout. Successful, accurate regeneration could occur whether axons grew along normal or along aberrant pathways. The distal stumps of some sensory axons severed from cell bodies and maintained in organ culture survived without their glial sheath for up to 3 weeks. These experiments show that, although loss of the glial cell affects sensory axon growth, the glial cell is not required for accurate axonal regeneration in the leech central nervous system.

Animals↗
PubMed1983

Regeneration of an identified central neuron in the cricket. I. Control of sprouting from soma, dendrites, and axon.

When the axon of the medial giant interneuron (MGI) of the cricket is axotomized close to the cell body, the normally stable, characteristic dendritic arborization is induced to sprout supernumerary neurites. The origin of the induced dendritic sprouts is not random; they emerge preferentially from the dentritic tips and branches close to the exit of the axon from the terminal ganglion. If any growth also occurred from the axon, there was a reciprocal relationship between the extent of dendritic and axonal sprouting. On the other hand, axotomy distant to the cell body induces sprouting only from the axon and does not alter the dendritic structure of the MGI. After crushing the ventral nerve cord distant to the cell body, the MGI sprouted neurites from the proximal axonal stump which crossed the site of lesion and continued growing within the distal cord. After a distant cut of the cord, however, the axonal neurites formed a neuroma in the proximal cord stump at the site of lesion and stopped elongating after 1 month. At this time, supernumerary sprouts first began to emerge from the normally smooth, rounded contours of the cell body. Based on these observations, we propose that axotomized neurons produce membrane at a constant rate. This newly synthesized membrane is preferentially inserted into neurites emerging from the proximal axonal stump. When axonal neurites stop growing in a neuroma following a distant cut, then this new membrane appears as supernumerary neurites from the soma. After a close cut, the axon often dies back into the ganglion and appears unable to receive the full complement of sprouting membrane. In such cases, the balance of the newly synthesized membrane is inserted into the dendrites and the characteristic structure of the arborization is significantly altered.

Animals↗
PubMed1982

4 S RNA in regenerating optic axons of goldfish.

Previous experiments have demonstrated that 4 S RNA is transported axonally during the reconnection period of optic nerve regeneration in goldfish. The present experiments were performed to determine whether 4 S RNA is transported axonally during later, maturational stages of nerve regeneration and to examine some of the characteristics of 4 S RNA in regenerating axons. [3H]Uridine was injected into both eyes of fish 18 days (near the time of reconnection) after bilateral optic nerve crush and the fish were sacrificed at various times up to 180 days after injection. [2H]RNA was isolated by phenol extraction and ethanol precipitation from 24 pooled tecta and fractionated by SDS-polyacrylamide tube gel electrophoresis. Data from these experiments showed that 70% of the [3H]RNA is present as 4 S RNA 12 days after injection, and 60 days after injection, this value is still approximately 50%. When nerves were cut 36 days after injection (54 days post-crush) and allowed to degenerate for 6 days before determining tectal [3H]RNA, the majority of the 4 S[3H]RNA was lost from the tectum. This indicates that up to 36 days after injection, 4 S [3H]RNA remains within regenerating axons and that it is unlikely that significant amounts of axonally transported 4 S RNA are transferred out of the axon to surrounding cells. In other experiments, the time of sacrifice after injection was held constant and the time of injection after nerve crush was varied. Analysis of tectal [3H]RNA showed that the major period of axonal transport of 4 S [3H]RNA was in early stages of regeneration at 24 and 36 days after nerve crush and that the amount of 4 S [3H]RNA which is transported axonally decreased at later time points. Calculations of the amount of axonal 4 S [3H]RNA versus what is synthesized in periaxonal cells gave results suggesting that 4 S RNA in regeneration axons turns over relatively slowly when compared with 4 S RNA in tectal cells.

Animals↗
PubMed1995

Presynaptic glutamate levels in tonic and phasic motor axons correlate with properties of synaptic release.

Synaptic glutamate release involves the accumulation of cytoplasmic glutamate in synaptic vesicles, whereafter it is released by triggered exocytosis. As glutamatergic terminals are known to be functionally diverse it was of interest to examine whether the presynaptic glutamate supply differs between individual axon terminals with distinct release properties. The glutamatergic terminals in the crustacean neuromuscular system system comprise a "phasic" type which shows fatigue of release during repetitive stimulation, and a "tonic" type which can maintain transmission for long periods. Quantitative immunogold analysis showed that the axons in a tonic nerve innervating slow muscles in the abdomen contained two times higher levels of glutamate labeling over axoplasmic matrix and over mitochondria, as compared to the corresponding elements in a phasic nerve. Similar results were obtained when adjacent phasic and tonic axons in a mixed nerve innervating leg muscles were compared. In the terminal regions of tonic and phasic axons the glutamate labeling differed correspondingly over axoplasmic matrix and mitochondria, while the synaptic vesicles showed a similar strong accumulation of labeling in both types of terminal. The level of labeling for glutamine, a glutamate precursor, was closely similar in phasic and tonic axons. The axoplasmic glutamate concentration was estimated to be in the low millimolar range, through comparison with coprocessed conjugates with known glutamate concentration. These results show that fatigue-resistant tonic axons and terminals contain higher levels of glutamate than fatiguable phasic axons, presumably representing an adaptation to the markedly different impulse activities in the two types of neuron. The axonal glutamate concentrations are in the range of the Km value for vesicular glutamate transport. Thus in tonic axons the high glutamate level appears to promote an efficient refilling of synaptic vesicles during sustained release, while in phasic axons the refilling should be slower which is compatible with an infrequent release.

Animals↗
PubMed1994

Axon-glia interactions regulate ECM patterning in the postnatal rat olfactory bulb.

It has been suggested that an inhibitory ECM containing chondroitin-6-sulfate proteoglycan (C-6S-PG) and tenascin (TN), which appears homogeneously in the core of the OB following afferent fiber arrival, helps position ingrowing olfactory axons in the prospective glomerular layer (GL) (Gonzalez and Silver, 1992; Gonzalez et al., 1993). Later, a similar ECM associated with astrocytes envelopes axonal glomeruli in rings, suggesting that axons may control the precise ECM patterning. The question remains whether formation of the matrix ring pattern around each axonal glomerulus is an intrinsic property of the matrix-producing cells or a response to developing axons. To determine if the organization of glial associated matrix in the OB was dependent on the presence of axons, we studied the effect of unilateral injection of a neurotoxin into the olfactory epithelium of postnatal rats. Using olfactory marker protein (OMP), beta-tubulin (TUJ1) antibodies, and Nissl staining, we found that at 5 and 10 d following neurotoxin administration the number of glomeruli decreased by an average of 77.0% in the injected side. At the same time, we observed that the TN/C-6S-PG rings and periglomerular cells were present only around the remaining small number of glomeruli. Elsewhere, ECM expression and the periglomerular cell configuration were more disorganized in the GL. The pattern of glial fibrillary acidic protein (GFAP) did not change significantly. We found that OMP staining, beta-tubulin immunoreactivity, and periglomerular cells reformed in a glomerular-like pattern as the olfactory axons reformed by 20 d. As the glomeruli-shaped collection of axon terminals reappeared, TN/C-6S-PG immunoreactivity also reoccurred in rings around the new axon bundles. Again, at this later stage, the expression of GFAP was similar in both sides. In our previous study (Gonzalez et al., 1993), we suggested that the initial gross positioning of glomeruli may be controlled by the overall positioning of TN/C-6S-PG. In the present study, we suggest that the formation of TN/C-6S-PG in the precise ring pattern around glomeruli appears to be dependent upon the presence of bundled olfactory axons. Various mechanisms are discussed that may explain the dynamic change in ECM expression that occurs inside the glomerulus after the neurotoxin treatment.

Animals↗
PubMed1995

Olfactory marker protein mRNA is found in axons of olfactory receptor neurons.

The separation between the cell bodies of olfactory receptor neurons in the nasal cavity and their axon terminals in the olfactory bulb make them attractive for studying axonal transport. Although high molecular weight RNAs are generally believed to be excluded from axons of mature neurons, we demonstrate here that mRNA for olfactory marker protein (OMP), an abundant cytoplasmic protein selectively expressed in mature receptor cells, is present in rodent olfactory receptor axons. OMP RNA was detected by in situ hybridization at the light microscope level in axons and in terminals. By nuclease protection, the level of OMP RNA in the olfactory bulb was 5-10% of that in the olfactory epithelium where the cell bodies reside. In contrast to axonally transported vasopressin and oxytocin mRNAs, which are deficient in their 3' polyA tails, axonal OMP RNA fractionated as polyA+. OMP RNA was lost from axons and terminals after deafferentation, suggesting that OMP RNA was synthesized in receptor cell bodies in the epithelium and was transported into axons and terminals in the olfactory bulb. RNA for G(olf), a G-protein highly expressed in dendrites of mature olfactory receptor neurons, was not detected in the olfactory bulb. We hypothesize that the immature nature of the cytoskeleton and, specifically, the lack of tightly bundled microtubules allows transport of particular mRNAs in olfactory receptor axons.

Afferent Pathways↗
PubMed1994

Extent and mechanism of sealing in transected giant axons of squid and earthworms.

Transected axons are often assumed to seal at their cut ends by the formation of continuous membrane barriers that allow for the restoration of function in the axonal stumps. We have used several electrophysiological measures (membrane potential, input resistance, injury current density) and several morphological measures (phase-contrast, video-enhanced differential interference contrast, light, and electron microscopies) of living and fixed material to assess the extent and mechanism of sealing within hours after transecting giant axons of squid (Loligo pealei and Sepioteuthis lessoniana) and earthworms (Lumbricus terrestris). Our electrophysiological data suggest that the proximal and distal ends of transected squid giant axons do not completely seal within 2.5 hr in physiological saline. In contrast, the same set of measures suggest that proximal and distal ends of transected earthworm giant axons seal within 1 hr in physiological saline. Our morphological data show that the cut ends of both squid and earthworm axons constrict, but that a 20-70-microns-diameter opening always remains at the cut end that is filled with vesicles. Axonal transection induces the formation of vesicles that are observed in the axoplasm within minutes in standard salines and that rapidly migrate to the cut ends. These injury-induced vesicles are loosely packed near the cut ends of squid giant axons, which do not functionally seal within 2.5 hr of transection. In contrast, vesicles formed a tightly packed plug at the cut ends of earthworm medial giant axons, which do functionally seal within 1 hr of transection in physiological saline. Since we detect no single continuous membrane that spans the cut end, sealing does not appear to occur by the fusion of constricted axolemmal membrane or the formation of a membranous partition at the cut end. Rather, our data are consistent with the hypothesis that a tightly packed vesicular plug is responsible for sealing of earthworm giant axons.

Animals↗
PubMed1994

T-cadherin expression delineates specific regions of the developing motor axon-hindlimb projection pathway.

T-cadherin is a unique member of the cadherin family anchored to the membrane by a glycosyl phosphatidylinositol moiety (Ranscht and Dours-Zimmermann, 1991). T-cadherin's distribution in the developing motor axon pathway was mapped by immunocytochemistry in the chick lumbosacral region as spinal neurons project to and innervate hindlimb muscle. On growing motor axons, T-cadherin was expressed biphasically. Initially, uniform T-cadherin expression occurred on motor neurons as they projected between the spinal cord and the base of the hindlimb (stage 21-24), and then decreased as the axons sorted to form dorsal, ventral and muscle nerve trunks (stage 25-27). Later, as motor axons entered and formed terminal axon arbors and synapses in muscle (stages 28-36), expression reoccurred heterogeneously among motor neuron pools. Thus, T-cadherin may guide the growth and fasciculation of all motor neurons during early axon extension, but only affect particular populations during the later expression period. In the mesenchyme of the motor axon pathway, T-cadherin was restricted to regions avoided by growing axons: the posterior-half sclerotome before and during the projection of motor axons through the T-cadherin-negative anterior half, and the extrasynaptic surfaces of developing muscle. The temporal and spatial expression patterns of T-cadherin and neurite outgrowth-promoting N-cadherin were complementary both in nerve and muscle tissues. Thus, in the posterior sclerotome and in maturing muscle, T-cadherin may act as a negative regulator that works in concert with neurite growth-promoting molecules to guide motor axons to their peripheral targets.

Animals↗
PubMed1994

Modulation of the axonal microtubule cytoskeleton by myelinating Schwann cells.

The Trembler PNS myelin-deficient mutant mouse offers a unique model for the study of axon-glial interactions. Previous work in our laboratory on Trembler mouse sciatic nerve established that myelinating Schwann cells exert a profound effect on the underlying neuronal cytoskeleton. Demyelinated axon segments exhibited decreases in the rate of slow axonal transport, axonal caliber, and neurofilament phosphorylation, as well as increases in neurofilament density. The present study considers effects on the microtubule cytoskeleton. At least two aspects of the microtubule cytoskeleton in Trembler PNS axons were altered by demyelination. First, the stability of the Trembler axonal microtubule cytoskeleton is decreased, as measured by decreased levels of insoluble tubulin (Sahenk and Brady, 1987). Second, the composition and phosphorylation of axonal microtubule-associated proteins, including tau, MAP 1A, and MAP 1B, are changed in Trembler demyelinated nerves. Further, the fraction of axonal tubulin moving at slow component b rates was increased (de Waegh and Brady 1990, 1991). These results provide further evidence that cell-cell interactions between myelinating glia and their underlying axons extend beyond a structural role, actively influencing biochemical and physiological properties of the axon.

Animals↗
PubMed1994

Long interfascicular axon growth from embryonic neurons transplanted into adult myelinated tracts.

In a previous study we used the species-specific marker M6 to demonstrate that transplanted mouse embryonic hippocampal neurons grow axons at a rate of at least 1 mm/d for a distance of at least 10 mm along the longitudinal axis of the fimbria in immunosuppressed adult rat hosts. We now show that hippocampal neurons are able to grow comparably long interfascicular axons in two other myelinated adult fiber tracts, the corpus callosum and the cingulum. Moreover, suspensions of cells from embryonic neocortex and superior colliculus transplanted into each of these three adult host sites also give interfascicular axon growth whose speed, intensity, and pattern of distribution are identical to those of transplanted hippocampal neurons. The axons of the donor cells grow in both directions along the longitudinal axis of the host tracts, where they are interspersed in parallel among the normal host axons, the rows of host interfascicular glial nuclei, and the longitudinal processes of host tract astrocytes. Serial section analysis through the complex trajectories of the host fiber bundles of the fimbria and corpus callosum shows that the course of the donor axons conforms to the underlying orientation of the axonal and glial structures of the host fiber tract. These observations indicate that long interfascicular axon growth can occur in several different adult myelinated fiber tracts. The donor axons become integrated with the host tract fibers and glia, and they respect intertract boundaries. Growth is not restricted to the types of axons normally present in the tracts.

Animals↗
PubMed1993

Occurrence and three-dimensional structure of multiple synapses between individual radiatum axons and their target pyramidal cells in hippocampal area CA1.

Recent physiological work has used quantal analysis to investigate the properties of synaptic transmission and long-term potentiation in hippocampal area CA1. These analyses have revealed changes in the strength of excitatory post-synaptic responses following long-term potentiation that could be mediated by cellular mechanisms in the presynaptic element, in the postsynaptic element, or in both elements. In these studies, either minimal stimulation, presumably involving a single presynaptic axon, or recordings from pairs of CA3 and CA1 cells have been used. Interpretation of these quantal analyses requires knowledge about whether single or multiple synapses occur between the presynaptic axon and its target CA1 pyramidal cells. Here, light and serial electron microscopy was used to begin to examine this question and a related question concerning the ultrastructure of spines on multiple-synapse boutons. Light microscopic analyses of Golgi preparations revealed that about 20% of the axons occurring in stratum radiatum come into close apposition with two to four different dendrites of a target CA1 cell. An "apposition" was defined as a point where the axons and dendrites crossed in the same focal plane and therefore were sufficiently close to allow a dendritic spine to reach the axon and possibly establish a synaptic contact. An additional 4% of the axons wound back and forth across individual dendrites, possibly forming multiple synapses closely spaced along the dendrites. Serial electron microscopy revealed that 24% of the individual axonal boutons in stratum radiatum make synapses with multiple dendritic spines arising from either the same or different dendritic segments. Two adjacent boutons of the same axon could also be found to synapse with different spines of the same dendrite. Together with the light microscopic analysis, these observations suggest that multiple synapses occur between single axons in stratum radiatum and their target CA1 cells, and that at least some of these synapses may occur at different electronic distances. If these multiple synapses have different physiological strengths, then they may obscure or smooth peaks in the frequency histograms that are used for quantal analyses. A three-dimensional analysis was done to compare the dimensions of pairs of dendritic spines synapsing with individual axonal boutons. When the pairs of spines associated with a single bouton arose from different dendrites, at least some of which were likely to have come from different cells, the differences between their volumes and the areas of the postsynaptic densities were on average 100% and ranged up to 650%.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Single mossy fiber axonal systems of human dentate granule cells studied in hippocampal slices from patients with temporal lobe epilepsy.

Previous histological and immunocytochemical studies suggest that reorganization of the dentate granule cell axons, the mossy fibers, can occur in epileptic human hippocampus (Sutula et al., 1989; Houser et al., 1990; Babb et al., 1991) and in animal models of epilepsy (Tauck and Nadler, 1985; Sutula et al., 1988; Cronin et al., 1992). However, neuroanatomical analyses of the trajectory and morphology of reorganized axons are not yet available. The present study was conducted to investigate single dentate granule cell axonal systems in human epileptic hippocampus. Individual mossy fibers were directly visualized by injecting a tracer (biocytin or Lucifer yellow) intracellularly in hippocampal slices prepared from temporal lobes that were surgically removed from patients for treatment of intractable epilepsy. Two major arborization patterns were identified: (1) the parent axons extended to and coursed through the hilus toward CA3, leaving collaterals along their paths in the hilus (N = 19 neurons); (2) in addition to the aforementioned axonal system, collateral(s) branched from the parent axon near the soma and projected to the granule cell layer and molecular layer, forming an aberrant axonal pathway (N = 9 neurons). These aberrant collaterals bore large boutons similar to those of the hilar axons and formed extensive plexuses in the granule cell layer and/or in the molecular layer. The summed length of collaterals in the granular/molecular layers was 1110.8 microns on average, which was one-fourth of the total summed length of the mossy fibers (3698.5 microns on average). The size of the somata in neurons that had aberrant collaterals was significantly larger than that of neurons without such collaterals (p < 0.025). In four cases, filopodium-like fine processes were present near the axon hillock and proximal parts of the parent axon, suggesting that the aberrant collateral formation might be an ongoing process in these tissues. The lack of control slices from normal living human hippocampus makes it difficult to assess to what extent the present findings are epilepsy associated. However, the presence of aberrant mossy fiber collaterals in the hippocampi used in the present study has been confirmed by Timm's staining and/or dynorphin immunohistochemistry in comparison with nonepileptic autopsy material, indicating its relation to epilepsy (Babb et al., 1991, 1992). At present, there seems to be a consensus that the projection of mossy fiber collaterals to the supragranular layer is a rare occurrence in normal rats (Lorento de Nó, 1934; Claiborne et al., 1986; Seress et al., 1991; present study), normal monkeys (Seress et al., 1991), and normal humans (Houser et al., 1990).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Mechanisms for the maintenance and eventual degradation of neurofilament proteins in the distal segments of severed goldfish mauthner axons.

Cellular mechanisms that might affect the degradation of neurofilament proteins (NFPs) were examined in the distal segments of severed goldfish Mauthner axons (M-axons), which do not degenerate for more than 2 months after severance. Calpain levels, as determined by reactivity to a polyclonal antibody, remained constant for 80 d postseverance in distal segments of M-axons and then declined from 80 to 85 d postseverance. Calpain activity in rat brain, as determined by a spectrophotometric assay, was much higher than calpain activity in control and severed goldfish brain, spinal cord, muscle, or M-axons. Calpain activity was extremely low in M-axons compared with that in all other tissues and remained low for up to 80 d postseverance in distal segments of M-axons. Phosphorylated NFPs, as determined by Stains-All treatment of SDS gels, were maintained for up to 72 d postseverance and then decreased noticeably at 75 d postseverance when NFP breakdown products appeared on silver-stained gels. By 85 d post-severance, phosphorylated NFPs no longer were detected, and NFP breakdown products were the most prominent bands on silver-stained gels. These results suggest that the distal segments of M-axons survive for months after severance, because NFPs are maintained in a phosphorylated state that stabilizes and protects NFPs from degradation by low levels of calpain activity in the M-axon; the distal segments of severed M-axons degenerate eventually when NFPs no longer are maintained in a phosphorylated state and become susceptible to degradation, possibly by low levels of calpain activity in the M-axon.

Animals↗