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PubMedDate not supplied

The distribution and morphology of LGN K pathway axons within the layers and CO blobs of owl monkey V1.

The lateral geniculate nucleus (LGN) of primates contains three classes of relay cells, the magnocellular (M), parvocellular (P), and koniocellular (K) cells. At present, very little is known about either the structure or function of the K relay cells in New or Old World monkeys (simian primates). In monkeys, K cells are located between the main LGN layers and adjacent to the optic tract. For convenience, these intercalated cell layers are numbered K1-K4 starting closest to the optic tract with K1. The objective of this study was to examine the details of K axon morphology in the primary visual cortex (V1) of owl monkeys and to determine if different K layers give rise to distinct axon types. For this purpose, injections of WGA-HRP or PHA-L were made into specific K LGN layers and the distribution and morphology of the resulting labeled axons were analyzed. Injections of fluorescent tracers also were made within the superficial layers of V1 to further document connections via analysis of the patterns of retrogradely labeled cells in the LGN. Our main finding is that K axons in owl monkeys terminate as delicate focused arbors within single cytochrome oxidase (CO) blob columns in cortical layer III and within cortical layer I. Overall, the morphology of the K axons in these monkeys is quite similar to what we described previously for K geniculocortical axons in the distantly related bush baby (prosimian primate), suggesting that the basic features of this pathway are common to all primates. Our results also provide evidence that the axon arbors from different K layers are morphologically distinct; axons from LGN layer K1 project mainly to cortical layer I, while axons from LGN layer K3 chiefly terminate in cortical layer III. Taken together, these results imply that the basic features of axons within the K pathway are conserved across primates, and that the K axons from different K layers are likely to differ in function based upon their different morphologies.

Animals↗
PubMed1998

Distribution of afferent axons in the bladder of rats.

The distribution of afferent axons in the bladder of rats was studied by means of immunohistochemistry for calcitonin gene-related peptide (CGRP), in frozen sections and in wholemount preparations of mucosa and muscle coat. Synaptophysin-immunofluorescence was used for the general detection of all intramural axons. The afferent axons were distributed over four distinct targets: at the base of the epithelium, inside the epithelium, on blood vessels (both arteries and veins) and along muscle bundles. In the mucosa, all the afferent axons, except the perivascular ones, lay either inside the epithelium or in a subepithelial plexus very close to the basal surface of the epithelium. The plexus was thickest in the neck of the bladder and in the initial portion of the urethra, and it became progressively less dense in the adjacent regions; it did not extend beyond the equatorial region, and therefore the mucosa of the cranial region of the bladder had no afferent axons. Most of the axons in the subepithelial plexus were terminal axons and included conspicuous varicosities arranged in very long chains; branching points were numerous, usually at right angles and located at the level of a varicosity; some axons split and then rejoined, forming closed axonal loops. The afferent innervation of the musculature was more diffuse, and appeared uniform throughout the bladder. After unilateral surgical denervation (by excision of the pelvic ganglion 5-7 days earlier) areas of complete denervation were observed, but there were large areas where the innervation was only reduced. The results showed that there is a bilateral innervation of many regions of the mucosa and the musculature, including individual muscle bundles. A substantial number of fibres crossed the midline into the contralateral side of the bladder. CGRP-immunofluorescence in mucosal afferent axons is enhanced in the surviving axons 5 days after contralateral denervation, a change which is interpreted as an early sign of regeneration.

Afferent Pathways↗
PubMed1980

Removal of the synaptic target permits terminal sprouting of a mature intact axon.

When the central nervous system (CNS) develops, neurones send out axons to make contact with appropriate synaptic target cells and then stop growing. If its usual target is missing, an axon may continue to grow until it synapses with a suitable but inappropriate target. This suggests that contact with a synaptic target is important in stopping axonal growth during development. Many classes of neurone in the adult CNS retain a capacity to grow towards denervated targets, but it is not known whether the synaptic contacts established during development continue to regulate the growth of individual mature, intact axons. This has been a difficult problem to investigate; in vertebrates most studies necessarily involve large populations of neurones, and the most direct approach, removal of a synaptic target, usually damages many neurones, including the axons that are to be studied. We report here a demonstration of target cell influences on the growth of a single mature, intact axon in the CNS of the leech by selectively destroying the axon's synaptic target without injuring the axon itself. Target removal, which itself does not trigger sprouting of intact axons, permits the intact axon to grow at its tip in response to injury of other axonal branches of the same cell.

Age Factors↗
PubMed1995

Alkylphosphocholines inhibit choline uptake and phosphatidylcholine biosynthesis in rat sympathetic neurons and impair axonal extension.

At least 50% of the major axonal membrane lipid, phosphatidylcholine, of rat sympathetic neurons is synthesized in situ in axons [Posse de Chaves, Vance, Campenot and Vance (1995) J. Cell Biol. 128, 913-918]. In the same study we reported that, in a choline-deficient model for neuron growth, phosphatidylcholine synthesis in cell bodies is neither necessary nor sufficient for growth of distal axons. Rather, the local synthesis of phosphatidylcholine in distal axons is required for normal axon growth. We have now used three alkylphosphocholines (hexadecylphosphocholine, dodecylphosphocholine and octadecylphosphocholine) as inhibitors of PtdCho biosynthesis in a compartmented model for culture of rat sympathetic neurons. The experiments reveal that alkylphosphocholines decrease the uptake of choline into these neurons and inhibit PtdCho synthesis, but not via an effect on the activity of the enzyme CTP: phosphocholine cytidylyltransferase. We also show that when the distal axons, but not the cell bodies, are exposed to alkylphosphocholines, axonal elongation is inhibited, which is consistent with the hypothesis that phosphatidylcholine synthesis in axons, but not in cell bodies, is required for axonal elongation. The inhibitory effect of alkylphosphocholines on axon growth is most likely not mediated via a decrease in the activity of protein kinase C, since when this enzyme activity is down-regulated by treatment of the cells with phorbol ester, the alkylphosphocholines retain their ability to inhibit axonal growth.

Animals↗
PubMed2000

Abnormal axonal physiology is associated with altered expression and distribution of Kv1.1 and Kv1.2 K+ channels after chronic spinal cord injury.

Dysfunction of surviving axons which traverse the site of spinal cord injury (SCI) has been linked to altered sensitivity to the K+ channel blocker 4-aminopyridine (4-AP) and appears to contribute to post-traumatic neurological deficits although the underlying mechanisms remain unclear. In this study, sucrose gap electrophysiology in isolated dorsal column strips, Western blotting and confocal immunofluorescence microscopy were used to identify the K+ channels associated with axonal dysfunction after chronic (6-8 weeks postinjury) clip compresssion SCI of the thoracic cord at T7 in rats. The K+ channel blockers 4-AP (200 microM, 1 mM and 10 mM) and alpha-dendrotoxin (alpha-DTX, 500 nM) resulted in a significant relative increase in the amplitude and area of compound action potentials (CAP) recorded from chronically injured dorsal column axons in comparison with control noninjured preparations. In contrast, TEA (10 mM) and CsCl (2 mM) had similar effects on injured and control spinal cord axons. Western blotting and quantitative immunofluorescence microscopy showed increased expression of Kv1.1 and Kv1.2 K+ channel proteins on spinal cord axons following injury. In addition, Kv1.1 and Kv1.2 showed a dispersed staining pattern along injured axons in contrast to a paired juxtaparanodal localization in uninjured spinal cord axons. Furthermore, labelled alpha-DTX colocalized with Kv1.1 and Kv1.2 along axons. These findings suggest a novel mechanism of axonal dysfunction after SCI whereby an increased 4-AP- and alpha-DTX-sensitive K+ conductance, mediated in part by increased Kv1.1 and Kv1.2 K+ channel expression, contributes to abnormal axonal physiology in surviving axons.

4-Aminopyridine↗
PubMed2002

Axons and glial interfaces: ultrastructural studies.

At most vertebrate nerve transitional zones (TZs) there is a glial barrier which is pierced by axons passing between the CNS and PNS. Myelinated axons traverse this in individual tunnels. The same is true of larger non-myelinated axons. This holds widely among the vertebrates, for example, the large motor axons of the sea-lamprey Petromyzon (which also possess TZ specializations not found in mammals). Smaller non-myelinated axons traverse the TZ glial tunnels as fascicles and so the barriers are correspondingly less comprehensive for them. Accordingly, in nerves composed of non-myelinated axons, such as the vomeronasal or the olfactory, a TZ barrier stretching across the nerve is effectivelyabsent. The chordateAmphioxus differsfrom the vertebrates in lacking a TZ barrier throughout. Invertebrates also lack glial barriers at the TZs between ganglia and interconnecting nerve trunks. The glial barrier at the dorsal spinal root TZ (DRTZ) has considerable value for analysing protocols aimed at achieving CNS regeneration, because it provides a useful model of the gliotic reaction at sites of CNS injury. Also, it is especially amenable to morphometric analysis, and so enables objective quantification of different protocols. Being adjacent to the subarachnoid space, it is accessible for experimental intervention. The DRTZ was used to investigate the value of neurotrophin 3 (NT3) in promoting axon regeneration across the TZ barrier and into the CNS following dorsal root crush. It promoted extensive regeneration and vigorous non-myelinated axonal ensheathment. On average, around 40% of regenerating axons grew across the interface, compared with virtually none in its absence. These may have traversed the interface through loci occupied by axons prior to degeneration. Many regenerating axons became myelinated, both centrally and peripherally.

Animals↗
PubMed2001

Ceramide inhibits axonal growth and nerve growth factor uptake without compromising the viability of sympathetic neurons.

Ceramide inhibits axonal growth of cultured rat sympathetic neurons when the ceramide content of distal axons, but not cell bodies, is increased (Posse de Chaves, E. I., Bussiere, M. Vance, D. E., Campenot, R. B., and Vance, J.E. (1997) J. Biol. Chem. 272, 3028-3035). We now report that inhibition of growth does not result from cell death since although ceramide is a known apoptotic agent, C(6)-ceramide given to the neurons for 24 h did not cause cell death but instead protected the neurons from death induced by deprivation of nerve growth factor (NGF). We also find that a pool of ceramide generated from sphingomyelin in distal axons, but not cell bodies, inhibits axonal growth. Analysis of endogenous sphingomyelinase activities demonstrated that distal axons are rich in neutral sphingomyelinase activity but contain almost no acidic sphingomyelinase, which is concentrated in cell bodies/proximal axons. Together, these observations are consistent with the idea that generation of ceramide from sphingomyelin by a neutral sphingomyelinase in axons inhibits axonal growth. Furthermore, we demonstrate that treatment of distal axons with ceramide inhibits the uptake of NGF and low density lipoproteins by distal axons by approximately 70 and 40%, respectively, suggesting that the inhibition of axonal growth by ceramide might be due, at least in part, to impaired endocytosis of NGF. However, inhibition of endocytosis of NGF by ceramide could not be ascribed to decreased phosphorylation of TrkA.

Animals↗
PubMed2004

Assessment of factors regulating axon growth between the cortex and spinal cord in organotypic co-cultures: effects of age and neurotrophic factors.

Axon growth failure in the central nervous system (CNS) of adult animals is thought to be attributable to several factors, including an inadequate intrinsic growth response, the presence of inhibitory molecules, and a lack of adequate neurotrophic support. Here we use a new in vitro assay system to quantitatively assess growth of axons in cortex/spinal cord organotypic co-cultures from neonatal rats. Co-cultures of cortex and spinal cord were prepared from neonatal rats at P3 or P7, and by pairing cortex and spinal cords from different ages. Axon growth from the cortex to the spinal cord was assessed using DiI tract tracing techniques. Axons could be traced from the cortex to the spinal cord in co-cultures in which both tissues were obtained from P3 animals, whereas few axons crossed the cortex/spinal cord boundary in co-cultures from P7 animals. A larger number of axons could be traced across the boundary in co-cultures from P3 animals that were treated with neurotrophins (NGF, BDNF, or NT3), whereas neurotrophins produced minimal growth enhancement in P7 co-cultures. In mixed age co-cultures of P7 cortex with P3 spinal cord, moderate numbers of axons extended between the cortex and spinal cord when cultures were treated with neurotrophins, but few if any crossing axons were detected in co-cultures of P3 cortex with P7 spinal cords. These results indicate that successful growth of axons from the cortex to the spinal cord depends on the developmental age of the tissue terrain (the spinal cord and/or the interface between cortex and spinal cord explants), and to a lesser extent on the developmental state of the cortical neurons, and that axon growth between cortex and spinal cord can be enhanced by exogenous neurotrophins. These co-cultures provide a potentially useful assay for factors that affect axon growth that is intermediate between assays based on dissociated neurons and the intact tissue terrain.

Age Factors↗
PubMed1996

Differences in the recovery of excitability in sensory and motor axons of human median nerve.

Following conduction of an action potential there is a stereotyped sequence of changes in excitability as axons are initially refractory, then superexcitable and finally subexcitable. These activity-dependent oscillations in excitability subside over 100 ms and together constitute the recovery cycle. The present study was undertaken first to document the recovery cycle of sensory and motor axons of different threshold and, secondly, to compare the changes in sensory axons with those in motor axons. A computerized threshold-tracking system was used to measure recovery cycles in six healthy subjects; stimuli were applied to the median nerve at the wrist. Changes in the threshold required to produce an antidromic compound sensory action potential (CSAP) and an orthodromic compound muscle action potential (CMAP) of fixed amplitude (30%, 50% and 70% of maximal) were recorded following a single supramaximal conditioning stimulus. Normalized recovery cycles were identical for axons of different threshold, whether sensory or motor, and were reproducible on repeat testing. However, there were significant differences between the changes in sensory and motor axons, with greater supernormality and greater late subnormality in motor axons. The greater changes in motor axons could not be explained by differences in the strength-duration properties of sensory and motor axons. There are biophysical differences in the properties of sensory and motor axons and these differences may underlie the differential susceptibility of sensory and motor axons in peripheral nerve disorders.

Adult↗
PubMed2003

Changes in the expression and localization of the paranodal protein Caspr on axons in chronic multiple sclerosis.

The presence of intact paranodal junctions on myelinated axons in the CNS and PNS is crucial for both myelin sheath attachment and saltatory impulse conduction. The axonal glycoprotein contactin-associated protein (Caspr) is expressed in the paranodal region and plays an important role in the creation and maintenance of these adhesive junctions. In the present study, antibodies to Caspr were used to assess the integrity of paranodal junctions on myelinated axons in brain and spinal cord tissue from subjects with longstanding multiple sclerosis, a neurological disorder that affects both myelin and axons. Triple immunofluorescence combined with confocal laser scanning microscopy showed that axons in the demyelinated centre of the 36 brain and 16 spinal cord multiple sclerosis lesions studied were devoid of Caspr immunoreactivity, suggesting that axons down regulate the expression of Caspr following demyelination. Additional data indicated that Caspr reappears in the paranodal region with the formation of new myelin sheaths. Immuno labelling further revealed that Caspr on myelinated axons in border regions was often no longer concentrated in the paranodal region, but was also present in the internodal region-a phenomenon particularly common in the borders of the more chronic lesions in the collection. Myelinated axons with long Caspr-positive stretches were often present at a considerable distance from the lesion edges. These findings raise the possibility that the aberrant location of Caspr is an early sign of impending myelin loss. This would imply that demyelination continues at a slow rate in established lesions. The diameters of Caspr-positive structures on some myelinated axons near the lesion edges were also increased. Moreover, the gap between individual myelin sheaths on these apparently swollen axons was widened occasionally and a very small myelin sheath plus additional Caspr-positive structures had sometimes formed in the enlarged space. This finding thus suggests that the formation of new myelin in multiple sclerosis is not only induced following the loss of complete internodes but also in response to broadening of the nodal region. Interestingly, alterations in the expression and localization of Caspr were observed in tissue from both subjects with the primary and secondary progressive form of multiple sclerosis. In summary, the present study provides immunohistochemical evidence that paranodal junctions on some myelinated axons in the borders of lesions of patients with chronic progressive multiple sclerosis are no longer intact. This may impair saltatory impulse conduction and lead to further myelin loss, thereby contributing to disease progression in multiple sclerosis.

Adult↗
PubMed2005

Axon and Schwann cell partnership during nerve regrowth.

Regeneration of peripheral nerve involves an essential contribution by Schwann cells (SCs) in collaboration with regrowing axons. We examined such collaboration between new axons and Schwann cells destined to reform peripheral nerve trucks in a regeneration chamber bridging transected rat sciatic nerves. There was a highly intimate "dance" between axons that followed outgrowing and proliferating SCs. Axons without SCs only grew short distances and almost all axon processes had associated SC processes. When regeneration chambers were infused through an external access port with local mitomycin, a mitosis inhibitor, SC proliferation, migration and subsequent axon regrowth were dramatically reduced. Adding laminin to mitomycin did not reverse this regenerative lag and indicated that SCs provide more than laminin synthesis alone. Laminin infused alone supplemented endogenous laminin and facilitated first SC then axon regrowth. "Wrong way" misdirected axons were associated with misdirected SC processes and were more numerous in bridges exposed to mitomycin, but were fewer in laminin supplemented bridges. Later, by 21 days, there was myelinated axon repopulation of regenerative bridges but those exposed to mitomycin alone at early time points had substantial impairments in axon investment. Reforming peripheral nerve trucks involves a very close and intimate relationship between axons and SCs that must proliferate and migrate, facilitated by laminin.

Animals↗
PubMed1990

The role of Schwann cells and basal lamina tubes in the regeneration of axons through long lengths of freeze-killed nerve grafts.

The ability of long acellular nerve grafts to support axonal regeneration was examined using inbred rats. Grafts (40 mm long) of tibial/plantar nerves were used either as live grafts or after freeze-drying to render the grafts acellular. The grafts were sutured to the proximal stump of severed tibial nerves in host animals which were then killed 1-12 weeks later. Axons rapidly regenerated through the living grafts but only extended 10-20 mm into the acellular grafts. This distance was achieved by 6 weeks and thereafter no significant further axonal extension occurred in the acellular grafts. A few naked axons lacking Schwann cell contact were identified in all acellular grafts, but became more numerous near the distal extent of axonal penetration into 6-12 week grafts. These axons contained large numbers of neurofilaments. When the distal 20 mm of 6 week acellular grafts (segments into which axons had not penetrated) were sutured to freshly severed tibial nerves, axons grew readily into the grafted tissue to a maximum distance of 9 mm. It is therefore likely that the limits to axonal regeneration through initially acellular grafts were set by factors intrinsic to the severed nerve. It is suggested that the limited migratory powers of Schwann cells may be one such factor. The concept that basal lamina tubes are not essential for axonal regeneration but may act as low resistance pathways for both axonal elongation and Schwann cell migration is discussed.

Animals↗
PubMed2005

The T1 domain of Kv1.3 mediates intracellular targeting to axons.

Shaker K+ channels play an important role in modulating electrical excitability of axons. Recent work has demonstrated that the T1 tetramerization domain of Kv1.2 is both necessary and sufficient for targeting of the channel to the axonal surface [Gu, C., Jan, Y.N. & Jan, L.Y. (2003) Science,301, 646-649]. Here we use a related channel, Kv1.3, as a model to investigate cellular mechanisms that mediate axonal targeting. We show that the T1 domain of Kv1.3 is necessary and sufficient to mediate targeting of the channel to the axonal surface in pyramidal neurons in slices of cortex from neonatal rat. The T1 domain is also sufficient to cause preferential axonal localization of intracellular protein, which indicates that the domain probably does not work through compartment-specific endocytosis or compartment-specific vesicle docking. To determine whether the T1 domain mediates axonal trafficking of transport vesicles, we compared the trafficking of vesicles containing green fluorescent protein-labelled transferrin receptor with those containing the same protein fused with the T1 domain in living cortical neurons. Vesicles containing the wild-type transferrin receptor did not traffic to the axon, in accord with previously published results; however, those containing the transferrin receptor fused to T1 did traffic to the axon. These results are consistent with the T1 domain of Kv1.3 mediating axonal targeting by causing transport vesicles to traffic to axons and they represent the first evidence that such a mechanism might underlie axonal targeting.

Animals↗
PubMed1975

The incidence and properties of beta axons to muscle spindles in the cat hind limb.

The distribution of beta axons to muscle spindles in the tenuissimus and abductor digiti quinti medius (A.D.Q.M.) muscles of the hind limb of the cat was determined by testing the action of single motor axons, capable of producing extrafusal contraction, isolated in the ventral spinal roots on the discharges of individual muscle spindle primary sensory endings recorded in the dorsal spinal roots. The proportion of spindles with beta innervation was 41% in A.D.Q.M. and 30% in tenuissimus. The proportion of fast motor axons that were beta axons was 28% in the A.D.Q.M. and 11% in tenuissimus; usually each beta axon innervated a single spindle while no spindle received more than two beta axons. The beta axons were dynamic in nature and those to any one muscle tended to have slightly lower conduction velocities than the alpha axons though some overlap did occur. The extent to which beta axons can account for the fact that in isolated spindles axons selective to either nuclear bag or nuclear chain fibres are found in about equal proportions whereas a ratio of three static to one dynamic gamma axons is found electrophysiologically is discussed. An explanation for the low incidence of beta innervation previously found electrophysiologically and the considerably higher incidence found histologically is given.

Action Potentials↗
PubMed1976

Kinetics and energetics of calcium efflux from intact squid giant axons.

The Ca efflux from intact squid axons consists of three major components: one that is activated by Cao, one that is activated by Nao and a residual flux that persists in the nominal absence of both Cao and Nao. The properties of these components have been investigated in unpoisoned axons and in axons poisoned with cyanide. 2. Under all conditions the shape of the curve relating Cao to Cao-activated Ca efflux approximates to a section of a rectangular hyperbola, consistent with simple Michaelis activation. 3. The external Ca concentration giving half-maximal activation of Cao-activated Ca efflux is about 2 muM in unpoisoned axons immersed in Na-ASW, but on poisoning changes progressively to values in the range 1-10 mM. The residual efflux from unpoisoned axons may reflect activation by traces of Ca present immediately external to the axolemma. 4. The apparent affinity for Cao of Cao-activated Ca efflux is very similar in unpoisoned axons immersed in sea waters containing Na, Li, Tris or K as major cation, whereas in poisoned axons the affinity in Na and Li is about the same but higher than that in choline and Tris. 5. In unpoisoned axons Ca influx increases linearly as Cao is increased from 2 muM to 110 mM. The absolute value of the Ca influx from 10 muM-Cao is less than 1% of the Cao-activated Ca efflux at this external Ca concentration. In poisoned axons the sizes of Cao-activated Ca efflux and Ca influx were similar at all Ca concentrations examined. 6. The shape of the curve relating Nao to Nao-activated Ca efflux approximates to a section of rectangular hyperbola in unpoisoned axons but is clearly sigmoidal in axons that have been fully poisoned with cyanide. The sigmoidal shape develops progressively during poisoning. ...

Adenosine Monophosphate↗
PubMed1976

Distribution of fusimotor axons to intrafusal muscle fibres in cat tenuissimus spindles as determined by the glycogen-depletion method.

1. The distribution of fusimotor axons to bag1, bag2 and chain muscle fibres in cat tenuissimus spindles has been studied using a modification of the glycogen-depletion technique of Edstrrom & Kugelberg (1968). Single fusimotor axons were stimulated intermittently at 40-100/sec for long periods (30-90 sec) during blood occlusion. Portions of muscle containing the activated spindles were quick-frozen, fixed in absolute ethanol during freeze-substitution, and then embedded in paraffin wax. Serial transverse sections were stained for glycogen using the periodic acid-Schiff method, and examined for depletion. 2. Dynamic gamma axons (i.e. those that increase the dynamic index of primary-ending responses to ramp stretches of large amplitude) depleted bag1 fibres almost exclusively. 3. Static gamma axons (i.e. those that reduce or abolish the dynamic index) depleted both bag and chain fibres. Bag1 and bag2 fibres were depleted about equally. 4. A single static gamma axon may activate both bag and chain fibres in one spindle (the most common pattern), chain fibres only in another, and bag fibres only in a third spindle. 5. Static gamma axons with conduction velocities less than 25 m/sec also had a non-selective distribution, but no depletion was observed in bag2 fibres. 6. The zones of depletion produced by dynamic gamma axons were distributed more or less equally in the intra- and extracapsular parts of spindle poles, whereas those produced by static gamma axons were mainly intracapsular. 7. The results are compared with the glycogen-depletion studies of Brown & Butler (1973, 1975) and our own study of the distribution of static gamma axons to spindles in which all other motor axons had degenerated (Barker, Emonet-Dénand, Laporte, Proske & Stacey, 1973). The implications of the finding that both static gamma and dynamic gamma axons activate bag1 fibres are discussed.

Animals↗
PubMed1983

Apportionment of the terminals from single preganglionic axons to target neurones in the rabbit ciliary ganglion.

We have studied the apportionment of terminals from single preganglionic axons to target neurones in the ciliary ganglion of adult rabbits. Both electrical recording and intra-axonal injection of horseradish peroxidase (HRP) showed that each preganglionic axon innervates only a small fraction of the ganglion cell population (about 10-20 of the approximately 400 ganglion cells). Examination of ganglia in whole mounts showed that neurones whose cell bodies were enveloped by HRP-labelled boutons from a single axon were often surrounded by other neurones which received no contacts from the labelled fibre. Electron microscopical examination of labelled presynaptic terminals on individual ganglion cells confirmed that the boutons of single axons were sharply confined to particular target cells. This suggests that individual target neurones (or portions of them) are the unit of innervation during the development of these synaptic connexions. Comparison of the amplitudes of synaptic responses in singly and multiply innervated ganglion cells indicated that, on average, an individual axon made a weaker synaptic connexion with a multiply innervated neurone than with neurone that received only one input. Moreover, neurones innervated by several different axons tended to have fewer synapses on their somata than neurones innervated by only one or two preganglionic axons. Individual post-synaptic profiles were often contacted exclusively by labelled terminals when examined in the electron microscope. Since many of these neurones are multiply innervated, this observation suggests some regional separation of the several inputs contacting the same cell. For several reasons, however, this inference must be regarded as tentative. Taken together, these findings provide a possible explanation of the correlation between the dendritic geometry of ganglion cells and the number of different axons that innervate them (Purves & Hume, 1981). The several axons that initially innervate ganglion cells without dendrites evidently compete during early life until only a single input remains. On ganglion cells with dendrites, however, the number of inputs that persists is proportional to dendritic complexity. The present results suggest that the diminished competition between axons innervating neurones with dendrites may result from some degree of terminal segregation on dendritic arborizations.

Action Potentials↗
PubMed1995

Electrical and morphological factors influencing the depolarizing after-potential in rat and lizard myelinated axons.

1. Intra-axonal recording and electron microscopy were applied to intramuscular myelinated axons in lizards and rats to investigate factors that influence the amplitude and time course of the depolarizing after-potential. 2. Depolarizing after-potentials in lizard axons had larger peak amplitudes and longer half-decay times than those recorded in rat axons (mean values 10 mV, 35 ms in lizard; 3 mV, 11 ms in rat). These differences were not due to differences in temperature, resting potential or action potential amplitude or duration. 3. For a given axon diameter, the myelin sheath in lizard fibres was thinner and had fewer wraps than in rat fibres. There was no significant difference in myelin periodicity. Calculations suggest that the thinner myelin sheath accounts for < 30% of the difference between depolarizing after-potential amplitudes recorded in lizard and rat axons. 4. Consistent with a passive charging model for the depolarizing after-potential, the half-time of the passive voltage transient following intra-axonal injection of current was shorter in rat than in lizard axons. 5. Aminopyridines prolonged the falling phase of the action potential and increased the amplitude of the depolarizing after-potential in both types of axon. 6. During repetitive stimulation the depolarizing after-potentials following successive action potentials exhibited little or no summation. Axonal input conductance in the interspike interval increased during the train. 7. These findings suggest that the amplitude and time course of the depolarizing after-potential are influenced not only by the passive properties of the axon and myelin sheath, but also by persisting activation of axolemmal K+ channels following action potentials.

Action Potentials↗