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PubMed2005

Action potential fidelity during normal and epileptiform activity in paired soma-axon recordings from rat hippocampus.

Although action potential initiation and propagation are fundamental to nervous system function, there are few direct electrophysiological observations of propagating action potentials in small unmyelinated fibres, such as the axons within mammalian hippocampus. To circumvent limitations of previous studies that relied on extracellular stimulation, we performed dual recordings: whole-cell recordings from hippocampal CA3 pyramidal cell somas and extracellular recordings from their axons, up to 800 micro m away. During brief spike trains under normal conditions, axonal spikes were more resistant to amplitude reduction than somatic spikes. Axonal amplitude depression was greatest at the axon initial segment < 150 microm from the soma, and initiation occurred approximately 75 microm from the soma. Although prior studies, which failed to verify spike initiation, suggested substantial axonal depression during seizure-associated extracellular K+([K+]o) rises, we found that 8 mm [K+]o caused relatively small decreases in axonal spike amplitude during brief spike trains. However, during sustained, epileptiform spiking induced in 8 mm [K+]o, axonal waveforms decreased significantly in peak amplitude. During epileptiform spiking, bursts of two or more action potentials > 20 Hz failed to propagate in most cases. In normal [K+]o at 25 and 32 degrees C, spiking superimposed on sustained somatic depolarization, but not spiking alone, produced similar axonal changes as the epileptiform activity. These results highlight the likely importance of steady-state inactivation of axonal channels in maintaining action potential fidelity. Such changes in axonal propagation properties could encode information and/or serve as an endogenous brake on seizure propagation.

Action Potentials↗
PubMedDate not supplied

Changes in retinal ganglion cell axons after optic nerve crush: neurofilament expression is not the sole determinant of calibre.

After injury in the central nervous system of adult mammals, many of the axons that remain attached to their intact cell bodies degenerate and decrease in calibre. To understand this process better, we have investigated the relationship between axonal loss, cell loss, and the time course of changes in axonal calibre. Optic nerves (ONs) were crushed and the numbers and sizes of axons remaining close to the cell bodies (2 mm from the eye) and near the site of the lesion (6 mm from the eye) were determined for nerves examined between 1 week and 3 months after injury. Comparison with the retinal ganglion cell (RGC) counts from the same animals revealed that axonal loss was concomitant with cell body loss for at least the first 2 weeks after injury. However, there was no significant change in the calibre of the surviving neurons until 1 month after injury. Thereafter, the axonal calibre was decreased equally along the ON. No progressive somatofugal atrophy was observed. These decreases in axonal calibre occur much later than the immediate drop in neurofilament (NF) expression that also follows injury. The late effect of injury on axonal calibre suggests that NF expression is not the sole determinant of axon size of the RGC fibers in the ON. Other factors are likely additional contributing factors, such as the decreased rate of axonal transport that would help maintain the axonal neurofilament content.

Animals↗
PubMed1988

Insulin improves rat soleus axon function by increasing glucose transport.

The effect of varying glucose and insulin concentration on neuromuscular transmission was investigated in rat soleus and extensor digitorum longus (EDL) nerve-muscle preparations using conventional microelectrode techniques. Soleus and EDL axons were similar in that both failed after approximately 70 min of glucose deprivation and often did not recover from glucose deprivation. Soleus and EDL axons differed in the following ways: 1) soleus axons required greater than 7.64 mM of glucose to give sustained function vs. greater than 2.78 mM of glucose for the EDL; 2) 30 microU/ml of insulin improved soleus axon function over a range of glucose concentrations from 4.17 to 9.72 mM vs. no effect of 1,000 microU/ml on EDL axons; 3) resting glucose transport was slow into soleus axons and rapid into EDL axons; and 4) 10 microU/ml of insulin increased glucose transport into soleus axons vs. no effect of 1,000 microU/ml of insulin on glucose transport into EDL axons. These results suggest that insulin improves soleus axon function by increasing glucose transport, whereas insulin has no effect on EDL axons.

Animals↗
PubMed1986

Fusimotor axons in the kitten.

In kittens 1- to 23-days old growth of axons in the soleus nerve has been studied using the structural parameters nerve length, internodal length, and axonal diameter. In addition, single functional fusimotor axons were isolated in lumbosacral ventral roots, and the responses of muscle spindles in soleus were studied during fusimotor stimulation. While nerve length over the soleus nerve to lumbar spinal root increased from 41 to 76 mm during the 22 days, mean internodal length increased from 250 to 410 microns. Mean axon diameter increased from 2.1 to 4.1 microns. In the youngest animals values for both internodal length and axon diameter were distributed uniformly about the mean. From day 11 onward the distributions became bimodal, including a growing number of new axons in the small-myelinated range. Filaments of ventral root were isolated that on repetitive stimulation had a specific excitatory effect on the discharge of muscle spindles. The responses could be attributed to axons that were not associated with measurable tension and were therefore likely to be fusimotor fibers. Measurements of the conduction velocity of skeletomotor and fusimotor axons showed that conduction speed increased progressively with age for both groups, but the rate of increase was more than three times faster in the most rapidly conducting skeletomotor axons compared with the fusimotor axons. The distribution of conduction velocities for fusimotor fibers showed two peaks, one in the range typical for conduction in unmyelinated fibers, 0.5-1.0 m/s, the second at 3-4 m/s. The small number of values in the range of 1-2 m/s was attributed to the process of myelination. It is suggested that conduction speed increases discontinuously over this part of the range as impulse conduction changes from continuous propagation to saltatory transmission. Eighteen fusimotor axons could be classified as having either a static or a dynamic action on spindle discharge. Repetitive stimulation of fusimotor fibers during a ramp-and-hold stretch of the muscle produced a characteristic response. Fibers classified as dynamic had little effect on the response of the spindle when the muscle was held at a particular length but greatly increased the response during a length change. Static fusimotor fibers, on stimulation, increased the response of the spindle at constant length but did not evoke a selective increase during the length change. Both kinds of fusimotor effects were characterized by overall low firing rates.

Aging↗
PubMed1995

Synaptic potentials and threshold currents underlying spike production in motor giant axons of Aglantha digitale.

1. Motor giant axons that excite swimming muscles in the jelly-fish Aglantha digitale interface with units of the inner and outer nerve rings in the margin at the base of the bell. External recording electrodes were used to monitor electrical activity at different sites within the nerve ring while events in the motor giant axon were recorded with intracellular micropipettes placed within 100 microns of the synaptic area. In some experiments, 4- to 6-micron-diam patch pipettes were used to record in situ from ion channel clusters at different locations along the axon. 2. Independently propagating calcium and sodium spikes in the motor giant axon were found to arise from different excitatory postsynaptic potentials (EPSPs). Two separate inputs were identified; one EPSP class represented an input from the pacemaker system in the inner nerve ring, whereas another represented an input from the giant axon in the outer nerve ring. EPSPs from the two nerve rings had significantly different time courses and amplitudes. EPSPs from the ring giant axon reached a peak in little more than 1 ms, whereas EPSPs from the pacemaker system reached a maximum in approximately 7 ms. These slower EPSPs may be compound events composed of postsynaptic potentials from multiple synapses excited in series by the passage of the pacemaker neuron signal. 3. The threshold for the production of calcium spikes by the slow EPSPs of the pacemaker system (-51 +/- 2.2 mV, mean +/- SD; n = 5) corresponded well with the voltage at which a net inward "T"-type calcium current first appeared in recordings from axon membrane patches (-55 to -50 mV); the threshold for the initiation of the sodium spike by the fast EPSPs of the ring giant system (-32 +/- 1.2 mV, mean +/- SD; n = 6) corresponded well with the voltage at which a net inward sodium current first appeared (-35 to -30 mV). 4. Inward currents were rarely observed in membrane patches formed using pipettes with tips of < 1 micron OD. Even with 4-micron pipettes, patches of membrane were sometimes obtained with a channel population consisting exclusively of potassium channels; calcium and sodium currents were found in highly discrete areas ("hot spots"). Preliminary findings on the undersurface of the axon, which makes synaptic contact with the myoepithelium, are consistent with a similar distribution. 5. The pathway by which the ring giant excites the motor giant axon is not definitely known. The synaptic delay between the peak of the ring giant action potential (monitored externally) and the initial rise of the fast EPSP (1.64 +/- 0.15 ms, mean +/- SD; n = 21) would allow for transmission at two synapses, because single synaptic delays at neuromuscular junctions in Aglantha are approximately 0.7 ms at 12 degrees C. The mean synaptic delay at the slow EPSP synapse was 0.88 +/- 0.09 (SD) ms (n = 12). 6. The delay between the impulse in the ring giant axon and the subsequent excitation of the motor giant axon may permit the animal to withdraw its tentacles and so lower the drag that would otherwise reduce the effectiveness of any escape swim and might induce tentacle autotomy.

Action Potentials↗
PubMed1997

Spinohypothalamic tract neurons in the cervical enlargement of rats: locations of antidromically identified ascending axons and their collateral branches in the contralateral brain.

Antidromic activation was used to determine the locations of ascending spinohypothalamic tract (SHT) axons and their collateral projections within C1, medulla, pons, midbrain, and caudal thalamus. Sixty-four neurons in the cervical enlargement were antidromically activated initially by stimulation within the contralateral hypothalamus. All but one of the examined SHT neurons responded either preferentially or specifically to noxious mechanical stimuli. A total of 239 low-threshold points was classified as originating from 64 ascending (or parent) SHT axons. Within C1, 38 ascending SHT axons were antidromically activated. These were located primarily in the dorsal half of the lateral funiculus. Within the medulla, the 29 examined ascending SHT axons were located ventrolaterally, within or adjacent to the lateral reticular nucleus or nucleus ambiguus. Within the pons, the 25 examined ascending SHT axons were located primarily surrounding the facial nucleus and the superior olivary complex. Within the caudal midbrain, the 23 examined SHT ascending axons coursed dorsally in a position adjacent to the lateral lemniscus. Within the anterior midbrain, SHT axons traveled rostrally near the brachium of the inferior colliculus. Within the posterior thalamus, all 17 examined SHT axons coursed rostrally through the posterior nucleus of thalamus. A total of 114 low-threshold points was classified as collateral branch points. Sixteen collateral branches were seen in C1; these were located primarily int he deep dorsal horn. Forty-five collateral branches were located in the medulla. These were primarily in or near the medullary reticular nucleus, nucleus ambiguus, lateral reticular nucleus, parvocellular reticular nucleus, gigantocellular reticular nucleus, cuneate nucleus, and the nucleus of the solitary tract. Twentysix collateral branches from SHT axons were located in the pons. These were in the pontine reticular nucleus caudalis, gigantocellular reticular nucleus, parvocellular reticular nucleus, and superior olivary complex. Twenty-three collateral branches were located in the midbrain. These were in or near the mesencephalic reticular nucleus, brachium of the inferior colliculus, cuneiform nucleus, superior colliculus, central gray, and substantia nigra. Int he caudal thalamus, two branches were in the posterior thalamic nucleus and two were in the medial geniculate. These results indicate that SHT axons ascend toward the hypothalamus in a clearly circumscribed projection in the lateral brain stem and posterior thalamus. In addition, large numbers of collaterals from SHT axons appears to project to a variety of targets in C1, the medulla, pons, midbrain, and caudal thalamus. Through its widespread collateral projections, the SHT appears to be capable of providing nociceptive input to many areas that are involved in the production of multifaceted responses to noxious stimuli.

Animals↗
PubMed1999

Experimental spinal cord injury: spatiotemporal characterization of elemental concentrations and water contents in axons and neuroglia.

To examine the role of axonal ion deregulation in acute spinal cord injury (SCI), white matter strips from guinea pig spinal cord were incubated in vitro and were subjected to graded focal compression injury. At several postinjury times, spinal segments were removed from incubation and rapidly frozen. X-ray microanalysis was used to measure percent water and dry weight elemental concentrations (mmol/kg) of Na, P, Cl, K, Ca, and Mg in selected morphological compartments of myelinated axons and neuroglia from spinal cord cryosections. As an index of axon function, compound action potentials (CAP) were measured before compression and at several times thereafter. Axons and mitochondria in epicenter of severely compressed spinal segments exhibited early (5 min) increases in mean Na and decreases in K and Mg concentrations. These elemental changes were correlated to a significant reduction in CAP amplitude. At later postcompression times (15 and 60 min), elemental changes progressed and were accompanied by alterations in compartmental water content and increases in mean Ca. Swollen axons were evident at all postinjury times and were characterized by marked element and water deregulation. Neuroglia and myelin in severely injured epicenter also exhibited significant disruptions. In shoulder areas (adjacent to epicenter) of severely injured spinal strips, axons and mitochondria exhibited modest increases in mean Na in conjunction with decreases in K, Mg, and water content. Following moderate compression injury to spinal strips, epicenter axons exhibited early (10 min postinjury) element and water deregulation that eventually recovered to near control values (60 min postinjury). Na(+) channel blockade by tetrodotoxin (TTX, 1 microM) perfusion initiated 5 min after severe crush diminished both K loss and the accumulation of Na, Cl, and Ca in epicenter axons and neuroglia, whereas in shoulder regions TTX perfusion completely prevented subcellular elemental deregulation. TTX perfusion also reduced Na entry in swollen axons but did not affect K loss or Ca gain. Thus graded compression injury of spinal cord produced subcellular elemental deregulation in axons and neuroglia that correlated with the onset of impaired electrophysiological function and neuropathological alterations. This suggests that the mechanism of acute SCI-induced structural and functional deficits are mediated by disruption of subcellular ion distribution. The ability of TTX to reduce elemental deregulation in compression-injured axons and neuroglia implicates a significant pathophysiological role for Na(+) influx in SCI and suggests Na(+) channel blockade as a pharmacotherapeutic strategy.

Animals↗
PubMedDate not supplied

A new type of biocompatible bridging structure supports axon regrowth after implantation into the lesioned rat optic tract.

We have developed a new type of polymer/cell/matrix implant and tested whether it can promote the regrowth of retinal ganglion cell (RGC) and other axons across surgically induced tissue defects in the CNS. The constructs, which consisted of 2-2.5-mm-long polycarbonate tubes filled with lens capsule-derived extracellular matrix coated with cultured neonatal Schwann cells, were implanted into lesion cavities made in the left optic tract (OT) of 18-21-day-old rats. In one group, to promote Schwann cell proliferation and perhaps also to stimulate axon regrowth, basic fibroblast growth factor (bFGF) was added to the lens capsule matrix prior to implantation. In another group, to determine whether application of growth factors to the somata of cells enhances the regrowth of distally injured axons, the neurotrophin NT-4/5 was injected into the eye contralateral to the OT lesion. NT-4/5 and bFGF treatments were combined in some rats. After medium-term (4-10 weeks) or long-term (15-20 weeks) survivals, axon growth into implants was assessed immunohistochemically using a neurofilament (RT97) antibody. RGC axons were visualized after injection of WGA/HRP into the right eye. Viable Schwann cells were present in implants at all times after transplantation. Large numbers of RT97+ axons were consistently found within the bridging implants, often associated with the peripheral glia. Axons were traced up to 1.7 mm from the nearest CNS neuropil and there was immunohistochemical evidence of myelination by Schwann cells and by host oligodendrocytes. There were fewer RGC axons in the implants, fibers growing up to 1.6 mm from the thalamus. Neither NT-4/5 nor bFGF, alone or in combination, significantly increased the extent of RGC axon growth within the implants. A group of OT-lesioned rats was implanted with polymer tubes filled with 2-2.5-mm-long pieces of predegenerate peripheral nerve. Surprisingly, polymer/cell/matrix constructs contained comparatively greater numbers of RGC and other axons and supported more extensive axon elongation. Thus, implants of this type may potentially be useful in bridging large tissue defects in the CNS.

Animals↗
PubMed1983

Unmyelinated axon subpopulations in the rat peripheral nervous system.

Using the neurotoxin capsaicin, we examined subpopulations of unmyelinated axons in mixed (sciatic), cutaneous (sural), and muscular (nerve to soleus) nerves. Administration of capsaicin to neonatal rats caused reduction of the sciatic nerve immunoreactive (IR)-substance P (by 45%) and IR-somatostatin (by 84%) contents. This correlated with a substantial reduction in unmyelinated axons in the sciatic and sural nerves (45% and 65%, respectively), although there was no significant decrease in unmyelinated axons in the nerve to soleus. In a parallel study, we have shown that sympathetic ganglia-derived unmyelinated axons account for about 20 to 25% of the total unmyelinated axon population in both the sural nerve and the nerve to soleus. Thus, in the sural nerve, the majority of unmyelinated axons are dorsal root ganglia-derived, contain either substance P or somatostatin, and are capsaicin-sensitive; whereas in the nerve to soleus, the majority of unmyelinated axons are dorsal root ganglia-derived but are insensitive to capsaicin and do not contain substance P or somatostatin. These latter unmyelinated axons presumably contain a yet to be defined neurotransmitter and may be the axons connecting with muscular ergoreceptors, a subpopulation of unmyelinated axons that are biochemically and functionally distinct from the unmyelinated axons of cutaneous nerves.

Animals↗
PubMed1991

Early ablation of target muscles modulates the arborisation pattern of an identified embryonic Drosophila motor axon.

The Drosophila RP3 motor axon establishes a stereotypic arborisation along the adjoining edges of muscles 6 and 7 by the end of embryogenesis. The present study has examined the role of the target muscles in determining this axonal arborisation pattern. Target muscles were surgically ablated prior to the arrival of the RP3 axon. Following further development of the embryo in culture medium, the morphology of target-deprived RP3 motor axons was assayed by intracellular injection with the dye Lucifer Yellow. Axonal arborisations were formed on a variety of non-target muscles when muscles 6 and 7 were removed and these contacts were maintained into stage 16. The pattern of axonal arborisations over non-target muscles varied between preparations in terms of the number of muscles contacted, and the distribution of arborisations on individual muscles. Following removal of muscle 6, the RP3 motor axon frequently contacted muscle 7, and axonal arborisations were present along the distal edge of the muscle. In the absence of muscle 7, the RP3 axon often did not contact muscle 6 and when muscle 6 was contacted, the arborisation of RP3 was poorly developed. Axonal processes were retained on non-target muscles when only one target muscle was present. Therefore, the establishment of a stereotypic arborisation by the RP3 motor axon is apparently dependent on growth cone contact with both target muscles.

Animals↗
PubMed2000

brakeless is required for lamina targeting of R1-R6 axons in the Drosophila visual system.

Photoreceptors in the Drosophila eye project their axons retinotopically to targets in the optic lobe of the brain. The axons of photoreceptor cells R1-R6 terminate in the first optic ganglion, the lamina, while R7 and R8 axons project through the lamina to terminate in distinct layers of the second ganglion, the medulla. Here we report the identification of the gene brakeless (bks) and show that its function is required in the developing eye specifically for the lamina targeting of R1-R6 axons. In mosaic animals lacking bks function in the eye, R1-R6 axons project through the lamina to terminate in the medulla. Other aspects of visual system development appear completely normal: photoreceptor and lamina cell fates are correctly specified, R7 axons correctly target the medulla, and both correctly targeted R7 axons and mistargeted R1-R6 axons maintain their retinotopic order with respect to both anteroposterior and dorsoventral axes. bks encodes two unusually hydrophilic nuclear protein isoforms, one of which contains a putative C(2)H(2) zinc finger domain. Transgenic expression of either Bks isoform is sufficient to restore the lamina targeting of R1-R6 axons in bks mosaics, but not to retarget R7 or R8 axons to the lamina. These data demonstrate the existence of a lamina-specific targeting mechanism for R1-R6 axons in the Drosophila visual system, and provide the first entry point in the molecular characterization of this process.

Amino Acid Sequence↗
PubMed2006

RhoA-kinase coordinates F-actin organization and myosin II activity during semaphorin-3A-induced axon retraction.

Axon guidance is mediated by the effects of attractant and repellent guidance cues on the cytoskeleton of growth cones and axons. During development, axon retraction is an important aspect of the pruning of inappropriately targeted axons in response to repellent guidance cues. I investigated the roles of RhoA-kinase and myosin II in semaphorin-3A-induced growth cone collapse and axon retraction. I report that semaphorin 3A activates myosin II in growth cones and axons. Myosin II activity is required for axon retraction but not growth cone collapse. Furthermore, semaphorin 3A promotes the formation of intra-axonal F-actin bundles in concert with the loss of F-actin in growth cone lamellipodia and filopodia. Formation of axonal F-actin bundles was independent of myosin II, but partially required RhoA-kinase activity. Conversely, RhoA-kinase activity was required to shut down F-actin polymerization underlying protrusive activity. Collectively, these observations suggest that guidance cues cause axon retraction through the coordinated activation of myosin II and the formation of intra-axonal F-actin bundles for myosin-II-based force generation. I suggest that in the context of semaphorin 3A signaling, RhoA-kinase serves as a switch to change the function of the F-actin cytoskeleton from promoting protrusive activity to generating contractile forces.

Actin Cytoskeleton↗
PubMed1990

In vitro experiments on axonal guidance and growth-cone collapse.

In the retinotectal projection, nasal retinal axons project to posterior tectum, while temporal axons project to the anterior part of the tectum. In in vitro experiments, a similar specificity can be observed: the nasal and temporal retinal axons can be guided by tectal membrane components so that, for example, temporal retinal axons, when growing on a striped substratum consisting of anterior and posterior tectal membranes, express a very strong preference for the anterior stripes. This preference is not due to attractivity of anterior membranes but rather to avoidance of posterior material, although the pure posterior membranes are a very good substratum for growth of temporal axons. The repellent guidance molecule has been identified. Interestingly, besides guidance this molecule causes another reaction: when growing temporal axons are exposed to medium containing either posterior membranes or artificial lipid vesicles containing the repellent guidance molecule, the axonal growth cones collapse. As in guidance, there is a clear regional specificity: e.g. the repellent guidance molecule derived from posterior tectum induces collapse of temporal but not of nasal axons. Since the guiding and the collapse-inducing activity are expressed by one and the same glycoprotein molecule (Mr 33 x 10(3), linked to the membrane by phosphatidylinositol) and since another molecule has been identified by Keynes' group which also expresses both guiding and collapse-inducing activity, one might speculate that axonal guidance and axonal collapse have something in common. Models of axonal guidance will be discussed.

Animals↗
PubMed1980

Electrophysiological and pharmacological properties of glial cells associated with the medial giant axon of the crayfish with implications four neuron-glial cell interactions.

Schwann-like glial cells surrounding the medial giant axon of the crayfish (Procambarus clarkii) were impaled with glass microelectrodes to study their responses to cholinomimetics, cholinergic receptor blockers and ouabain. Axon electrical properties were simultaneously monitored. Glial cells have a low membrane potential compared to the axon; -42 mV and -85 mV, respectively. Acetylcholine, carbachol and nicotine hyperpolarized the glial cells but did not affect the axon steady-state or active membrane potentials. The action of the cholinergics was completely blocked by d-tubocurarine and alpha-bungarotoxin. Ouabain hyperpolarized the glial cell but depolarized the axon. Tubocurarine blocked the ouabain hyperpolarization but not the delayed depolarization of the glia cell or the axon. It is concluded that ouabain causes the release of acetylcholine from the glial cell-axon preparation, inducing the glial hyperpolarization. Studies of the axon-glial cell interaction suggest that a function of the glial cell is to actively modulate the periaxonal potassium concentration on a signal from the axon. Periaxonal potassium can strongly affect axon membrane potential through electrogenic Na transport, modifying axon signalling properties.

Animals↗
PubMed1999

Intrinsic determinants of retinal axon collateralization and arborization patterns.

Permanent, novel retinal projections to the principal thalamic somatosensory (ventrobasal) or auditory (medial geniculate) nuclei can be produced in adult hamsters if the superior colliculus is ablated bilaterally and the somatosensory and auditory lemniscal axons are transected unilaterally on the day of birth. We studied the development of those novel projections by labeling retinal axons with the fluorescent tracer 1,1'-dioctadecyl-3,3,3', 3'-tetramethylindocarbocyanine perchlorate to examine the relative roles of intrinsic factors and axon-target interactions in the specification of retinal axon connections. Our principal findings are as follows: (1) In hamsters operated on the day of birth to produce the novel retinal projections, retinal ganglion cell axons projecting to the ventrobasal or medial geniculate nuclei develop in three morphologically distinct stages, i.e., elongation, collateralization, and arborization, as do retinal axons projecting to the dorsal lateral geniculate nucleus, the principal thalamic visual nucleus, in normal hamsters. (2) In both the ventrobasal and medial geniculate nuclei of operated hamsters, as in the dorsal lateral geniculate nucleus of normal hamsters, collateral branches were initially formed by retinal ganglion cell axons in both the superficial and internal components of the optic tract and only collaterals from the superficial component formed permanent projections. (3) The retinofugal axon terminal arbors in the ventrobasal and medial geniculate nuclei of mature, operated hamsters resemble the same three morphologic classes that are observed in the lateral geniculate nucleus of normal hamsters, although their absolute size appears to be altered. These data suggest that both superficial and internal optic tract axons can produce thalamic collaterals during development but that only superficial optic tract axons can permanently retain thalamic collaterals. Furthermore, the same morphologic types of retinofugal axons appear to contribute to normal and surgically induced retinal projections.

Animals↗
PubMed1999

Morphology of single olivocerebellar axons labeled with biotinylated dextran amine in the rat.

The morphology of olivocerebellar (OC) axons originating from the inferior olive (IO) was investigated in the rat by reconstructing the entire trajectories of single axons that had been labeled with biotinylated dextran amine. Virtually all of the OC axons entered the cerebellum through the inferior cerebellar peduncle (ICP) contralateral to the IO, with a few exceptions. Although most OC projection was contralateral, a few axons projected bilaterally by crossing the midline within the cerebellum. Collaterals of OC axons could be classified into thick branches and thin collaterals. Thick branches of each OC axon (6.1 +/- 3.7/OC axon, mean +/- SD for n = 16 axons) terminated as climbing fibers (CFs) on single Purkinje cells (PCs) in a one-to-one relationship. Besides terminal arborization around PC thick dendrites, CFs had terminals that surrounded a PC soma, fine branchlets that extended transversely in the molecular layer, and thin retrograde collaterals that re-entered the PC and granular layers. Innervation of a single PC by two CFs originating from the same axon was seen, although infrequently. Concerning thin collaterals, about half of the OC axons had one or only a few collaterals terminating in the white matter of the ICP, most had 1 to 6 collaterals terminating in a single cerebellar nucleus, and all had 3 to 16 collaterals that terminated mainly in the granular layer, but occasionally in the cerebellar white matter and the PC layer. Some swellings of thin collaterals touched somata of presumed Golgi cells and PCs. No OC axons terminated solely in the ICP, cerebellar nucleus or granular layer without giving rise to CFs.

Animals↗
PubMed2000

Stabilization of growing retinal axons by the combined signaling of nitric oxide and brain-derived neurotrophic factor.

The pattern of axonal projections early in the development of the nervous system lacks the precision present in the adult. During a developmental process of refinement, mistargeted projections are eliminated while correct projections are retained. Previous studies suggest that during development nitric oxide (NO) is involved in the elimination of mistargeted retinal axons, whereas brain-derived neurotrophic factor (BDNF) may stabilize retinal axon arbors. It is unclear whether these neuromodulators interact. This study showed that NO induced growth cone collapse and retraction of developing retinal axons. This effect was not attributable to NO-induced neurotoxicity. BDNF protected growth cones and axons from the effects of NO. This effect was specific to BDNF, because neither nerve growth factor (NGF) nor neurotrophin-3 (NT-3) prevented NO-induced growth cone collapse and axon retraction. Exposure to both BDNF and NO, but not either factor alone, stabilized growth cones and axons. Stabilized axons exhibited minimal retraction or extension. This response appears to be a new axon "state" and not simply a partial amelioration of the effect of NO, because lower doses of BDNF or NO allowed axon extension. Furthermore, BDNF/NO-induced growth cone stabilization correlated with the appearance of a cytochalasin D-resistant population of actin filaments. BDNF protection from NO likely was mediated locally at the level of the growth cone, because growth cones or individual filopodia in contact with BDNF-coated beads were protected from NO-induced collapse. These findings suggest a cellular mechanism by which some axonal connections are stabilized and some are eliminated during development.

Animals↗
PubMed2000

Thalamic terminal fields of individual axons from the ventral part of the dentate nucleus of the cerebellum in Macaca mulatta.

This study examined organization of the projection from the dentate nucleus of the cerebellum to the ventral lateral nucleus (VL) of the thalamus in Macaca mulatta. Small injections of biotinylated dextran amine were placed in the ventral parts of dentate nuclei. The distribution of all contralateral terminal fields in the thalamus was charted, and representative individual axons that terminated in the VL were traced in serial sections under the light microscope. These axons were reconstructed with all their branches and terminal fields in the thalamus. The geometry and size of the terminal fields as well as the number and distribution of boutons and neurons in them were analyzed. The terminal fields of all labeled axons were distributed widely over the VL either singly or in clusters. Two types of axons were found: simple axons formed only one terminal field and complex axons formed multiple terminal fields at a distance. Individual terminal fields were focal, had the form of flattened discs, and generated up to 200 boutons distributed between 10 and 29 nerve cell bodies. These findings suggest that a simple axon activates a small group of neurons at one site. The complex axons, in turn, influence similar size cell groups at different VL locations. The total number of boutons generated by a single complex axon was up to 300. Future studies should determine whether simple axons could be branches of complex axons that took off below the thalamus. The results reveal a complex organization of the input from the ventral dentate to the VL that only partially fits into the traditional concept of somatotopic organization of the nucleus.

Animals↗