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PubMed2004

Differential effects of Rho GTPases on axonal and dendritic development in hippocampal neurones.

Formation of neurites and their differentiation into axons and dendrites requires precisely controlled changes in the cytoskeleton. While small GTPases of the Rho family appear to be involved in this regulation, it is still unclear how Rho function affects axonal and dendritic growth during development. Using hippocampal neurones at defined states of differentiation, we have dissected the function of RhoA in axonal and dendritic growth. Expression of a dominant negative RhoA variant inhibited axonal growth, whereas dendritic growth was promoted. The opposite phenotype was observed when a constitutively active RhoA variant was expressed. Inactivation of Rho by C3-catalysed ADP-ribosylation using C3 isoforms (Clostridium limosum, C3(lim) or Staphylococcus aureus, C3(stau2)), diminished axonal branching. By contrast, extracellularly applied nanomolar concentrations of C3 from C. botulinum (C3(bot)) or enzymatically dead C3(bot) significantly increased axon growth and axon branching. Taken together, axonal development requires activation of RhoA, whereas dendritic development benefits from its inactivation. However, extracellular application of enzymatically active or dead C3(bot) exclusively promotes axonal growth and branching suggesting a novel neurotrophic function of C3 that is independent from its enzymatic activity.

ADP Ribose Transferases↗
PubMed1994

Effects of prenatal exposure to ethanol on the number of axons in the pyramidal tract of the rat.

We examined the effect of gestational ethanol exposure on the number of axons in the caudal pyramidal tract. Between gestational day (G) 6 and G21, inclusive, pregnant rats were fed a liquid ethanol-containing diet (Et), an isocaloric liquid control diet (Ct), or a diet of chow and water (Ch). On postnatal day 30, the offspring of these rats were killed and their caudal medullas were processed for electron microscopy. The overall size of the pyramidal tract and the space occupied by the axons was smaller in the Et-treated rats than in the Ct-treated rats. The myelinated axons were smaller and the myelin was thinner in the Et-treated rats than in the Ct-treated rats. These decreases produced an ethanol-induced increase in the density of axons in the pyramidal tract. In particular, the density of myelinated axons (but not nonmyelinated axons) was greater in Et-treated rats. The net result was that the estimated number of axons in the pyramidal tracts of the Et-treated rats was not significantly different than the number in the Ch- and Ct-treated rats. The present data demonstrate that ethanol does not affect the absolute number of axons in the pyramidal tract. As a result of the ethanol-induced microencephaly, however, the data translate into a relative increase in the number of pyramidal tract axons. This relative increase matches the ethanol-induced increase in the density of corticospinal projection neurons that may result from the retention of a developmentally exuberant projection.

Animals↗
PubMed2006

Ultrastructural study of extraocular muscle tendon axonal profiles in infantile and intermittent exotropia.

PURPOSE: To investigate the ultrastructures of tendon axonal profiles in infantile and intermittent exotropia. Tendon axonal profiles are composed of myotendinous nerve endings that are presumed to serve as sensorial receptors in ocular proprioception. METHODS: The study subjects included 10 patients with exotropia who had undergone surgery in one eye (recession and resection). They were divided into two equal groups. Five patients with infantile exotropia that had developed at under 12 months of age were allocated to group A. Another five, with intermittent exotropia that had developed at over 12 months of age, were allocated to group B. In all patients, medial recti were resected by 3-4 mm in order to obtain tissue samples, which were then examined under an electron microscope. RESULTS: In group A, we noted many axonal degenerative findings, such as the retraction of axons from myelin sheaths with considerable shrinkage, axonal disintegration, and Schwann cell proliferation. On the other hand, we identified three unique findings in group B: intact axons with incomplete Schwann cell wrapping; intact Schwann cells not associated with axons, and disorganized Schwann cells with shrunken axons. CONCLUSION: Different patterns of tendon axonal profiles were seen in association with the two types of exotropia. These differences may be related to the pathogenesis of these exotropia types.

Age of Onset↗
PubMed1993

Sabeluzole administration does not enhance fast axonal transport in normal adult rat sciatic nerve.

Sabeluzole (R58735, Janssen Research Foundation) increased rates of axonal transport in short term tissue culture experiments and in rats with streptozotocin-induced diabetes. The drug was tested for its subacute (3 days) net effect on axonally transported substances in motor, sensory, and adrenergic axons of normal adult rats. Sabeluzol was given once daily for 3 days, 1 or 10 mg/kg/day intraperitoneally. Immunofluorescence was used to identify transported material. Three or 6 hr after crushing the sciatic nerves, to interrupt anterograde and retrograde intraaxonal transport, cytofluorimetric scanning was used to quantitate accumulated immunoreactive material. Compared with vehicle treated control rats, no clear differences in the net amounts of accumulated material, or in rates of accumulation, were detected in any axonal type. Since the short-term crush procedure interrupts ongoing axonal transport, the accumulation pattern reflects the transport characteristics in the crushed axons. The absence of clear increases in transport of several substances in this study indicates that sabeluzole did not enhance net axonal transport above control levels in peripheral axons of normal adult rats. Possible reasons for the discrepancy with earlier observations on the effect of sabeluzole on fast axonal transport is discussed.

Animals↗
PubMed1998

Accumulation of immunoreactivity to ubiquitin carboxyl-terminal hydrolase PGP 9.5 in axons of human cases with spinal cord lesions.

The protein gene product PGP 9.5 is one of the major polypeptides in neurons. It can act as a ubiquitin carboxyl-terminal hydrolase in ubiquitin-mediated degradation of proteins. The present study was performed to find out if human cases with spinal cord trauma present immunohistochemical signs of PGP 9.5 accumulation in injured axons known to accumulate ubiquitin. For comparison, we used six autopsy cases without spinal cord pathology, one case with syringomyelia, one case with ischaemic injury of the cord, and six ALS cases. Controls presented PGP 9.5-immunostained axons of weak to moderate intensity in the longitudinal tracts. Immunoreactivity was not detected in nerve cell bodies, glial cells or axons of the grey matter. All nine trauma cases showed axonal swellings, but their numbers varied. Intensely immunostained axonal swellings were particularly abundant in cases with a survival period up to 1 month after trauma. Strongly immunoreactive axons were present also in the cases with infarct and syringomyelia. In conclusion, human cases with spinal cord trauma and other focal injuries present signs of PGP 9.5 accumulation in severed axons possibly resulting from disturbed axonal transport. PGP 9.5 thus seems to be present and may take part in ubiquitin-mediated degradation of proteins in injured axons of the spinal cord.

Adult↗
PubMed1992

Diversity and homogeneity within endplates associated with physiologically identified static gamma-axons in cat tenuissimus muscle.

The terminations of static gamma-axons on chain fibres may be associated with a muscle surface contour thrown into complex folds at one extreme, ranging through lesser degrees of folding to being apparently uninfluenced by the presence of the terminals. The folding is not necessarily confined to the postsynaptic membrane. As a quantitative indicator of the degree of folding seen in cross-sections, the perimeters of the two halves of the intrafusal fibre with, and without the ending were compared. Both complexity of endplate structure and an undifferentiated appearance could co-exist within individual endings (of six static gamma-axons on thirteen chain fibres), associated with axons that supplied only chain fibres in the spindle isolated. (It should be noted, however, that the type of intrafusal fibres innervated by a particular axon was definitively identified only for the spindle isolated.) Endings of three other static gamma-axons on six chain fibres had a more homogeneous and less complex endplate structure; these supplied bag2 fibres in addition to the chain fibres and their endplates on the bag2 fibres were less folded than those of three axons which supplied bag2 fibres only. A sensory inhibitory influence on folding was not apparent because complexly folded endplates on chain fibres lay close (less than 500 microns) to sensory endings. All the endings studied were functional. In our experimental conditions all nine static gamma-axons which innervated chain fibres, alone, or together with a bag2 fibre, drove the Ia afferent at some stimulus frequencies; none of the three static gamma-axons innervating bag2 fibres alone caused driving at any frequency. These findings are discussed in relation to the concept of a dynamic remodelling of ending structure during life, to the relationship between the motor axon and the intrafusal fibre it innervates, and to the possibility that subgroups of static gamma-motoneurones might exist which could release different amounts of the trophic substances responsible for moulding the endplate structure.

Animals↗
PubMed1975

Functional and structural changes in mammalian sympathetic neurones following interruption of their axons.

The effects of interrupting the axons of principal neurones in the superior cervical ganglion of adult guinea-pigs were studied by means of intracellular recording, and light and electron microscopy. 1. Within 72 hr of axon interruption, the amplitude of exitatory postsynaptic potentials potentials (e.p.s.p.s) recorded in principal neurons in response to maximal preganglionic stimulation declined. E.p.s.p.s were maximally reduced (by more than 70% on average) 4-7 days following interruption, and failed to bring many cells to threshold. E.p.s.p.s. recorded in nearby neurones whose axons remained intact were unaffected. 2. In ganglia in which axon interruption was achieved by means of nerve crush (thus allowing prompt regeneration), mean e.p.s.p. amplitudes began to increase again after about 1-2 weeks. One month after the initial injury many neurones had e.p.s.p.s of normal amplitude, and by 2 months affected neurones were indistinguishable from control cells. Functional peripheral connexions were re-established during the period of synaptic recovery. 3. The mean number of synapses identified electron microscopically in ganglia in which all the major efferent branches had been crushed decreased by 65-70% in parallel with synaptic depression measured by intracellular recording. However synapse counts did not return to normal levels even after 3 months. 4. During the period of maximum synaptic depression, numerous abnormal profiles which contained accumulations of vesicular and tubular organelles, vesicles, and mitochondria were observed in electron microscopic sections. Injection of horseradish peroxidase into affected neurones demonstrated dendritic swelling which probably correspond to these profiles. 5. Little or no difference was found in the electrical properties of normal neurones and neurones whose axons had been interrupted 4-7 days previously. However, the mean amplitude of spontaneously occurring synaptic potentials was reduced, and the amplitude distribution was shifted. This abnormality of the synapses which remain on affected neurones also contributes to synaptic depression. 6. Counts of neurones in normal and experimental ganglia showed that approximately half the principal cells died 1-5 weeks after crushing the major efferent brances. This finding presumably explains the failure of synapse counts to return to control levels after recovery. 7. If axons were prevented from growing back to their target organ by chronic ligation, surviving neurones whose axons were enclosed by the ligature did not generally recover normal synaptic function. Following ligation, most affected cells died within a month. 8. Thus the integrity of a principal cell's axon is necessary for the maintenance of preganglionic synaptic contacts, and ultimately for neuronal survival. The basis of neuronal recovery from the effects of axon interruption appears to be some aspect of regeneration to the peripheral target.

Animals↗
PubMed1978

The influence of extracellular calcium binding on the calcium efflux from squid axons.

1. The Ca efflux from unpoisoned squid axons seems to consist of three components: Cao-dependent Ca efflux and a 'residual' flux that persists in the nominal absence of external Ca and Na and is little affected by the further removal of external Mg. 2. Evidence is presented to show that much of the apparent dependence on Cao of the Ca efflux from unpoisoned axons probably does not reflect a membrane process but results instead from the existence of a Ca-binding matrix external to the plasma membrane. Removal of external Ca produces a fall in efflux which is not maintained but returns to its original level over 20-60 min. Readmission of Ca produces only a transient increase in Ca efflux. Addition of EGTA to nominally Ca-free media also produces only a transient rise in Ca efflux. 3. Direct measurement of Ca binding to the surface of highly cleaned axons reveals appreciable binding over a wide range of Ca concentrations. A high affinity component of superficial binding can be recognized which has a capacity of about 60 p-mole/cm2 axon membrane and is half-maximal about 0.3 micrometer-Ca in Na-ASW. This component of binding is unaltered in cyanide-poisoned axons and in media in which Na is replaced isosmotically by Tris; but is reduced in the presence of 1 mM-La or after brief exposure of the axon to pronase. There is also a component of large capacity and lower affinity which was not saturated by 100 mM-Cao. 4. After brief pronase treatment the sensitivity of the Ca efflux to external Ca is markedly reduced although the Na-dependent Ca efflux persists apparently unaltered. 5. Addition of La produces a transient increase in Ca efflux followed by a maintained fall. 300 micrometer-La largely inhibits the component of the Ca efflux that persists in the nominal absence of external Na and Ca. Higher concentrations of La also inhibit Nao-dependent Ca efflux. 6. The Cao-dependent Ca efflux and Nao-dependent Ca efflux seen in poisoned axons persist in the presence of EGTA or after pronase treatment, suggesting that both are genuine membrane processes. 7. We conclude that in unpoisoned axons 50-90% of the Ca efflux can continue in the absence of external Ca, Na and Mg and may reflect an uncoupled extrusion of Ca. Most of the remaining efflux from these axons is Nao-dependent although a small Cao-dependent component can be distinguished in the absence of Na. Poisoning results in the loss of uncoupled Ca efflux, the appearance of appreciable Cao-dependent Ca efflux and alteration in the kinetics of Nao-dependent Ca efflux.

Animals↗
PubMed1986

Interaction between the soma and the axon terminal of retinal horizontal cells in Cyprinus carpio.

Intracellular recordings were made from the monophasic horizontal cells of the carp retina which are known to respond with a sustained hyperpolarization to all visible monochromatic light. The receptive field of each subcellular structure, the soma and the axon terminal, was determined using a long narrow slit of light. Somata and axon terminals showed receptive fields that encompassed almost the entire retina. This observation suggests that each aggregate of the subcellular parts forms a synctial structure. However, with increasing distance from the slit, the response peak decayed more steeply in somata than in axon terminals. The spatial decline of the peak consisted of two exponential functions in somata, while a single exponential function in axon terminals. The length constant of the axon terminal was similar to the larger length constant revealed in the soma. This finding suggests an electrical communication at work between the soma and the axon terminal. A quantitative account was made in light of a discrete resistive network model which consists of a pair of syncytia coupled through connecting axons; one represents the contiguous layer of somata and the other the contiguous layer of axon terminals. Relevant response properties computed from the model analysis were in satisfactory agreement with experimental data. It was concluded that the soma and the axon terminal of the horizontal cell are electrically connected in the cyprinid retina.

Animals↗
PubMed1987

Comparison of the after-effects of impulse conduction on threshold at nodes of Ranvier along single frog sciatic axons.

1. Single axons were teased from the distal end of whole frog sciatic nerve and impulses were recorded with a suction electrode. The whole nerve trunk was stimulated using a gross electrode that was slowly moved for several centimetres along the length of the nerve. The threshold for initiation of an action potential showed periodic minima which were interpreted as the location of nodes of Ranvier. 2. Internodal distances were uniform along individual fibres but differed among fibres having matching conduction velocities, suggesting that other individuating characteristics are also important in determining the spacing of nodes. 3. A standard protocol was used to measure the activity dependence of threshold. Nodes along any given fibre were found to be alike in the dependence of threshold on impulse activity. Both the superexcitable phase and the depressed phase of the after-effects of impulse activity were similar for successive nodes. This suggests that the activity dependence of an unbranched length of axon can be well characterized by looking at any one of its nodes. 4. Comparison of nodes from different axons showed large variations in activity dependence. Depressibility, denoting the relative tendency of an axon to show depression, was quantified either as the initial rate of rise in threshold (percentage increase/min) following the onset of repetitive stimulation or as the total rise in threshold (percentage increase) after 5 min of exposure to a standardized rate of repetitive stimulation. By either measure depressibility differed among axons more than it differed among nodes from a single axon. 5. Superexcitability following single impulses was measured in the absence of depression. Axons exhibiting a larger decrease in threshold during the superexcitable phase also tended to show larger depressions relative to other axons when stimulated at a given rate. 6. There was little correlation between conduction velocity and the magnitude of either the depressed phase or the superexcitable phase within the population of fibres studied. This suggests that axon diameter alone (as indicated by conduction velocity) cannot be responsible for the wide variations in the amplitude of the depressed phase or the superexcitable phase. 7. The results suggest that some process exists to constrain the nodes along a fibre to have a uniform activity dependence.

Action Potentials↗
PubMed1987

The extensibility of Aplysia nerve and the determination of true axon length.

1. Characteristics of Aplysia nerves in response to extension were examined in comparison with nerves of the cat, frog and lobster. 2. Only the Aplysia nerve was easily elongated up to about 5 times its resting or relaxing length without impairing propagation of the action potential along the axon in the nerve. 3. The conduction velocity along the elongated nerve increased linearly in proportion to the nerve length in the range from the relaxing length to about 1.2-1.5 times extension (the first phase). However, upon further extension it stayed constant regardless of the nerve length (the second phase). 4. In the relaxed nerve bundle the course of the axons was zigzagging and the axon membrane had numerous foldings or wrinklings. 5. The true length of the zigzagging axon was measured by analysing the length of intra-axonal diffusion following intracellular injection of radioactive acetylcholine ([3H]ACh) whose diffusion kinetics in the axoplasm have been studied in detail (Koike & Nagata, 1979). The length of the axon coincided with the nerve length at which the first phase shifted to the second phase. 6. Cat and frog nerves shrank after dissecting out from the body. When extended, they showed the first phase from the shortened length to their original length in the body. These nerves lacked the second phase. The lobster nerve did not shrink and lacked both phases. 7. Thus the zigzagging course of the axon is suggested to be responsible for the first phase during which the axon length did not change but took a straight course upon nerve extension. 8. On the other hand, the second phase appears to be caused by actual extension of the axon itself and could be explained by reduction of the wrinklings of the membrane.

Action Potentials↗
PubMed1989

Depolarization changes the mechanism of accommodation in rat and human motor axons.

1. We have previously studied accommodation in rat and human motor axons by testing excitability with combinations of long and short current pulses. We found that normally polarized axons accommodate slowly and partially (over about 50 ms) to subthreshold depolarizing currents, and that the principal mechanism is the activation of slow potassium channels (Bostock & Baker, 1988). To understand the response of human nerves to ischaemia, we have now extended these observations to axons already depolarized before the testing currents were applied. 2. Rat ventral root axons were depolarized by passing continuous currents or by raising the extracellular potassium concentration. Human forearm nerves were depolarized by ischaemia, induced by inflating a sphygmomanometer cuff on the upper arm. Depolarized rat and human motor axons accommodated much more rapidly and completely than normally polarized axons (e.g. accommodation in rat axons was 50% complete within 2 ms at about 15 mV depolarized to rest). 3. The fast component of accommodation in depolarized rat fibres was not blocked by tetraethylammonium ions or 4-aminopyridine, was not accompanied by a conductance or potential change, and had a time constant of 1.7 ms at 30 degrees C. It was attributed to inactivation of closed sodium channels. 4. In depolarized rat fibres exhibiting fast accommodation, a brief rise in excitability was seen at the break of an anodal current. Our prediction that human motor axons would show anode-break excitation during ischaemia was readily confirmed. 5. The results are discussed in relation to Hill's (1936) mathematical description of accommodation in nerve, and it is concluded that his description is only applicable to depolarized axons.

Action Potentials↗
PubMed2004

Differences in activity-dependent hyperpolarization in human sensory and motor axons.

The present study was undertaken to determine whether activity-dependent changes in axonal excitability are greater in motor axons than cutaneous afferents for the same impulse load. In nine healthy subjects, supramaximal stimulation at 8 Hz was delivered to the median nerve at the wrist. Changes in the threshold current required to generate compound motor and sensory potentials approximately 50% of maximum and other indices of axonal excitability were tracked before and after repetitive stimulation for 10 min. The long-lasting stimulation produced a prolonged depression in the excitability of both cutaneous afferents and motor axons, with gradual recovery to control levels over 15-20 min. These changes in threshold were associated with a reduction in refractoriness, an increase in supernormality and a decrease in the strength-duration time constant, changes consistent with axonal hyperpolarization. Greater changes in threshold occurred in motor axons: threshold increased by 9.9% and 16.4% for test stimulus durations of 0.1 and 1 ms, respectively, for motor axons and by 5.4% and 8.3% for cutaneous afferents. With higher stimulus frequencies and thereby greater impulse loads, greater threshold changes could be induced in cutaneous afferents. It is argued that the hyperpolarization resulted from activity of the electrogenic Na(+)-K+ pump, that it requires > 125 ms to restore the resting state following an action potential, and that significant intracellular Na+ accumulation occurs during a steady 8-Hz train. These findings imply that physiological discharge rates will activate the pump and thereby produce axonal hyperpolarization, the extent of which will vary with impulse load. A plausible explanation is that greater activity-dependent hyperpolarization in motor axons is due to less inward rectification as a result of less activity of the hyperpolarization-activated cation conductance (IH) than in cutaneous afferents.

Action Potentials↗
PubMed2006

Kv7/KCNQ/M-channels in rat glutamatergic hippocampal axons and their role in regulation of excitability and transmitter release.

M-current (I(M)) plays a key role in regulating neuronal excitability. Mutations in Kv7/KCNQ subunits, the molecular correlates of I(M), are associated with a familial human epilepsy syndrome. Kv7/KCNQ subunits are widely expressed, and I(M) has been recorded in somata of several types of neurons, but the subcellular distribution of M-channels remains elusive. By combining field-potential, whole-cell and intracellular recordings from area CA1 in rat hippocampal slices, and computational modelling, we provide evidence for functional M-channels in unmyelinated axons in the brain. Our data indicate that presynaptic M-channels can regulate axonal excitability and synaptic transmission, provided the axons are depolarized into the I(M) activation range (beyond approximately -65 mV). Here, such depolarization was achieved by increasing the extracellular K(+) concentration ([K(+)](o)). Extracellular recordings in the presence of moderately elevated [K(+)](o) (7-11 mm), showed that the specific M-channel blocker XE991 reduced the amplitude of the presynaptic fibre volley and the field EPSP in a [K(+)](o)-dependent manner, both in stratum radiatum and in stratum lacknosum moleculare. The M-channel opener, retigabine, had opposite effects. The higher the [K(+)](o), the greater the effects of XE991 and retigabine. Similar pharmacological modulation of EPSPs recorded intracellularly from CA1 pyramidal neurons, while blocking postsynaptic K(+) channels with intracellular Cs(+), confirmed that active M-channels are located presynaptically. Computational analysis with an axon model showed that presynaptic I(M) can control Na(+) channel inactivation and thereby affect the presynaptic action potential amplitude and Ca(2+) influx, provided the axonal membrane potential is sufficiently depolarized. Finally, we compared the effects of blocking I(M) on the spike after-depolarization and bursting in CA3 pyramidal neuron somata versus their axons. In standard [K(+)](o) (2.5 mm), XE991 increased the ADP and promoted burst firing at the soma, but not in the axons. However, I(M) contributed to the refractory period in the axons when spikes were broadened by a low dose 4-aminopyridine (200 microm). Our results indicate that functional Kv7/KCNQ/M-channels are present in unmyelinated axons in the brain, and that these channels may have contrasting effects on excitability depending on their subcellular localization.

4-Aminopyridine↗
PubMed2005

Heterogeneity of a fluorescent tegument component in single pseudorabies virus virions and enveloped axonal assemblies.

The molecular mechanisms responsible for long-distance, directional spread of alphaherpesvirus infections via axons of infected neurons are poorly understood. We describe the use of red and green fluorescent protein (GFP) fusions to capsid and tegument components, respectively, to visualize purified, single extracellular virions and axonal assemblies after pseudorabies virus (PRV) infection of cultured neurons. We observed heterogeneity in GFP fluorescence when GFP was fused to the tegument component VP22 in both single extracellular virions and discrete puncta in infected axons. This heterogeneity was observed in the presence or absence of a capsid structure detected by a fusion of monomeric red fluorescent protein to VP26. The similarity of the heterogeneous distribution of these fluorescent protein fusions in both purified virions and in axons suggested that tegument-capsid assembly and axonal targeting of viral components are linked. One possibility was that the assembly of extracellular and axonal particles containing the dually fluorescent fusion proteins occurred by the same process in the cell body. We tested this hypothesis by treating infected cultured neurons with brefeldin A, a potent inhibitor of herpesvirus maturation and secretion. Brefeldin A treatment disrupted the neuronal secretory pathway, affected fluorescent capsid and tegument transport in the cell body, and blocked subsequent entry into axons of capsid and tegument proteins. Electron microscopy demonstrated that in the absence of brefeldin A treatment, enveloped capsids entered axons, but in the presence of the inhibitor, unenveloped capsids accumulated in the cell body. These results support an assembly process in which PRV capsids acquire a membrane in the cell body prior to axonal entry and subsequent transport.

Animals↗
PubMed2002

Corticostriatal combinatorics: the implications of corticostriatal axonal arborizations.

The complete striatal axonal arborizations of 16 juxtacellularly stained cortical pyramidal cells were analyzed. Corticostriatal neurons were located in the medial agranular or anterior cingulate cortex of rats. All axons were of the extended type and formed synaptic contacts in both the striosomal and matrix compartments as determined by counterstaining for the mu-opiate receptor. Six axonal arborizations were from collaterals of brain stem-projecting cells and the other 10 from bilaterally projecting cells with no brain stem projections. The distribution of synaptic boutons along the axons were convolved with the average dendritic tree volume of spiny projection neurons to obtain an axonal innervation volume and innervation density map for each axon. Innervation volumes varied widely, with single axons occupying between 0.4 and 14.2% of the striatum (average = 4%). The total number of boutons formed by individual axons ranged from 25 to 2,900 (average = 879). Within the innervation volume, the density of innervation was extremely sparse but inhomogeneous. The pattern of innervation resembled matrisomes, as defined by bulk labeling and functional mapping experiments, superimposed on a low background innervation. Using this sample as representative of all corticostriatal axons, the total number of corticostriatal neurons was estimated to be 17 million, about 10 times the number of striatal projection neurons.

Animals↗
PubMed1980

Glycogen-depletion method of intrafusal distribution of gamma-axons that increase sensitivity of spindle secondary endings.

1. The glycogen-depletion method was used in cat tenuissimus muscles to investigate whether the action of static gamma-axons that increase the sensitivity of spindle secondary endings to muscle length is associated with a specific pattern of distribution of these axons to intrafusal muscle fibers. 2. In each experiment, a single gamma-axon acting on a secondary ending of a precisely located spindle was repetitively stimulated, and subsequently the intrafusal muscle fibers of that spindle were examined for glycogen depletion. 3. The gamma-axons whose repetitive stimulation increased the length sensitivity of secondary endings depleted all the chain fibers in one or both poles of the spindle, with the bag fibers being inconstantly involved. The gamma-axons whose stimulation did not exert this effect produced much more restricted patterns of glycogen depletion. 4. The length sensitivities of two secondary endings belonging to the same spindle were similarly affected by a single gamma-axon, whereas a gamma-axon could increase the sensitivity of a secondary ending without altering that of the primary ending of the same spindle. 5. The action exerted by single gamma-axons on secondary endings appears related to their intrafusal distribution since enhancement of the secondary endings sensitivity was observed only when all the chain fibers of at least one spindle pole were activated. 6. If several static gamma-axons supplying a given spindle are firing together, an increase in the length sensitivity of the secondary endings of that spindle can be expected since probably all chain fibers are activated.

Animals↗
PubMed1993

Posttetanic hyperpolarization produced by electrogenic Na(+)-K+ pump in lizard axons impaled near their motor terminals.

1. The hyperpolarization that follows tetanic stimulation was recorded intra-axonally from the internodal region of intramuscular myelinated motor axons. 2. The peak amplitude of the posttetanic hyperpolarization (PTH) that followed stimulation at 20-100 Hz for < or = 35 s increased with increasing train duration, reaching a maximum of 22 mV. PTH decayed over a time course that increased from tens to hundreds of seconds with increasing train duration. For a given frequency of stimulation the time integral of PTH was proportional to the number of stimuli in the train, averaging 3-4 mV.s per action potential. 3. Ouabain (0.1-1 mM) and cyanide (1 mM) depolarized the resting potential and abolished PTH. Tetanic stimulation in ouabain was followed by a slowly decaying depolarization (probably due to extra-axonal K+ accumulation) whose magnitude and duration increased as the duration of the train increased. 4. Axonal input resistance showed no consistent change during PTH in normal solution but increased during PTH in the presence of 3 mM Cs+ (which blocks axonal inward rectifier currents). 5. PTH was abolished when bath Na+ was replaced by Li+ or choline. PTH persisted after removal of bath Ca2+ and addition of 2 mM Mn2+. 6. Removal of bath K+ abolished the PTH recorded after brief stimulus trains and greatly reduced the duration of PTH recorded after longer stimulus trains. 7. A brief application of 10 mM K+, which normally depolarizes axons, produced a ouabain-sensitive hyperpolarization in axons bathed in K(+)-free solution. 8. These observations suggest that in these myelinated axons PTH is produced mainly by activation of an electrogenic Na(+)-K(+)-ATPase, rather than by changes in K+ permeability or transmembrane [K+] gradients. This conclusion is supported by calculations showing agreement between estimates of Na+ efflux/impulse based on PTH measurements and estimates of Na+ influx/impulse based on nodal voltage-clamp measurements. Pump activity also appears to contribute to the resting potential. 9. The stimulus intensity required to initiate a propagating action potential increased during PTH but decreased during the posttetanic depolarization recorded in ouabain. Thus changes in axonal excitability after tetanic stimulation correlate with changes in the posttetanic membrane potential. 10. Action potentials that propagated during PTH had a larger peak amplitude and were followed by a larger and longer depolarizing afterpotential than action potentials elicited at the resting potential. This enhancement of the depolarizing afterpotential is consistent with previous reports of an increased superexcitable period after action potentials evoked during PTH.

Animals↗