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I G McQuarrie

Publications and source records attributed to I G McQuarrie.

At least 19 recordsLinked to original sources
PubMed2001

Calcium/calmodulin-dependent protein kinase IIalpha in optic axons moves with slow axonal transport and undergoes posttranslational modification.

In neurons, the mRNA for calcium/calmodulin-dependent protein kinase II alpha (CKIIalpha) is known to be targeted to dendrites-where the enzyme is synthesized and supports postsynaptic functions. We are interested in knowing how neuronal proteins enter axons from the nerve cell body, and the mechanism for protein transport to terminals. Because CKIIalpha immunofluorescence can be demonstrated in over 80% of retinal ganglion cells, we asked whether this regulatory protein is being transported into optic axons. Using Sprague-Dawley rats, [(35)S] methionine was injected into the vitreous humor of the eye. Four days later, the optic nerves, tracts, lateral geniculate ganglia, and superior colliculi were removed and processed for 2D-PAGE and Western blotting. Radiolabeled CKIIalpha appears to move with slow component b (SCb) of axonal transport, as is the case in rodent sciatic motor neurons. In addition, the radiolabeled CKIIalpha isoform that enters the optic nerve is found to be 4 kDa heavier (in SDS-PAGE molecular mass) than the isoform in the optic tract, superior colliculus, and lateral geniculate nucleus. This reduction is likely the result of dephosphorylation, which is a mechanism used to regulate the enzyme's activity.

Animals↗
PubMed2001

Diagnostic status and treatment recommendations for Persian Gulf War Veterans with multiple nonspecific symptoms.

BACKGROUND: Unexplained symptoms have frequently been observed in deployed Persian Gulf War veterans (GWVs). Using factor analysis, the Centers for Disease Control and Prevention (CDC) has established criteria for Gulf War illness (GWI). We report here on the prevalence of GWI, identify comorbidities, and compare these with those of veterans without GWI. METHODS: GWVs who consented to complete questionnaires and laboratory measures were given complete physical and mental health examinations. Outcome measures included CDC criteria for GWI, the Medical Outcomes Study Short Form 36 (SF-36), clinical and laboratory evaluations, and structured psychiatric interviews. RESULTS: One hundred twenty GWVs were enrolled, and 89 received complete physical and mental health examinations; 83% met CDC criteria for GWI. Veterans with GWI (1) were older, (2) reported more combat exposure, (3) scored higher on measures of depression, post-traumatic stress disorder, and fibromyalgia, and (4) had poorer health-related quality of life. More than half had anxiety or depressive disorders, and 93% had at least one medical and/or psychiatric diagnosis. The SF-36 predicted mental health status with a positive predictive value of 81.58. By adding the Hamilton D rating for depression, the positive predictive value increased to 88.57. INTERPRETATION: The CDC criteria accurately identified GWVs negative for GWI. Most GWVs were positive for GWI. Neither CDC criteria nor CDC severity rankings distinguish between veterans with psychiatric syndromes and those without: both groups endorsed the same symptoms. More than half of those with GWI had a treatable anxiety or depressive disorder. The SF-36 was a valid predictor of mental health status, particularly when paired with the Hamilton depression interview.

Adult↗
PubMed2000

Hydrocephalus in coccidioidal meningitis: case report and review of the literature.

OBJECTIVE AND IMPORTANCE: Coccidioidomycosis was once confined to the southwest United States and northern Mexico. It has become a larger concern because of the concentration of military bases in these areas, the increasing mobility of populations, and the rising population of immunocompromised persons. Outside endemic areas, the diagnosis is rarely considered. Patients with coccidioidomycosis may develop occult basilar meningitis progressing to communicating hydrocephalus and death. CLINICAL PRESENTATION: A 60-year-old white man presented with a 1-month history of vertigo, falls, and vomiting. Computed tomography of the head revealed mild hydrocephalus. Lumbar puncture results were remarkable for 1065 mg/dl protein; acid-fast bacillus stain, Gram's stain, and culture results were negative. Postgadolinium magnetic resonance imaging demonstrated enhancement of basilar and cervical meninges, suggesting inflammation, and communicating hydrocephalus. For 48 hours, the patient's level of consciousness decreased progressively. INTERVENTION: A ventriculoperitoneal shunt was placed, and antifungal agents were initiated on an emergent basis. CONCLUSION: Coccidioidomycosis should be considered in the differential diagnosis of occult basilar meningitis. The diagnosis is established by the discovery of a high (>1:2) titer of complement-fixing antibody in the cerebrospinal fluid. Communicating hydrocephalus is a common complication of untreated coccidioidal meningitis, and it may develop during appropriate treatment (oral fluconazole, 200-400 mg/d, continued indefinitely). Patients with hydrocephalus and evidence of increased intracranial pressure require a shunt.

Antifungal Agents↗
PubMed1997

Calcium/calmodulin-dependent protein kinase II expression in motor neurons: effect of axotomy.

Although Ca2+/calmodulin-dependent (CaM) protein kinase II isoforms are present in the nervous system in high amounts, many aspects of in vivo expression, localization, and function remain unexplored. During development, CaM kinase IIalpha and IIbeta are differentially expressed. Here, we examined CaM kinase II isoforms in Sprague-Dawley rat sciatic motor neurons before and after axotomy. We cut the L4-5 spinal nerves unilaterally and exposed the proximal nerve stumps to a fluoroprobe, to retrogradely label the neurons of origin. Anti-CaM kinase IIbeta antibody showed immunoreactivity in motor neurons, which decreased to low levels by 4 days after axotomy. We found a similar response by in situ hybridization with riboprobes. The decrease in expression of mRNA and protein was confined to fluorescent motor neurons. For CaM kinase IIalpha, in situ hybridization showed that the mRNA was in sciatic motor neurons, with a density unaffected by axotomy. However, these neurons were also enlarged, suggesting an up-regulation of expression. Northern blots confirmed an mRNA increase. We were unable to find CaM kinase IIalpha immunoreactivity before or after axotomy in sciatic motor neuron cell bodies, suggesting that CaM kinase IIalpha is in the axons or dendrites, or otherwise unavailable to the antibody. Using rats with crush lesions, we radiolabeled axonal proteins being synthesized in the cell body and used two-dimensional polyacrylamide gel electrophoresis with Western blots to identify CaM kinase IIalpha as a component of slow axonal transport. This differential regulation and expression of kinase isoforms suggests separate and unique intracellular roles. Because we find CaM kinase IIbeta down-regulates during axonal regrowth, its role in these neurons may be related to synaptic transmission. CaM kinase IIalpha appears to support axonal regrowth.

Animals↗
PubMed1996

Assembly of microfilaments and microtubules from axonally transported actin and tubulin after axotomy.

The slow component (SC) of axonal transport conveys structural proteins, regulatory proteins, and glycolytic enzymes toward the axon tip at 1-6 mm/day. Following axon interruption (axotomy), the rate of outgrowth corresponds to the rate of SCb-the fastest subcomponent of SC. Both axonal outgrowth and SCb accelerate 20-25% after axotomy. Tubulin and actin are the major proteins being carried by SCb. To further characterize the acceleration of SCb, we measured the equilibrium between subunits and polymers for both actin and tubulin. We radiolabeled newly synthesized proteins in rat motor neurons by microinjecting [35S]methionine into the spinal cord 7 days after crushing the sciatic nerve (85 mm from the spinal cord). Nerves were removed 7 days later for homogenization in polymer-stabilizing buffer (PSB) and centrifugation, followed by SDS-PAGE of supernatants (S) and pellets (P). We removed beta-tubulin, actin, and the medium-weight neurofilament protein (NF-M) from each gel by using the fluorogram as a template. After solubilizing gel segments for liquid scintillation spectrometry, we expressed counts as a polymerization ratio: P/[S+P]. In the nerve segments that contained radiolabeled Scb proteins, located 24-36 mm from the spinal cord, axotomy increased the polymerization ratio of SCb actin from 0.23 to 0.36 (P < 0.05) but had no effect on SCb beta-tubulin. In a separate experiment, we added 12 microM taxol to PSB to stabilize newly assembled microtubules. Adding taxol did not alter the polymerization ratio for SCb beta-tubulin in sham-axotomized nerves but aid increase the ratio in axotomized nerves, from 0.44 to 0.63 (P < 0.05); polymerization ratios for SCb actin were unaffected. We conclude that the assembly of microfilaments and microtubules increases to provide cytoskeletal elements for axon sprouts. The resulting loss of actin and tubulin subunits may play a role in the acceleration of SCb.

Actin Cytoskeleton↗
PubMed1996

Axonal regrowth upregulates beta-actin and Jun D mRNA expression.

When quiescent cells are perturbed, mRNAs encoding proteins that regulate gene transcription and the cell cycle are expressed at higher level. Jun and Fos are examples of proteins that mediate mitogenic signals and influence differentiation. In neurons, axon interruption (axotomy) increases the content of actin, tubulin, Jun D, and c-Jun proteins in association with increases in actin mRNA levels. Jun D protein binds to gene promoter regions, and its expression has been linked to several aspects of cell differentiation. Because Jun D and beta-actin messages have been described as "constitutive" in expression, we wanted to know whether these messages were responsive to axotomizing lesions of the sciatic motor nerve. We crushed the right sciatic nerve in Sprague-Dawley rats and extracted mRNA from the half spinal cord that serves each leg. At 4 days, Northern blots showed a 2.3-fold increase in beta-actin mRNA and a 2.5-fold increase in Jun D mRNA in the right hemicord. In situ hybridization showed either an undiminished or increased concentration of both mRNAs in motor neurons ipsilateral to the lesion at 4 days, even though many had enlarged two-to threefold. By introducing Fluoro-Ruby at the axotomy site, we were able to show that only the axotomized neurons have enlarged. We conclude that aspects of axonal regeneration resemble the embryonic program for neuronal differentiation and are reinitiated by axotomy.

Actins↗
PubMed1993

Retardation of fast axonal transport in wobbler mice.

To investigate axonal function in a model of early motor neuron disease, we examined fast and slow components of anterograde axonal transport in the less-affected hindlimb motor neurons of wobbler mice. To study the fast component (FC), we injected tritiated amino acids into the lumbar spinal cord and retrieved the sciatic nerve after 2 or 3 h. The transport distance was the extent of the plateau of labeling; regression analysis indicated that FC was 25% slower in wobbler mice than in unaffected littermates (P < 0.01). To study slow component (SC), [35S]methionine was injected. Transport distances were to the peaks of labeling for structural proteins after 2 or 3 weeks. Rates for each subcomponent (SCa and SCb) were unaffected by wobbler disease. Because the rate of retrograde FC is also unaffected (Mitsumoto et al., Muscle & Nerve 13:121-126, 1990), we conclude that wobbler disease specifically retards anterograde FC in less-affected hindlimb motor neurons, whereas all components of axonal transport are retarded in forelimb motor neurons.

Animals↗
PubMed1993

Acceleration of axonal outgrowth in rat sciatic nerve at one week after axotomy.

Following injury of sciatic motor axons in the rat, the rate of axonal outgrowth is faster if there has been a prior "conditioning" axotomy. The acceleration of outgrowth is due to an acceleration of SCb, the rate [slow (SC)] component of axonal transport that carries cytomatrix proteins; this occurs throughout the axon by 7 days after the conditioning axotomy (Jacob and McQuarrie, 1991a, J. Neurobiol. 22:570-583). To further characterize the conditioning lesion effect (CLE), it is important to know (1) the minimum effective conditioning interval (time between conditioning and testing lesions), (2) whether the cell body reaction is required, and (3) whether outgrowth accelerates after a single axotomy. Outgrowth distances were measured by radiolabeling all newly synthesized neuronal proteins and detecting those carried to growth cones by fast axonal transport. When the conditioning and testing lesions were made simultaneously (0 day conditioning interval), there was no CLE. With a conditioning interval of 3 days, there was a shortening of the initial delay (before the onset of outgrowth) without a change in outgrowth rate. With conditioning intervals of 7, 14, and 21 days, the rates of outgrowth were increased by 8%, 22%, and 11%, respectively. To determine whether the cell body reaction to axotomy is necessary for the CLE, a nonaxotomizing stimulus to axonal growth (partial denervation) was used in place of a conditioning axotomy. This had no effect on the rate of outgrowth from a testing lesion made 14 days later. Finally, we examined the possibility that outgrowth accelerates after a single lesion. Outgrowth was faster at 6-9 days after axotomy than at 3-6 days (p < 0.001), and accelerated further at 9-12 days (p < 0.001). We conclude that (1) the shortest effective conditioning interval is 3 days; (2) the cell body reaction is necessary for the CLE; (3) axonal outgrowth from a single axotomy accelerates in concert with the anabolic phase of the cell body reaction. The SCb motor is, in turn, upregulated by this reaction. This suggests that the SCb motor responds to a fast-transported signal that is a product of the cell body reaction.

Animals↗
PubMed1991

Conditioning nerve crush accelerates cytoskeletal protein transport in sprouts that form after a subsequent crush.

To examine the relationship between axonal outgrowth and the delivery of cytoskeletal proteins to the growing axon tip, outgrowth was accelerated by using a conditioning nerve crush. Because slow component b (SCb) of axonal transport is the most rapid vehicle for carrying cytoskeletal proteins to the axon tip, the rate of SCb was measured in conditioned vs. sham-conditioned sprouts. In young Sprague-Dawley rats, the conditioning crush was made to sciatic nerve branches at the knee; 14 days later, the test crush was made where the L4 and L5 spinal nerves join to form the sciatic nerve in the flank. Newly synthesized proteins were labeled in motor neurons by injecting 35S-methionine into the lumbar spinal cord 7 days before the test crush. The wave of pulse-labeled SCb proteins reached the crush by the time it was made and subsequently entered sprouts. The nerve was removed and sectioned for SDS-PAGE and fluorography 4-12 days after the crush. Tubulins, neurofilament proteins, and representative "cytomatrix" proteins (actin, calmodulin, and putative microtubule-associated proteins) were removed from gels for liquid scintillation counting. Labeled SCb proteins entered sprouts without first accumulating in parent axon stumps, presumably because sprouts begin to grow within hours after axotomy. The peak of SCb moved 11% faster in conditioned than in sham-conditioned sprouts: 3.0 vs. 2.7 mm/d (p less than 0.05). To confirm that sprouts elongate more rapidly when a test crush is preceded by a conditioning crush, outgrowth distances were measured in a separate group of rats by labeling fast axonal transport with 3H-proline 24 hours before nerve retrieval.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Axotomy accelerates slow component b of axonal transport.

Because the integrity of an axon depends on the supply of proteins synthesized in the cell body, we examined the effect of axotomy on the transport of structural proteins in rat motor axons, and the effect of altered transport on the rate of outgrowth after a subsequent testing axotomy. To examine the axonal transport of structural proteins, we labeled newly synthesized proteins with 35S-methionine 7 days after a "conditioning" lesion of the sciatic nerve, and removed the nerve 7-21 days later for SDS-PAGE. Tubulin, actin, calmodulin, and the 68-kD light neurofilament protein (NF-L) were identified by fluorography and removed for liquid scintillation counting. The fastest moving structural proteins were carried by slow component b (SCb) of axonal transport, which advanced 20% faster in conditioned axons: 4.2 versus 3.5 mm/day (p less than 0.01). NF-L was not accelerated, indicating that the motor for subcomponent a (SCa) of slow axonal transport was unaffected by axotomy. To measure outgrowth distances, the testing lesions was made 7 days after the conditioning lesion, and growth cones were located by the fast transport method 3 or 9 days later. The regression analysis of outgrowth distance on time showed that sprouts elongated 25% faster in conditioned axons: 4.0 versus 3.2 mm/day (p less than 0.001). These accelerated sprouts were formed too far from the spinal cord to contain SCb proteins that were synthesized after axotomy. Because the rate of outgrowth correlated closely with the rate of SCb in outgrowing sprouts (McQuarrie and Jacob, J. Comp. Neurol. 305:139-147, 1991), we conclude that SCb is accelerated throughout the length of the axon by 7 days after axotomy.

Actins↗
PubMed1990

Impairment of retrograde axonal transport in wobbler mouse motor neuron disease.

The earliest horseradish peroxidase (HRP) neuronal labeling (the fastest retrograde transport) was determined by histochemical techniques at various intervals after intramuscular HRP injection in wobbler mice and normal littermates. In the clinically impaired forelimb system, the retrograde transport rate was 150-170 mm/day in wobbler mice and 170-230 mm/day in controls. However, there was no statistical difference between the two groups. The neuronal HRP accumulation at the early intervals was significantly less in wobbler mice than controls, suggesting that the amount of HRP transport was diminished in each axon. For the clinically intact hindlimb nerves, the rate was normal in wobbler mice, but the amount of neuronal HRP was significantly increased. Retrograde axonal transport appeared to be affected in a differential fashion, depending on the extent of disease.

Animals↗
PubMed1990

Increased slow transport in axons of regenerating newt limbs after a nerve conditioning lesion.

We have previously shown that a nerve conditioning lesion (CL) made 2 weeks prior to amputation results in an earlier onset of limb regeneration in newts. Studies in fish and mammals demonstrate that when a CL precedes a nerve testing lesion, slow component b (SCb) of axonal transport is increased compared to axons that had not received a CL. We wanted to know whether the earlier initiation of limb regeneration after a CL was associated with an increase in SCb transport. The transport of [35S]methionine labeled SCb proteins was measured by using SDS-PAGE, fluorography, and scintillation counting. The rate of transport and quantity of SCb proteins was determined at 7, 14, 21, and 28 days after injection of [35S]methionine into the motor columns of normal; single lesioned (i.e., transection axotomy, amputation axotomy, or sham CL followed by amputation); and double-lesioned limb axons (i.e., nerve transection CL followed 2 weeks later by amputation axotomy). The rate of SCb transport in axons of unamputated newt limbs was 0.19 mm/day. There was an increase in the amount of labeled SCb proteins transported in axons regenerating as the result of a single lesion but no acceleration in the rate of SCb transport, which was 0.21 mm/day in axons that received a sham CL followed by limb amputation. The rate of SCb transport doubled (0.40 mm/day) and the amount of labeled SCb proteins being transported was increased when amputation was preceded by a CL. This study demonstrates that the earlier onset of limb regrowth, seen when amputation follows a CL, is associated with an increased transport of SCb proteins. This suggests that limb regeneration is, in part, regulated by axonal regrowth. We propose that the blastema requires a minimum quantity of innervation before progressing to the next stage of limb regeneration, and that the transport of SCb proteins determines when that quantity will be available.

Actins↗
PubMed1990

Histometric characteristics and regenerative capacity in wobbler mouse motor neuron disease.

In wobbler mice, histometric features and the response to injury in the less affected hindlimb nerves were compared with the severely affected forelimb nerves which were studied previously. The frequency of vacuolated anterior horn cells was not different at the individual ages studied (3 and 6 weeks, 3 months), but with the three ages combined, the frequency in the two systems differed significantly, being 1.7 +/- 0.9% in the cervical and 0.6 +/- 0.7% in the lumbar anterior horns (P = 0.005). The number of large myelinated nerve fibres (greater than or equal to 6 microns in diameter) became progressively reduced in ventral roots as the disease advanced, particularly for the forelimb. The total number of myelinated axons was well preserved in the hindlimb ventral roots because of an increase in the number of small myelinated nerve fibres. The regenerative capacity of motor neurons after axotomy (tested by radiolabelling growth cones) was well preserved. In the hindlimb, the increased numbers of small myelinated fibres in ventral roots and the normal regenerative capacity in the sciatic nerve and its branches contrast with the severely affected forelimb system. Our studies suggest that cervical and lumbar anterior horn cells have different susceptibilities to the wobbler gene, producing vulnerability in one system and disease resistance in the other.

Animals↗
PubMed1989

Ganglioside synthesis and transport in regenerating sensory neurons of the rat sciatic nerve.

The sciatic nerves of rats were crushed with fine forceps and allowed to survive for 3 or 7 days, at which time the 5th lumbar dorsal root ganglion was injected with [3H]glucosamine. Animals were killed 18 h later and the nerves proximal and distal to the crush site were cut into 3 mm segments. Gangliosides were purified from these segments, and radioactivity was separately measured in gangliosides, neutral glycolipids and glycoproteins. For all 3 fractions, radioactivity was distributed similarly between the crush site and point of maximum axonal elongation. A second smaller peak of ganglioside radioactivity was seen to span a few segments immediately distal to the point of maximum axonal elongation. We propose two possible explanations for this: (1) it represents ganglioside synthesis by Schwann cells (from blood-borne [3H]glucosamine) as part of the mitogenic response of these cells to the reappearance of axons; or (2) recently synthesized, transported gangliosides are released from the growth cone and taken up by adjacent mitogenic Schwann cells.

Animals↗
PubMed1989

Transport of cytoskeletal elements from parent axons into regenerating daughter axons.

The kinetics of slow axonal transport in newly regenerating axonal sprouts were compared with those in nonelongating axons. The slowly transported cytoskeletal proteins of ventral motor axons were prelabeled by microinjection of 35S-methionine into the spinal cord. Pulse-labeled slow transport "waves" were observed as they progressed from the surviving "parent" axon stumps (located proximal to a crush lesion) into regenerating "daughter" axon sprouts (located distal to the lesion). Prelabeled cytoskeletal elements of the parent axons were transported into daughter axons, to become distributed into 2 transport waves, "a" and "b." The rate and composition of these waves corresponded to the slow transport subcomponents, SCa and SCb. The shapes of the "a" and "b" waves suggested that the cytoskeletal elements had been reorganized at the junction between the parent and daughter axons. This hypothesis was supported by quantitative analyses of the transport distribution for individual radiolabeled cytoskeletal proteins (actin, spectrin, a 58-67 kDa group that includes microtubule-associated proteins, calmodulin, and tubulin). Specifically, during the first week of outgrowth, the amounts of radiolabeled calmodulin and 58-67 kDa proteins were greater in daughter axons than in nonregenerating control axons. These results support Paul Weiss's "conservative" model of axonal regeneration, which holds that the preexisting transported cytoskeletal elements that continually maintain axonal structure can also provide the cytoskeletal elements required for axonal regeneration. In addition, the results elucidate some of the reorganizational changes in cytoskeletal elements that occur when these are recruited from the parent axon to form daughter axons.

Actins↗
PubMed1987

Cytotypic differences in the protein composition of the axonally transported cytoskeleton in mammalian neurons.

Many of the structural and functional differences between axons are thought to reflect underlying differences in the biochemical composition and dynamic aspects of the axonal cytoskeleton and cytomatrix. In this study we investigated how the composition of the 2 slow components of axonal transport, SCa and SCb, which convey the cytoskeleton and cytomatrix, differs in axons that are structurally and functionally distinct. For this comparison we analyzed axons of retinal ganglion cells in the optic nerve (ON), axons of dorsal root ganglion (DRG) cells, and axons of ventral motor neurons (VMN) in adult rats. 35S-Methionine-labeled proteins transported with the peak of SCa and SCb were analyzed using high-resolution 2-dimensional polyacrylamide gels (2D-PAGE) and fluorography, and the amounts of major SCa and SCb proteins were quantified. The polypeptide composition of both SCa and SCb was found to be largely similar in DRG and VMN axons, but major qualitative as well as quantitative differences between these axons and ON axons were found. Notable among these were higher ratios of neurofilament protein to tubulin in SCa in DRG and VMN axons compared to ON axons, and significantly larger amounts of 2 microtubule-associated proteins relative to tubulin in SCa of ON axons than in both VMN and DRG axons. Tubulin was the major SCb protein in VMN and DRG axons, but it was not present in SCb in ON axons. Additionally, relatively larger amounts of 2 metabolic enzymes, creatine phosphokinase and nerve-specific enolase, were present in SCb in ON axons than in DRG or VMN axons. The results indicate that significant biochemical heterogeneity among different types of axons can be identified by examining the slow components of axonal transport.

Actins↗
PubMed1986

Structural protein transport in elongating motor axons after sciatic nerve crush. Effect of a conditioning lesion.

In elongating motor axons of the rat sciatic nerve, the maximum outgrowth rate increased from 4.6 to 5.3 mm/d (5.3-6.1 X 10(-8) m/s) when a testing lesion of spinal nerves L4 and L5 was preceded 2 wk earlier by a conditioning lesion of the sciatic nerve. Axonal outgrowth was examined by measuring the transport of 35[S]methionine-labeled structural proteins (tubulin, actin, and neurofilament triplet) from "parent" axon stumps into "daughter" axon sprouts. Since these proteins are conveyed by the slow component of axonal transport at 1-5 mm/d (1.2-6.0 X 10(-8) m/s), the isotope was injected into the spinal cord 1 wk before the testing lesion. Nerves were removed 8 d after the testing lesion, sectioned into 3-mm segments, and homogenized; soluble proteins were separated by polyacrylamide gel electrophoresis. Fluorographs were used as templates to identify gel segments for removal, solubilization, and liquid scintillation counting. Distributions of mean radioactivity for tubulin, actin, and neurofilament triplet were plotted for animals receiving a conditioning vs sham-conditioning lesion. Greater amounts of tubulin and actin were transported into daughter axons in the conditioned group. Tubulin was mainly increased in axon shafts, whereas actin was mainly increased in axon tips. These findings suggest that the axonal transport of tubulin and actin governs the rate of elongation.

Actins↗