Conduction Deficits and Membrane Disruption of Spinal Cord Axons as a Function of Magnitude and Rate of Strain

2006 ◽  
Vol 95 (6) ◽  
pp. 3384-3390 ◽  
Author(s):  
Riyi Shi ◽  
Jim Whitebone
Keyword(s):  
Spinal Cord ◽  
Strain Rate ◽  
Structural Damage ◽  
Ex Vivo ◽  
Membrane Damage ◽  
Compound Action Potential ◽  
Strain And Strain Rate ◽  
Gap Technique ◽  
Sucrose Gap ◽  
Compound Action

White matter strips extracted from adult guinea pig spinal cords were subjected to tensile strain (stretch) injury ex vivo. Strain was carried out at three magnitudes (25, 50, and 100%) and two strain rate regimens: slow (0.006–0.008 s−1) and fast (355–519 s−1). The cord samples were monitored physiologically using a double sucrose-gap technique and anatomically using a horseradish peroxidase assay. It seems that a higher magnitude of strain inflicted significantly more functional and structural damage within each strain rate group. Likewise, a higher strain rate inflicted more damage when the strain magnitude was maintained. It is evident that axons have remarkable tolerance to strain injury at a slow strain rate. Even a 100% strain at the slow rate only eliminated two-thirds of the compound action potential amplitude and resulted in almost no membrane damage when examined 30 min after strain. It is also clear that the spontaneous recovery is evident yet not complete compared with preinjury levels at the fast strain rate. To examine the factors that might influence the vulnerability of axons to strain, we have shown that the axonal diameters did not play a significant role in dictating the susceptibility of axons to strain. Rather, it is speculated that the location of axons might be a more important factor in this regard. The knowledge gained from this study is likely to be informative in elucidating the spinal cord biomechanical response to strain and strain rate.

Effect of DSPE-PEG on compound action potential, injury potential and ion concentration following compression in ex vivo spinal cord

2016 ◽  
Vol 620 ◽  
pp. 50-56 ◽  
Author(s):  
Aihua Wang ◽  
Xiaolin Huo ◽  
Guanghao Zhang ◽  
Xiaochen Wang ◽  
Cheng Zhang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Action Potential ◽  
Ex Vivo ◽  
Compound Action Potential ◽  
Ion Concentration ◽  
Compound Action ◽  
Injury Potential

scholarly journals Bioassay-Guided Evaluation of Antinociceptive Effect ofN-Salicyloyltryptamine: A Behavioral and Electrophysiological Approach

2010 ◽  
Vol 2010 ◽  
pp. 1-6 ◽  
Author(s):  
Lucindo J. Quintans-Júnior ◽  
Davi A. Silva ◽  
Jullyana S. Siqueira ◽  
Adriano A. S. Araújo ◽  
Rosana S. S. Barreto ◽  
...  
Keyword(s):  
Action Potential ◽  
Neuronal Excitability ◽  
Antinociceptive Effect ◽  
Compound Action Potential ◽  
Nerve Excitability ◽  
Gap Technique ◽  
Antinociceptive Effects ◽  
Sucrose Gap ◽  
Second Phases ◽  
Compound Action

We investigated the antinociceptive and nerve excitability effects of theN-salicyloyltryptamine (NST) NST-treated mice exhibited a significant decrease in the number of writhes when 100 and 200 mg/kg (i.p.) were administered (i.p.). This effect was not antagonized by naloxone (1.5 mg/kg, i.p.). NST inhibited the licking response of the injected paw when 100 and 200 mg/kg were administered (i.p.) to mice in the first and second phases of the formalin test. Because the antinociceptive effects could be associated with neuronal excitability inhibition, we performed the single sucrose gap technique and showed that NST (3.57 mM) significantly reduced (29.2%) amplitude of the compound action potential (CAP) suggesting a sodium channel effect induced by NST. Our results demonstrated an antinociceptive activity of the NST that could be, at least in part, associated to the reduction of the action potential amplitude. NST might represent an important tool for pain management.

Control of Membrane Sealing in Injured Mammalian Spinal Cord Axons

2000 ◽  
Vol 84 (4) ◽  
pp. 1763-1769 ◽  
Author(s):  
Riyi Shi ◽  
Tomoko Asano ◽  
Neil C. Vining ◽  
Andrew R. Blight
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Compound Action Potential ◽  
Calpain Inhibitor ◽  
Compression Injury ◽  
Gap Technique ◽  
Sucrose Gap ◽  
Axonal Transection ◽  
Membrane Sealing

The process of sealing of damaged axons was examined in isolated strips of white matter from guinea pig spinal cord by recording the “compound membrane potential,” using a sucrose-gap technique, and by examining uptake of horseradish peroxidase (HRP). Following axonal transection, exponential recovery of membrane potential occurred with a time constant of 20 ± 5 min, at 37°C, and extracellular calcium activity ([Ca2+]o) of 2 mM. Most axons excluded HRP by 30 min following transection. The rate of sealing was reduced by lowering calcium and was effectively blocked at [Ca2+]o ≤ 0.5 mM, under which condition most axons continued to take up HRP for more than 1 h. Sealing at higher [Ca2+]o was blocked by calpain inhibitors (calpeptin and calpain inhibitor-1) indicating a requirement for type II (mM) calpain in the sealing process. Following compression injury, the amplitude of the maximal compound action potential conducted through the injury site was reduced. The extent of amplitude reduction was increased when the tract was superfused with calcium-free Krebs' solution (Ca2+ replaced by Mg2+). These results suggest that the fall in [Ca2+]o seen following injury in vivo is sufficient to prevent membrane sealing and may paradoxically contribute to axonal dieback, retrograde cell death, and “secondary” axonal disruption.

Critical roles of decompression in functional recovery of ex vivo spinal cord white matter

2009 ◽  
Vol 10 (2) ◽  
pp. 161-170 ◽  
Author(s):  
Hui Ouyang ◽  
Beth Galle ◽  
Jianming Li ◽  
Eric Nauman ◽  
Riyi Shi
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Ex Vivo ◽  
Membrane Damage ◽  
Compound Action Potential ◽  
Axonal Membrane ◽  
Cord Injury ◽  
Decompression Procedure ◽  
Spinal Cord Decompression ◽  
Type Of Injury

Object The correlations between functional deficits, the magnitude of compression, and the role of sustained compression during traumatic spinal cord injury remain largely unknown. Thus, the functional outcome of this type of injury with or without surgical intervention is rather unpredictable. To elucidate how severity and duration of compression affect cord function, the authors have developed a method to study electrophysiological characteristics and axonal membrane damage in white matter from guinea pig spinal cord. Methods Ventral white matter strips isolated from adult guinea pigs were compressed by a compression rod at a level of either 60 or 80% and held briefly, for 30 minutes, or for 60 minutes. In half the experimental groups, a decompression phase consisting of probe withdrawal and 30 minutes of recovery was also applied. For all cord samples, functional response was continuously monitored through compound action potential (CAP) recording. In addition, axonal membrane damage was assessed by a horseradish peroxidase (HRP) exclusion assay. Results After 30 minutes of sustained compression at levels of 60 or 80%, a spinal cord decompression procedure caused a significant CAP recovery, with specimens reaching 97.5 ± 6.84% (p < 0.05) and 56.2 ± 6.14% (p < 0.05) of preinjury amplitude, respectively. After 60 minutes of compression, the amount of CAP recovery following the decompression stage was only 65.5 ± 9.33% for 60% compression (p < 0.05) and 29.8 ± 6.31% for 80% compression (p < 0.05). Unlike the CAP response, HRP uptake did not increase during sustained compression, and the data showed that HRP staining was primarily time dependent. Conclusions The degree of axonal membrane damage is not exacerbated during sustained compression. However, the electrical conductivity of the cord white matter weakens throughout the duration of compression. Therefore, decompression is a viable procedure for preservation of neurological function following compressive injury.

Specific effects of α-D,L-aminoadipic acid on synaptic transmission in frog spinal cord

1980 ◽  
Vol 58 (6) ◽  
pp. 692-698 ◽  
Author(s):  
Ante L. Padjen ◽  
Peter A. Smith
Keyword(s):  
Amino Acids ◽  
Spinal Cord ◽  
Dorsal Root ◽  
Lateral Column ◽  
Specific Effects ◽  
Acidic Amino Acids ◽  
Frog Spinal Cord ◽  
Gap Technique ◽  
Root Potential ◽  
Sucrose Gap

The sucrose gap technique was employed to investigate both synaptic and amino acid evoked responses from motoneurones or primary afferents of frog spinal cord. α-D,L-Aminoadipic acid (α-D,L-AAD) selectively antagonized responses to acidic amino acids, especially aspartate. The drug was most effective in antagonizing the polysynaptic components of synaptic potentials evoked by dorsal root or lateral column stimulation but had little effect on their monosynaptic components. The ventral root dorsal root potential which is thought to be mediated by a pathway that does not involve acidic amino acids was insensitive to α-D,L-AAD. These data, which were confirmed by intracellular recording from motoneurones, provided further evidence for the role of acidic amino acids in polysynaptic pathways in frog spinal cord.

Development of 4-AP and TEA sensitivities in mammalian myelinated nerve fibers

1988 ◽  
Vol 60 (6) ◽  
pp. 2168-2179 ◽  
Author(s):  
D. L. Eng ◽  
T. R. Gordon ◽  
J. D. Kocsis ◽  
S. G. Waxman
Keyword(s):  
Sciatic Nerve ◽  
Action Potential ◽  
Compound Action Potential ◽  
Nerve Fibers ◽  
Repetitive Firing ◽  
Base Line ◽  
Channel Blockers ◽  
Myelinated Nerve ◽  
Sucrose Gap ◽  
Compound Action

1. The sensitivities of mammalian myelinated axons to potassium channel blockers was studied over the course of development using in vitro sucrose gap and intra-axonal recording techniques. 2. Application of 4-aminopyridine (4-AP; 1.0 mM) to young nerves led to a delay in return to base line of the sciatic nerve compound action potential and to a postspike positivity (indicative of hyperpolarization) lasting for tens of milliseconds. These effects were very much attenuated during the course of maturation. 3. Tetraethylammonium chloride (TEA; 10 mM) application alone had little effect on the waveform of the compound action potential at any age. However, the 4-AP-induced postspike positivity was blocked by TEA, Ba/+, and Cs+. This block was observed in Ca2+-free electrolyte solutions containing EGTA (1.0 mM). 4. Immature sciatic nerves (approximately 3 wk postnatal) were incubated in a potassium-free electrolyte solution containing 120 mM CsCl for up to 1 h in an attempt to replace internal potassium with cesium. When the nerves were tested in the sucrose gap chamber using solutions containing 3.0 mM CsCl substituted for KCl, the compound action potential was broadened and a prolonged depolarization appeared, but there was no postspike positivity; the CsCl effect was similar to the combined effects of 4-AP and TEA. 5. Intra-axonal recordings were obtained to study the effects of 4-AP and TEA on individual axons. In the presence of 4-AP a single stimulus led to a burst of action potentials followed by a pronounced afterhyperpolarization (AHP) in sensory fibers. The AHP was blocked by TEA. In motor fibers 4-AP application resulted in action potential broadening with no AHP. 6. Repetitive stimulation (200-500 Hz; 100 ms) was followed by a pronounced AHP in both sensory and motor fibers at all ages studied. This activity-elicited AHP was sensitive to TEA at all ages. 7. The results indicate that 4-AP and TEA sensitivity change over the course of development in rat sciatic nerve. The effects of 4-AP are much more pronounced in immature nerves than in mature nerves, suggesting that 4-AP-sensitive channels become masked as they are covered by myelin during maturation. However, the TEA-sensitive channels, demonstrable after repetitive firing, remain accessible to TEA after myelination. These channels therefore may have a nodal representation.

Strain and strain rate generated by shear wave elastography in ex vivo porcine aortas

2017 ◽  
Author(s):  
Elira Maksuti ◽  
David Larsson ◽  
Matthew W. Urban ◽  
Kenneth Caidahl ◽  
Matilda Larsson
Keyword(s):  
Strain Rate ◽  
Shear Wave ◽  
Ex Vivo ◽  
Shear Wave Elastography ◽  
Strain And Strain Rate
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