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.

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.

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.

scholarly journals TRPA1 block protects against loss of white matter function during ischaemia in the mouse optic nerve

2021 ◽  
Author(s):  
Grace Flower ◽  
Vincenzo Giacco ◽  
Angela Roxas ◽  
Nicola B Hamilton-Whitaker ◽  
Andra Braban
Keyword(s):  
White Matter ◽  
Optic Nerve ◽  
Action Potential ◽  
Neuronal Excitability ◽  
Glucose Deprivation ◽  
Compound Action Potential ◽  
Oxygen And Glucose Deprivation ◽  
Loss And Damage ◽  
Compound Action Potentials ◽  
Compound Action

Oligodendrocytes produce myelin which provides insulation to axons and speeds up neuronal transmission. In ischaemic conditions myelin is damaged, resulting to mental and physical disabilities. Therefore, it is important to understand how the functionality of oligodendrocytes and myelin is affected by ischaemia. Recent evidence suggests that oligodendrocyte damage during ischaemia is mediated by TRPA1, whose activation raises intracellular Ca2+ concentrations and damages compact myelin. Here, we show that TRPA1 is tonically active in oligodendrocytes and the optic nerve, as the specific TRPA1 antagonist, A-967079, decreases basal oligodendrocyte Ca2+ concentrations and increases the size of the compound action potential. Conversely, TRPA1 agonists reduce the size of the optic nerve compound action potential, and this effect is significantly reduced by the TRPA1 antagonist. These results indicate that glial TRPA1 regulates neuronal excitability in the white matter under physiological as well as pathological conditions. Importantly, we find that inhibition of TRPA1 prevents loss of compound action potentials during oxygen and glucose deprivation (OGD) and improves the recovery. TRPA1 block was effective when applied before, during or after OGD, indicating that the damage is occurring during ischaemia, but that therapeutic intervention is possible after the ischaemic insult. These results indicate that TRPA1 has an important role in the brain, and that its block may be effective in treating oligodendrocyte loss and damage in many white matter diseases.

The Effect of Nitric Oxide on Compound Action Potential Thresholds in the Cochlea

1995 ◽  
Vol 113 (2) ◽  
pp. P151-P151
Author(s):  
C. G. Dean Dais ◽  
Jiri Prazma ◽  
Steven S. Ball ◽  
Vincent Carrasco ◽  
Harold C. Pillsbury
Keyword(s):  
Nitric Oxide ◽  
Action Potential ◽  
Compound Action Potential ◽  
Compound Action
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