Changes in intra‐axonal calcium distribution following nerve crush

Abstract

We used the oxalate-pyroantimonate method to demonstrate the ultrastructural distribution of calcium within rat sciatic nerve 4 h after a crush injury. In normal nerve there are discrete gradients of axoplasmic calcium precipitate with the amount of precipitate decreasing in the axoplasm beneath the Schmidt Lantermann clefts and in the paranodal regions at the node of Ranvier. Near the crush site a marked increase in endoneurial and intra-axonal calcium precipitate correlated with morphologic evidence of axonal degeneration. More distant from the crush site, both in the distal segment destined to degenerate and in the proximal segment destined to regenerate, the most prominent finding was a loss of the normal gradient of precipitate beneath the Schmidt Lantermann clefts. The calcium influx at the crush site corresponds to the known role of calcium in triggering degeneration. The alterations in the distal axon may be an early stage leading to degeneration. Alteration in calcium distribution in the proximal nerve stump may play a role in the regulation of the response to injury.

Intra-axonal calcium changes after axotomy in wild-type and slow Wallerian degeneration axons

“…The vast majority of SLCs in the sciatic nerve display a characteristic calcium distribution profile along the axis of the axons, which was demonstrated with the same oxalatepyroantimonate technique as used in the present study (Mata et al, 1986(Mata et al, , 1987. The highest density values of the EDDs were detected outside the cleft, while minimal amounts or none were present just under the cleft, as illustrated in Fig.…”

“…Using the oxalatepyroantimonate method to fix and identify calcium at the ultrastructural level, it was shown that in uninjured, wildtype axons there are discrete gradients of axoplasmic calcium that produce a characteristic pattern of precipitate, decreasing in the axoplasm beneath the Schmidt-Lantermann clefts (SLCs) and in the paranodal regions at the node of Ranvier (Mata et al, 1987). Within 4 h of nerve injury, long before any steady increase in total calcium levels, the uneven distribution of calcium precipitate below the majority of SLCs is lost (Mata et al, 1986).…”

Role of subconcussion in repetitive mild traumatic brain injury

“…22 In addition to primary and secondary injury, the concept of a tertiary phase of TBI may now be thought of as ongoing abnormalities in glucose utilization and cellular metabolism as well as membrane fluidity, synaptic function, and structural integrity. 3,35,[43][44][45]66,67,71,78 This phase of TBI may become chronic and compounded if the individual is subjected to repetitive minor head impacts.…”

Localized and Transient Elevations of Intracellular Ca2+Induce the Dedifferentiation of Axonal Segments into Growth Cones

“…Axotomy causes a large increase of the free intracellular Ca 2ϩ concentration in the transected axon, mainly because of Ca 2ϩ influx through the cut end (Borgens et al, 1980;Happel et al, 1981;Mata et al, 1986;Strautman et al, 1990;Rehder et al, 1991Rehder et al, , 1992Spira, 1993, 1995). This influx forms a steep [Ca 2ϩ ] i gradient along the severed axon, in which Ca 2ϩ concentrations Ͼ1 mM are recorded near the cut end.…”