Literature DB >> 80448

Anoxic block and recovery of axoplasmic transport and electrical excitability of nerve.

J Leone, S Ochs.   

Abstract

Axoplasmic transport of cat sciatic nerves was studied in vitro in a chamber in which maximal alpha action potentials could also be elicited. After initiation of N2 anoxia, electrical responses fell to zero at an average time of 22 min. A shorter time to zero of 11 min was seen during a second period of anoxia. A good recovery of both action potential responses and axoplasmic transport occurs after a period of anoxia lasting 1--1.5 hr. An apparent failure of recovery of axoplasmic transport was seen after 2 hr of anoxia with a good recovery of electrical responses. Axoplasmic transport tended to return toward normal when more time was allowed for recovery after anoxia. An adequate supply of approximately P was shown to be present by measurement of ATP and creatine phosphate levels. The delay in recovery of transport thus signifies a failure of utilization of approximately P by the transport mechanism. Longer periods of anoxia and recovery were limited in vitro and for this reason, ischemic anoxia was produced in vivo. Blood pressure cuffs were placed on the upper thigh of cats and maintained for times of 1--8 hr at pressures of 300-310 mm Hg. Then, recovery times up to 7 days were allowed. It was shown that axoplasmic transport could gradually recovery after an anoxia lasting up to 6-7 hr if sufficient recovery times were allowed. A possible explanation for the delay in the recovery of axoplasmic transport and the disassociation in the earlier recovery of electrical responses as against the recovery of transport was discussed.

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Year:  1978        PMID: 80448     DOI: 10.1002/neu.480090305

Source DB:  PubMed          Journal:  J Neurobiol        ISSN: 0022-3034


  8 in total

1.  Changes in human sensory axonal excitability induced by focal nerve compression.

Authors:  S Eric Han; Cindy S-Y Lin; Robert A Boland; Lynne E Bilston; Matthew C Kiernan
Journal:  J Physiol       Date:  2010-03-29       Impact factor: 5.182

2.  Pressure-induced inhibition of fast axonal transport of proteins in the rabbit vagus nerve in galactose neuropathy: prevention by an aldose reductase inhibitor.

Authors:  W G McLean
Journal:  Diabetologia       Date:  1988-07       Impact factor: 10.122

3.  Blockage of axonal transport induced by acute, graded compression of the rabbit vagus nerve.

Authors:  B Rydevik; W G McLean; J Sjöstrand; G Lundborg
Journal:  J Neurol Neurosurg Psychiatry       Date:  1980-08       Impact factor: 10.154

4.  Morphology of axonal transport abnormalities in primate eyes.

Authors:  R L Radius; D R Anderson
Journal:  Br J Ophthalmol       Date:  1981-11       Impact factor: 4.638

5.  Changes in nerve function and nerve fibre structure induced by acute, graded compression.

Authors:  B Rydevik; C Nordborg
Journal:  J Neurol Neurosurg Psychiatry       Date:  1980-12       Impact factor: 10.154

6.  Proteomic analysis of neuronal hypoxia in vitro.

Authors:  K Jin; X O Mao; D A Greenberg
Journal:  Neurochem Res       Date:  2004-06       Impact factor: 3.996

7.  [32P]orthophosphate and [35S]methionine label separate pools of neurofilaments with markedly different axonal transport kinetics in mouse retinal ganglion cells in vivo.

Authors:  R A Nixon; S E Lewis; M Mercken; R K Sihag
Journal:  Neurochem Res       Date:  1994-11       Impact factor: 3.996

8.  Impaired rat sciatic nerve sodium-potassium adenosine triphosphatase in acute streptozocin diabetes and its correction by dietary myo-inositol supplementation.

Authors:  D A Greene; S A Lattimer
Journal:  J Clin Invest       Date:  1983-09       Impact factor: 14.808

  8 in total

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