Divalent cations and fast axonal transport in chemically desheathed (triton X-treated) frog sciatic nerve
(1982) In Brain Research 241(1). p.67-74- Abstract
We have studied the ability of divalent cations to restore to normal axonal transport (AXT) which was inhibited by deprivation of Ca2+ and/or Mg2+ ions. The epi- and perineurium of the frog sciatic nerve were damaged by a 30-s wash in Triton X-100 containing frog Ringer's. This treatment did not affect either AXT or nerve levels of Ca2+ and Mg2+, but made the ions more easily extractable with a Ca2+- and Mg2+-free Ringer's solution (CMFR). Inhibition of AXT was achieved by incubating Triton X-100-treated nerves in CMFR + EGTA for 5 h, followed by an additional incubation for 12 h in CMFR or Ringer's devoid of only Ca2+ (CFR). These treatments reduced... (More)
We have studied the ability of divalent cations to restore to normal axonal transport (AXT) which was inhibited by deprivation of Ca2+ and/or Mg2+ ions. The epi- and perineurium of the frog sciatic nerve were damaged by a 30-s wash in Triton X-100 containing frog Ringer's. This treatment did not affect either AXT or nerve levels of Ca2+ and Mg2+, but made the ions more easily extractable with a Ca2+- and Mg2+-free Ringer's solution (CMFR). Inhibition of AXT was achieved by incubating Triton X-100-treated nerves in CMFR + EGTA for 5 h, followed by an additional incubation for 12 h in CMFR or Ringer's devoid of only Ca2+ (CFR). These treatments reduced Ca2+ and Mg2+ contents by 77% and 38% respectively. Addition of Ca2+ (1.1 mM) during the 12-h period stimulated AXT, measured as accumulation of 3H-labelled components in front of a ligature, several fold. Mg2+ could not substitute for Ca2+ but potentiated the stimulating effect of Ca2+. Addition of other divalent cations did not affect AXT (Sr2+ and Ba2+) or potentiated the inhibition caused by Ca2+-deprived medium (Mn2+ and Co2+). ATP and creatine phosphate contents were similar in nerves incubated in Ca2+-deprived medium and in Ca2+-containing Ringer's. Thus, inhibition of AXT in the former situation was not due to a decreased availability of high energy phosphates. Two calcium antagonists, D-600 and nifedipin, which are potent smooth muscle relaxants, effectively blocked AXT. The present ressults suggest that Ca2+ is specifically required to maintain AXT and that an anlogy exists between Ca2+ regulation during smooth muscle contraction and AXT.
(Less)
- author
- Kanje, Martin LU ; Edström, Anders LU and Ekström, Per LU
- organization
- publishing date
- 1982-06-03
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- axonal transport, calcium, calcium antagonists, divalent cations
- in
- Brain Research
- volume
- 241
- issue
- 1
- pages
- 8 pages
- publisher
- Elsevier
- external identifiers
-
- scopus:0020066182
- pmid:6179567
- ISSN
- 0006-8993
- DOI
- 10.1016/0006-8993(82)91229-X
- language
- English
- LU publication?
- yes
- id
- 12510102-4918-4772-8e49-3007b25e0c21
- date added to LUP
- 2016-12-07 14:22:33
- date last changed
- 2024-01-04 18:17:50
@article{12510102-4918-4772-8e49-3007b25e0c21,
abstract = {{<p>We have studied the ability of divalent cations to restore to normal axonal transport (AXT) which was inhibited by deprivation of Ca<sup>2+</sup> and/or Mg<sup>2+</sup> ions. The epi- and perineurium of the frog sciatic nerve were damaged by a 30-s wash in Triton X-100 containing frog Ringer's. This treatment did not affect either AXT or nerve levels of Ca<sup>2+</sup> and Mg<sup>2+</sup>, but made the ions more easily extractable with a Ca<sup>2+</sup>- and Mg<sup>2+</sup>-free Ringer's solution (CMFR). Inhibition of AXT was achieved by incubating Triton X-100-treated nerves in CMFR + EGTA for 5 h, followed by an additional incubation for 12 h in CMFR or Ringer's devoid of only Ca<sup>2+</sup> (CFR). These treatments reduced Ca<sup>2+</sup> and Mg<sup>2+</sup> contents by 77% and 38% respectively. Addition of Ca<sup>2+</sup> (1.1 mM) during the 12-h period stimulated AXT, measured as accumulation of <sup>3</sup>H-labelled components in front of a ligature, several fold. Mg<sup>2+</sup> could not substitute for Ca<sup>2+</sup> but potentiated the stimulating effect of Ca<sup>2+</sup>. Addition of other divalent cations did not affect AXT (Sr<sup>2+</sup> and Ba<sup>2+</sup>) or potentiated the inhibition caused by Ca<sup>2+</sup>-deprived medium (Mn<sup>2+</sup> and Co<sup>2+</sup>). ATP and creatine phosphate contents were similar in nerves incubated in Ca<sup>2+</sup>-deprived medium and in Ca<sup>2+</sup>-containing Ringer's. Thus, inhibition of AXT in the former situation was not due to a decreased availability of high energy phosphates. Two calcium antagonists, D-600 and nifedipin, which are potent smooth muscle relaxants, effectively blocked AXT. The present ressults suggest that Ca<sup>2+</sup> is specifically required to maintain AXT and that an anlogy exists between Ca<sup>2+</sup> regulation during smooth muscle contraction and AXT.</p>}},
author = {{Kanje, Martin and Edström, Anders and Ekström, Per}},
issn = {{0006-8993}},
keywords = {{axonal transport; calcium; calcium antagonists; divalent cations}},
language = {{eng}},
month = {{06}},
number = {{1}},
pages = {{67--74}},
publisher = {{Elsevier}},
series = {{Brain Research}},
title = {{Divalent cations and fast axonal transport in chemically desheathed (triton X-treated) frog sciatic nerve}},
url = {{http://dx.doi.org/10.1016/0006-8993(82)91229-X}},
doi = {{10.1016/0006-8993(82)91229-X}},
volume = {{241}},
year = {{1982}},
}