TY - JOUR
T1 - Hypoxia on hippocampal slices from mice deficient in dystrophin (mdx) and isoforms (mdx(3cv))
AU - Godfraind, Jean Marie
AU - Tekkök, Selva Baltan
AU - Krnjević, Krešimir
N1 - Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2000
Y1 - 2000
N2 - Slices from control C57, mdx, and mdx(3cv) mice were made hypoxic until both field excitatory postsynaptic potential (fEPSP) and presynaptic afferent volley (AV) disappeared (H1). After reoxygenation and recovery of fEPSP, a second and longer hypoxic test (H2) lasted 3 minutes beyond the time required to block AV. When slices were kept in 10 mmol/L glucose, H1 abolished AV 37 and 19% earlier in slices from mdx and mdx(3cv) mutants than in control slices (where H1 = 12 ± 4.6 minutes, mean ± SD). During H2 or when slices were kept in 4 mmol/L glucose, AV vanished even more quickly, but the times to block did not differ significantly between slices from controls and mutants. After reoxygenation, AV fully recovered in most slices. Rates of blockade of fEPSPs were comparable in all slices, and most fEPSPs recovered fully after H1. But even in the presence of 10 mmol/L glucose, the second hypoxia suppressed fEPSPs irreversibly in some slices: 2 of 10 from control, 3 of 7 from mdx, and 1 of 6 from md(3cv) mice. Most slices in 4 mmol/L glucose showed no recovery at all: six of seven from control, three of five from mdx, and four of five from mdx(3cv) mice. Thus, slices from mdx mice were more susceptible than other slices to irreversible hypoxic failure when slices were kept in 10 mmol/L glucose, but they were less susceptible than other slices when kept in 4 mmol/L glucose. In conclusion, the lack of full- length dystrophin (427 kDa) predisposes to quicker loss of nerve conduction in slices from mdx and mdx(3cv) mutants and improved posthypoxic recovery of fEPSPs in 4 mmol/L glucose in slices from mdx but not mdx(3cv) mutants, perhaps because the 70-kDa and other C-terminal isoforms are still present in mdx mice.
AB - Slices from control C57, mdx, and mdx(3cv) mice were made hypoxic until both field excitatory postsynaptic potential (fEPSP) and presynaptic afferent volley (AV) disappeared (H1). After reoxygenation and recovery of fEPSP, a second and longer hypoxic test (H2) lasted 3 minutes beyond the time required to block AV. When slices were kept in 10 mmol/L glucose, H1 abolished AV 37 and 19% earlier in slices from mdx and mdx(3cv) mutants than in control slices (where H1 = 12 ± 4.6 minutes, mean ± SD). During H2 or when slices were kept in 4 mmol/L glucose, AV vanished even more quickly, but the times to block did not differ significantly between slices from controls and mutants. After reoxygenation, AV fully recovered in most slices. Rates of blockade of fEPSPs were comparable in all slices, and most fEPSPs recovered fully after H1. But even in the presence of 10 mmol/L glucose, the second hypoxia suppressed fEPSPs irreversibly in some slices: 2 of 10 from control, 3 of 7 from mdx, and 1 of 6 from md(3cv) mice. Most slices in 4 mmol/L glucose showed no recovery at all: six of seven from control, three of five from mdx, and four of five from mdx(3cv) mice. Thus, slices from mdx mice were more susceptible than other slices to irreversible hypoxic failure when slices were kept in 10 mmol/L glucose, but they were less susceptible than other slices when kept in 4 mmol/L glucose. In conclusion, the lack of full- length dystrophin (427 kDa) predisposes to quicker loss of nerve conduction in slices from mdx and mdx(3cv) mutants and improved posthypoxic recovery of fEPSPs in 4 mmol/L glucose in slices from mdx but not mdx(3cv) mutants, perhaps because the 70-kDa and other C-terminal isoforms are still present in mdx mice.
KW - Afferent volley
KW - Anoxia
KW - CA1 synaptic transmission
KW - Glucose
KW - Mutants
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U2 - 10.1097/00004647-200001000-00019
DO - 10.1097/00004647-200001000-00019
M3 - Article
C2 - 10616803
AN - SCOPUS:17544364407
VL - 20
SP - 145
EP - 152
JO - Journal of Cerebral Blood Flow and Metabolism
JF - Journal of Cerebral Blood Flow and Metabolism
SN - 0271-678X
IS - 1
ER -