Effects of Calcium, Magnesium, and Calcium Chelating Agent on Recovery from Hypoxia in Hippocampal Tissue Slices.
- Author:
Woo Jae KIM
1
;
Jung Yul PARK
;
Youn Kwan PARK
;
Heung Seob CHUNG
;
Ki Chan LEE
;
Hoon Kap LEE
Author Information
1. Departmentof Neurosurgery,College ofMedicine,Korea UniversityMedical Center, Seoul, Korea.
- Publication Type:In Vitro ; Original Article
- Keywords:
Hypoxia;
Calcium;
Magnesium;
BAPTA-AM
- MeSH:
Anoxia*;
Calcium*;
Ischemia;
Magnesium*;
N-Methylaspartate;
Neurons
- From:Journal of Korean Neurosurgical Society
1997;26(4):491-498
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
To providean evidence tosupport thecalcium hypothesis ofcerebral ischemia, we examinedthe effectsoftheextracellular calciumandcalciumchelating agent(Bapta-AM), and magnesiumon in vitro ischemia usingrat hippocampal slices. Loss of the populationspike on thehippocampal CA1 region afterelectrical stimulation was usedas indexof damageon thesynaptictransmission andspike amplitudeof the population spikeas index ofrecovery level.Recovery from theloss of orthodromic responses aftertransient hypoxia in lowcalcium treated sliceswas more rapid than nontreated normal calciumslices, and remained robust for4 hours in slices exposed in lowcalcium, whileresponses inslices madehypoxic in normalcalcium remained depressed or more slowlyrecovered. There were statistical significant differences of amplitude between the two group at 5, 10 15, 30, 60, 90 and 120 minute after 10 minute hypoxia (p<0.05).To thelesserextent, similarresults wasobservedin calcium chelating agent, BAPTA-AM, treatedslices, with statistical significant difference at 10minute afterhypoxia(p<0.05). Butin additionto reducingcalcium, elevating magnesium levelwhich is knownas voltagedependent NMDA receptorblocker, did not improve recoverycompared to reducingcalcium alone. We concludethat recovery from the lossof function afterhypoxia was improved bydecreasing extracellular calcium concentration of neuronsand activation of NMDA receptorsprobably played no part in early neuronal damage.
