17β-estradiol pretreatment reduces CA1 sector cell death and the spontaneous hyperthermia that follows forebrain ischemia in the gerbil

W. C. Plahta, D. Clark, F. Colbourne

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Pretreatment with 17β-estradiol attenuates ischemia-induced hippocampal cornu ammonis 1 (CA1) neuronal death. We assessed whether this is mediated through prevention of hyperthermia that normally follows ischemia in gerbils. Male gerbils were given sustained-released 17β-estradiol pellets or sham operation. Later, a guide cannula was implanted for brain temperature measurement and some were implanted with core temperature telemetry probes. Gerbils were subjected to either 5 min bilateral carotid artery occlusion or sham procedures 2 weeks after pellet surgery. Brain temperature was normothermic during surgery in all cases. In experiment 1, only core temperature was measured afterward in untreated and estrogen-treated gerbils. In experiment 2, postischemic core temperature was measured in untreated and two estrogen-treated ischemic groups, one of which had their postischemic temperature increased, via infrared lamp, to mimic the untreated group. Habituation was assessed on days 5 and 6. Hyperthermia, like that which occurs spontaneously, was forced on untreated and estrogen-treated ischemic animals in the third experiment, where brain temperature was measured. CA1 cell counts were assessed after a 7-day survival. A fourth experiment measured brain and core temperature simultaneously in normal gerbils during heating with an infrared lamp. Estrogen did not affect core temperature of non-ischemic gerbils whereas spontaneous postischemic hyperthermia was blocked. Estrogen reduced cell death and provided behavioral protection when gerbils regulated their own core temperature, but not when core hyperthermia was enforced. Conversely, estrogen reduced cell death in gerbils that had their brain temperature elevated. Experiment 4 showed that the brain becomes overheated (by approximately 1°C) when core temperature is elevated. Accordingly, estrogen likely failed to reduce CA1 injury in experiment 2, when core hyperthermia was enforced, because of overheating the brain. In conclusion, estrogen reduces CA1 cell death by mechanisms other than preventing hyperthermia. Our results also suggest that future studies regulate brain instead of body temperature.

Original languageEnglish
Pages (from-to)187-193
Number of pages7
JournalNeuroscience
Volume129
Issue number1
DOIs
Publication statusPublished - 2004

Fingerprint

Gerbillinae
Prosencephalon
Estradiol
Hippocampus
Cell Death
Fever
Ischemia
Temperature
Estrogens
Brain
Telemetry
Body Temperature
Carotid Arteries
Heating
Cell Count

Keywords

  • estrogen
  • habituation
  • hippocampus
  • rodent
  • stroke
  • temperature

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

17β-estradiol pretreatment reduces CA1 sector cell death and the spontaneous hyperthermia that follows forebrain ischemia in the gerbil. / Plahta, W. C.; Clark, D.; Colbourne, F.

In: Neuroscience, Vol. 129, No. 1, 2004, p. 187-193.

Research output: Contribution to journalArticle

@article{963d22e933854002b4760755c210224d,
title = "17β-estradiol pretreatment reduces CA1 sector cell death and the spontaneous hyperthermia that follows forebrain ischemia in the gerbil",
abstract = "Pretreatment with 17β-estradiol attenuates ischemia-induced hippocampal cornu ammonis 1 (CA1) neuronal death. We assessed whether this is mediated through prevention of hyperthermia that normally follows ischemia in gerbils. Male gerbils were given sustained-released 17β-estradiol pellets or sham operation. Later, a guide cannula was implanted for brain temperature measurement and some were implanted with core temperature telemetry probes. Gerbils were subjected to either 5 min bilateral carotid artery occlusion or sham procedures 2 weeks after pellet surgery. Brain temperature was normothermic during surgery in all cases. In experiment 1, only core temperature was measured afterward in untreated and estrogen-treated gerbils. In experiment 2, postischemic core temperature was measured in untreated and two estrogen-treated ischemic groups, one of which had their postischemic temperature increased, via infrared lamp, to mimic the untreated group. Habituation was assessed on days 5 and 6. Hyperthermia, like that which occurs spontaneously, was forced on untreated and estrogen-treated ischemic animals in the third experiment, where brain temperature was measured. CA1 cell counts were assessed after a 7-day survival. A fourth experiment measured brain and core temperature simultaneously in normal gerbils during heating with an infrared lamp. Estrogen did not affect core temperature of non-ischemic gerbils whereas spontaneous postischemic hyperthermia was blocked. Estrogen reduced cell death and provided behavioral protection when gerbils regulated their own core temperature, but not when core hyperthermia was enforced. Conversely, estrogen reduced cell death in gerbils that had their brain temperature elevated. Experiment 4 showed that the brain becomes overheated (by approximately 1°C) when core temperature is elevated. Accordingly, estrogen likely failed to reduce CA1 injury in experiment 2, when core hyperthermia was enforced, because of overheating the brain. In conclusion, estrogen reduces CA1 cell death by mechanisms other than preventing hyperthermia. Our results also suggest that future studies regulate brain instead of body temperature.",
keywords = "estrogen, habituation, hippocampus, rodent, stroke, temperature",
author = "Plahta, {W. C.} and D. Clark and F. Colbourne",
year = "2004",
doi = "10.1016/j.neuroscience.2004.07.037",
language = "English",
volume = "129",
pages = "187--193",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "Elsevier Limited",
number = "1",

}

TY - JOUR

T1 - 17β-estradiol pretreatment reduces CA1 sector cell death and the spontaneous hyperthermia that follows forebrain ischemia in the gerbil

AU - Plahta, W. C.

AU - Clark, D.

AU - Colbourne, F.

PY - 2004

Y1 - 2004

N2 - Pretreatment with 17β-estradiol attenuates ischemia-induced hippocampal cornu ammonis 1 (CA1) neuronal death. We assessed whether this is mediated through prevention of hyperthermia that normally follows ischemia in gerbils. Male gerbils were given sustained-released 17β-estradiol pellets or sham operation. Later, a guide cannula was implanted for brain temperature measurement and some were implanted with core temperature telemetry probes. Gerbils were subjected to either 5 min bilateral carotid artery occlusion or sham procedures 2 weeks after pellet surgery. Brain temperature was normothermic during surgery in all cases. In experiment 1, only core temperature was measured afterward in untreated and estrogen-treated gerbils. In experiment 2, postischemic core temperature was measured in untreated and two estrogen-treated ischemic groups, one of which had their postischemic temperature increased, via infrared lamp, to mimic the untreated group. Habituation was assessed on days 5 and 6. Hyperthermia, like that which occurs spontaneously, was forced on untreated and estrogen-treated ischemic animals in the third experiment, where brain temperature was measured. CA1 cell counts were assessed after a 7-day survival. A fourth experiment measured brain and core temperature simultaneously in normal gerbils during heating with an infrared lamp. Estrogen did not affect core temperature of non-ischemic gerbils whereas spontaneous postischemic hyperthermia was blocked. Estrogen reduced cell death and provided behavioral protection when gerbils regulated their own core temperature, but not when core hyperthermia was enforced. Conversely, estrogen reduced cell death in gerbils that had their brain temperature elevated. Experiment 4 showed that the brain becomes overheated (by approximately 1°C) when core temperature is elevated. Accordingly, estrogen likely failed to reduce CA1 injury in experiment 2, when core hyperthermia was enforced, because of overheating the brain. In conclusion, estrogen reduces CA1 cell death by mechanisms other than preventing hyperthermia. Our results also suggest that future studies regulate brain instead of body temperature.

AB - Pretreatment with 17β-estradiol attenuates ischemia-induced hippocampal cornu ammonis 1 (CA1) neuronal death. We assessed whether this is mediated through prevention of hyperthermia that normally follows ischemia in gerbils. Male gerbils were given sustained-released 17β-estradiol pellets or sham operation. Later, a guide cannula was implanted for brain temperature measurement and some were implanted with core temperature telemetry probes. Gerbils were subjected to either 5 min bilateral carotid artery occlusion or sham procedures 2 weeks after pellet surgery. Brain temperature was normothermic during surgery in all cases. In experiment 1, only core temperature was measured afterward in untreated and estrogen-treated gerbils. In experiment 2, postischemic core temperature was measured in untreated and two estrogen-treated ischemic groups, one of which had their postischemic temperature increased, via infrared lamp, to mimic the untreated group. Habituation was assessed on days 5 and 6. Hyperthermia, like that which occurs spontaneously, was forced on untreated and estrogen-treated ischemic animals in the third experiment, where brain temperature was measured. CA1 cell counts were assessed after a 7-day survival. A fourth experiment measured brain and core temperature simultaneously in normal gerbils during heating with an infrared lamp. Estrogen did not affect core temperature of non-ischemic gerbils whereas spontaneous postischemic hyperthermia was blocked. Estrogen reduced cell death and provided behavioral protection when gerbils regulated their own core temperature, but not when core hyperthermia was enforced. Conversely, estrogen reduced cell death in gerbils that had their brain temperature elevated. Experiment 4 showed that the brain becomes overheated (by approximately 1°C) when core temperature is elevated. Accordingly, estrogen likely failed to reduce CA1 injury in experiment 2, when core hyperthermia was enforced, because of overheating the brain. In conclusion, estrogen reduces CA1 cell death by mechanisms other than preventing hyperthermia. Our results also suggest that future studies regulate brain instead of body temperature.

KW - estrogen

KW - habituation

KW - hippocampus

KW - rodent

KW - stroke

KW - temperature

UR - http://www.scopus.com/inward/record.url?scp=5444274657&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=5444274657&partnerID=8YFLogxK

U2 - 10.1016/j.neuroscience.2004.07.037

DO - 10.1016/j.neuroscience.2004.07.037

M3 - Article

C2 - 15489041

AN - SCOPUS:5444274657

VL - 129

SP - 187

EP - 193

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

IS - 1

ER -