Neuroscience 2003 Abstract
| Presentation Number: | 307.9 |
|---|---|
| Abstract Title: | Preconditioning with the anesthetic isoflurane: possible role of MAP kinase mek1/2 (p42/44). |
| Authors: |
Bickler, P. E.*1
; Fahlman, C. S.1
; Schuyler, J. A.1
1Dept. Anesthesia, UCSF, San Francisco, CA |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Ischemia -- Neuroprotection and tolerance |
| Session: |
307. Ischemia: Neuroprotection & Tolerance - Preconditioning Poster |
| Presentation Time: | Sunday, November 9, 2003 1:00 PM-2:00 PM |
| Location: | Morial Convention Center - Hall F-I, Board # II3 |
| Keywords: | ischemia, hippocampus, slice culture, MAPK |
The volatile anesthetic isoflurane is neuroprotective when administered just before or concurrent with brain ischemia. In hippocampal slice cultures, isoflurane administered concurrently with OGD reduces cell death in CA1, CA3 and dentate neurons by >75% (Anesthesiol., 96:189, 2002). In the heart, isoflurane pre-conditioning (a bout of anesthetic administration <1hr before ischemia) reduces myocardial injury during subsequent ischemia, but a phenomenon similar to classic ischemic preconditioning with isoflurane has not been described in the brain. In cortical neurons in mice and in organotypic hippocampal slice cultures from rats, isoflurane increases intracellular calcium concentration, activates MAPK p42/44 (ERK), pC-JUN, MKK3/6 and Raf, events possibly linked to neuroprotective gene expression (Fahlman, C.S. SFN Abstract, 2003). Therefore, in organotypic hippcampal cultures, we determined whether isoflurane (2% vapor in 95%O2/5%CO2 for 2 hrs at 37 C) 24 hours before a one hour period of oxygen-glucose deprivation at 37C (OGD) reduces the extent of neuron death 2-3 days later. Control cultures were treated identically except for the absence of isoflurane. Isoflurane preconditioning reduced cell death in CA1 neurons from 32±5% to 23±3% at 48 hrs post OGD (-28%) and from 41±4.7% to 30±4.4% (-27%, both p<0.05) at 72 hrs post OGD. After 1 hr of 1% isoflurane, immunostaining of the MAP kinase MEK1/2 in the CA1 region of the slice cultures was increased for at least 24 hrs. In cultured mouse cortical neurons, inhibition of MEK1/2 with U0126 prevented isoflurane neuroprotection during 1hr of anoxia (viability assay with calcein and propidium iodide) , suggesting that events in the MAP kinase axis may also be the basis of isoflurane preconditioning.
Supported by NIH GM52212
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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