PMID- 20298758
OWN - NLM
STAT- MEDLINE
DCOM- 20100820
LR  - 20181113
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Print)
IS  - 0306-4522 (Linking)
VI  - 168
IP  - 1
DP  - 2010 Jun 16
TI  - Is age-dependent, ketamine-induced apoptosis in the rat somatosensory cortex 
      influenced by temperature?
PG  - 253-62
LID - 10.1016/j.neuroscience.2010.03.016 [doi]
AB  - General anesthetics have long been thought to be relatively safe but recent 
      clinical studies have revealed that exposure of very young children (4 years or 
      less) to agents that act by blocking the N-methyl-D-aspartate receptor (NMDAR) 
      can lead to cognitive deficits as they mature. In rodent and non-human primate 
      studies, blockade of this receptor during the perinatal period leads to a number 
      of molecular, cellular and behavioral pathologies. Despite the overwhelming 
      evidence from such studies, doubt remains as to their clinical relevance. A key 
      issue is whether the primary injury (apoptotic cell death) is specific to 
      receptor blockade or due to non-specific, patho-physiological changes. Principal 
      to this argument is that loss of core body temperature following NMDAR blockade 
      could explain why injury is observed hours later. We therefore examined the 
      neurotoxicity of the general anesthetic ketamine in P7, P14 and P21 rats while 
      monitoring core body temperature. We found that, at P7, ketamine induced the 
      pro-apoptotic enzyme activated caspase-3 in a dose-dependent manner. As expected, 
      injury was greatly diminished by P14 and absent by P21. However, contrary to 
      expectations, we found that core body temperature was not a factor in determining 
      injury. Our data imply that injury is directly related to receptor blockade and 
      is unlikely to be overcome by artificially changing core body temperature.
CI  - 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Gutierrez, S
AU  - Gutierrez S
AD  - Department of Neurobiology & Anatomy, Wake Forest University School of Medicine, 
      1 Medical Center Boulevard, Winston-Salem, NC 27157-1010, USA.
FAU - Carnes, A
AU  - Carnes A
FAU - Finucane, B
AU  - Finucane B
FAU - Musci, G
AU  - Musci G
FAU - Oelsner, W
AU  - Oelsner W
FAU - Hicks, L
AU  - Hicks L
FAU - Russell, G B
AU  - Russell GB
FAU - Liu, C
AU  - Liu C
FAU - Turner, C P
AU  - Turner CP
LA  - eng
GR  - R01 NS051632/NS/NINDS NIH HHS/United States
GR  - R01 NS051632-04/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20100315
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Anesthetics, General)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 690G0D6V8H (Ketamine)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Age Factors
MH  - Anesthetics, General/*pharmacology
MH  - Animals
MH  - *Apoptosis
MH  - Caspase 3/biosynthesis
MH  - Female
MH  - Ketamine/*pharmacology
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, N-Methyl-D-Aspartate/*antagonists & inhibitors
MH  - Somatosensory Cortex/cytology/*drug effects
MH  - *Temperature
PMC - PMC2871987
MID - NIHMS189719
EDAT- 2010/03/20 06:00
MHDA- 2010/08/21 06:00
PMCR- 2011/06/16
CRDT- 2010/03/20 06:00
PHST- 2009/12/08 00:00 [received]
PHST- 2010/02/09 00:00 [revised]
PHST- 2010/03/08 00:00 [accepted]
PHST- 2010/03/20 06:00 [entrez]
PHST- 2010/03/20 06:00 [pubmed]
PHST- 2010/08/21 06:00 [medline]
PHST- 2011/06/16 00:00 [pmc-release]
AID - S0306-4522(10)00367-2 [pii]
AID - 10.1016/j.neuroscience.2010.03.016 [doi]
PST - ppublish
SO  - Neuroscience. 2010 Jun 16;168(1):253-62. doi: 10.1016/j.neuroscience.2010.03.016. 
      Epub 2010 Mar 15.