Xenon Inhibits but N2O Enhances Ketamine-Induced c-Fos Expression in the Rat Posterior Cingulate and Retrosplenial Cortices

@article{Nagata2001XenonIB,
  title={Xenon Inhibits but N2O Enhances Ketamine-Induced c-Fos Expression in the Rat Posterior Cingulate and Retrosplenial Cortices},
  author={A. Nagata and S. Nakao and Nobuyasu Nishizawa and M. Masuzawa and T. Inada and K. Murao and E. Miyamoto and K. Shingu},
  journal={Anesthesia \& Analgesia},
  year={2001},
  volume={92},
  pages={362–368}
}
Both nitrous oxide (N2O) and xenon are N-methyl-d-aspartate receptor antagonists that have psychotomimetic effects and cause neuronal injuries in the posterior cingulate and retrosplenial cortices. We investigated the effect of xenon, xenon with ketamine, N2O, and N2O with ketamine on c-Fos expression in the rat posterior cingulate and retrosplenial cortices, a marker of psychotomimetic effects. Brain sections were prepared, and c-Fos expression was detected with immunohistochemical methods. A… Expand
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References

SHOWING 1-10 OF 37 REFERENCES
Halothane and Diazepam Inhibit Ketamine‐induced c‐fos Expression in the Rat Cingulate Cortex
TLDR
Halothane and diazepam inhibited ketamine‐induced c‐Fos expression in the cingulate and retrosplenial cortices, leaving the thalamus relatively unaffected. Expand
Propofol Inhibits Ketamine-Induced c-fos Expression in the Rat Posterior Cingulate Cortex
TLDR
It is demonstrated that the clinically relevant dose of propofol significantly inhibited ketamine-induced c-fos expression in the rat posterior cingulate cortex, implying that prop ofol may inhibit ketamines-induced psychotomimetic activity and neuronal damage. Expand
Haloperidol prevents induction of the hsp70 heat shock gene in neurons injured by phencyclidine (PCP), MK801, and ketamine
TLDR
It is shown that PCP, MK801, and ketamine drug induced injury occurs in 30 day and older rats, but not in 0–20 day old rats, and is prevented by prior administration of the antipsychotic drugs haloperidol and rimcazole. Expand
Effects of phencyclidine on immediate early gene expression in the brain
TLDR
It is demonstrated that PCP produces neural activation not only in the cingulate and retrosplenial cortex, but also in many other regions of forebrain and cerebellum, suggesting that IEGs could mediate neurotoxic/neuroprotective effects in these brain regions. Expand
Phencyclidine-induced expression of c-Fos-like immunoreactivity in mouse brain regions
TLDR
It is suggested the possibility that such a c-Fos expression may underlie the behavioral and/or psychotomimetic effects of phencyclidine. Expand
Induction and suppression of immediate early genes in specific rat brain regions by the non-competitive N-methyl-d-aspartate receptor antagonist MK-801
TLDR
MK-801-elicited expression of immediate early gene-encoded proteins seems to identify reversibly injured neurons, mainly in layer III of the posterior cingulate and retrosplenial cortex, and is a more rapid and more sensitive indicator of non-lethal neuronal injury. Expand
High-dose ketamine does not induce c-Fos protein expression in rat hippocampus
TLDR
Findings disagree with the reports that ketamine depresses the neuronal function of the neocortex and thalamus, while it stimulates the limbic system. Expand
Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs.
TLDR
These findings raise new questions regarding the safety of these agents in the clinical management of neurodegenerative diseases and reinforce concerns about the potential risks associated with illicit use of PCP. Expand
The use of c-fos as a metabolic marker in neuronal pathway tracing
The use of c-fos protein (Fos) immunocytochemistry as a metabolic marker for tracing neuroanatomical connections, seizure pathways and sites of action of neuroactive drugs is discussed in thisExpand
Ketamine acts as a non-competitive N-methyl-d-aspartate antagonist on frog spinal cord in vitro
TLDR
Experiments in which combinations of drugs were tested indicated that these substances act by three distinct mechanisms to cause antagonism of the actions of NMDA. Expand
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4
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