Hydrogen cyanide generation by μ-opiate receptor activation: possible neuromodulatory role of endogenous cyanide

@article{Borowitz1997HydrogenCG,
  title={Hydrogen cyanide generation by $\mu$-opiate receptor activation: possible neuromodulatory role of endogenous cyanide},
  author={Joseph L. Borowitz and Palur G. Gunasekar and Gary E. Isom},
  journal={Brain Research},
  year={1997},
  volume={768},
  pages={294-300}
}
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A mitochondria-specific coumarin pyrrolidinium-derived fluorescence probe (MRP1) that permits the real-time ratiometric imaging ofHCN in living cells and has proved effective in visualizing different concentrations of exogenous HCN in the mitochondria of HepG2 cells, as well as the imaging of endogenous HCN within neurons.
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  • 2009
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A critical analysis of acute CO and CN poisonings evidences that the lone toxicological similarity between CO andCN is their ability to avidly bind iron ions in the different hemoproteins, further supporting different mechanisms of action.
Inhibition by naloxone of promoter activity of the neurofilament gene in SK-N-SH cells.
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It is suggested that naloxone has the ability to suppress transcriptional activity in some neurons by inhibition by dose-dependent and not reversed by morphine.
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References

SHOWING 1-10 OF 36 REFERENCES
Cyanide‐induced alteration of the adenylate energy pool in a rat neurosecretory cell line
TLDR
Since PC12 cells rapidly respond to cyanide, with predictable depletions of the cell adenylate energy pool, this cell line can serve as a suitable in vitro model for studies of neurotoxicity involving ischemic/hypoxic conditions.
The possible role of hydrogen sulfide as an endogenous neuromodulator
  • K. Abe, H. Kimura
  • Biology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1996
TLDR
It is shown that physiological concentrations of H2S selectively enhance NMDA receptor-mediated responses and facilitate the induction of hippocampal long-term potentiation, suggesting that endogenous H 2S functions as a neuromodulator in the brain.
Modulation of the NMDA receptor by cyanide: enhancement of receptor-mediated responses.
TLDR
Results indicate that cyanide interacts directly with the NMDA receptor channel complex to enhance receptor-mediated responses and increase the amplitude and duration of NMDA-stimulated whole-cell currents in patch-clamp studies.
Activation of a calcium- and pH-dependent phospholipase A2 by cyanide in PC12 cells.
TLDR
Data indicate that in PC12 cells KCN activates a Ca(2+)- and pH-dependent PLA2 which may contribute to cyanide-induced cell damage.
Accumulation of labeled cyanide in neuronal tissue.
Since cyanide is a reactive chemical substance and has the potential of forming a variety of adducts in biological systems, the rate of accumulation of labeled cyanide was studied in neural tissue, a
Opioid-glutamate interactions in rat locus coeruleus neurons.
TLDR
The results suggest that the mu-opioid-mediated potentiation of the glutamate response is dependent on membrane hyperpolarization.
Dopaminergic neurotoxicity of cyanide: neurochemical, histological, and behavioral characterization.
TLDR
Under these treatment conditions, cyanide produces a central dopaminergic toxicity which is characterized by decreased DA levels in select brain areas, impaired locomotor activity, and neuronal damage.
Reduced nicotinamide adenine dinucleotide-selective stimulation of inositol 1,4,5-trisphosphate receptors mediates hypoxic mobilization of calcium
TLDR
Findings indicate that direct regulation of IP3R by NADH is responsible for elevated cytoplasmic [Ca2+] occurring in the earliest phase of hypoxia, and may be relevant to both hypoxic damage and metabolic regulation ofIP3 signaling processes.
Nitric oxide release from a single cell measured in situ by a porphyrinic-based microsensor
TLDR
A porphyrinic microsensor is developed and applied to monitoring NO release in a microsystem and selectively measured in situ the NO released from a single cell with a response time of less than 10 ms.
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