Kynurenine potentiates the DOI head shake in mice

@article{McCreary1995KynureninePT,
  title={Kynurenine potentiates the DOI head shake in mice},
  author={Andrew C McCreary and Sheila L. Handley},
  journal={Journal of Psychopharmacology},
  year={1995},
  volume={9},
  pages={69 - 70}
}
Kynurenine is the first stable metabolite of the kynurenine pathway [which metabolises > 9007o of body tryptophan (Wolf, 1974) ]. A number of kynurenine pathway metabolites are known to have biological activity, including 3-hydroxykynurenine, xanthurenic acid, quinolinic acid and kynurenic acid (for reviews, see Schwarcz, 1993; Heyes, 1993; Stone and Connick, 1985). Recent studies have demonstrated that plasma kynurenine concentrations were elevated in all of seven patients suffering from… 
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References

SHOWING 1-10 OF 15 REFERENCES
Metabolism and neuropathologic significance of quinolinic acid and kynurenic acid.
  • M. Heyes
  • Biology, Chemistry
    Biochemical Society transactions
  • 1993
TLDR
A significantly different picture of how QUIN and KYNA are metabolized has emerged from studies of the consequences of immune activation, and a review will summarize these responses.
Metabolism and function of brain kynurenines.
  • R. Schwarcz
  • Biology
    Biochemical Society transactions
  • 1993
From Molecular Pharmacology to Behavior (Mandel, P. and DeFeudis, F. V., eds.), pp. 163-174, Raven Press, New York 25. Mayer, M. L. and Westbrook, G. L. (1985) J. Physiol. (London) 361,65-90 26.
Potencies of antagonists indicate that 5‐HT1C receptors mediate 1–3(chlorophenyl)piperazine‐induced hypophagia
TLDR
Results strongly support the hypothesis that mediation of mCPP‐induced hypophagia is by stimulation of 5‐HT1C receptors and the mediation of 4‐HT2‐induced head twitches by 5‐ HT2 receptors.
In vivo properties of SB 200646A, a 5‐HT2C/2B receptor antagonist
TLDR
The results indicate that SB 200646A has in vivo efficacy and that 5‐HT2C or 5‐ HT2B receptors are indeed likely to mediate mCPP‐induced hypolocomotion, hypophagia and anxiogenesis and suggest that5‐HT 2C/2B receptor blockade induces anxiolysis.
Elevated plasma kynurenine in Tourette syndrome.
Fasting plasma kynurenine concentrations were significantly elevated in a group of 7 patients (4 female) conforming to DSM-III-R of the American Psychiatric Association (1987) criteria for Tourette
5-HT1 and 5-HT2 binding characteristics of 1-(2,5-dimethoxy-4-bromophenyl)-2-aminopropane analogues.
TLDR
Of the DOB analogues examined, DOB (1a) possesses optimal selectivity for 5-HT2 binding, and the S-(+) isomer of the iodo analogue of 1a was found to possess one-third the affinity of its R-(-) enantiomer at 5- HT2 sites and also resulted in DOM-stimulus generalization.
1C receptors mediate the 1-3 (chlorophenyl) piperazine-induced hypophagia
  • Br J Pharmacol
  • 1994
Serotonin and Tourette’s Syndrome: movements
  • 1992
Potencies of antagonists
  • 1991
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