Kynurenine potentiates the DOI head shake in mice

  title={Kynurenine potentiates the DOI head shake in mice},
  author={Andrew C McCreary and Sheila L. Handley},
  journal={Journal of Psychopharmacology},
  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… 
7 Citations

Figures from this paper

Effects of nicotine on head-shakes and tryptophan metabolites
The acute studies indicate that head-shakes induced by DOI are indeed inhibited by nicotinic receptor agonists and suggest that this is not a consequence of an increase in kynurenine.
Plasma kynurenine and related measures in tic disorder patients
While the observed elevation in plasma neopterin is consistent with immune activation in a subset of tic Disorder patients, metabolism of tryptophan through the kynurenine pathway appears to be unaltered in tic disorder patients.
Is Tourette's syndrome an autoimmune disease?
We provide a review of recent research findings which support the involvement of autoimmunity in childhood-onset tic disorders, in particular the presence of antineuronal autoantibodies, D8/17 B
Role of Autoimmunity and Infections in Tourette Syndrome
The classically proposed autoimmunity model of TS is analogous to Sydenham’s chorea, and antibodies directed against the streptococci are thought to cross-react with structures of the central nervous system, subsequently leading to damage to these structures, which eventually is thought to result in tics and associated features.


Metabolism and neuropathologic significance of quinolinic acid and kynurenic acid.
  • M. Heyes
  • Biology, Chemistry
    Biochemical Society transactions
  • 1993
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
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
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.
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