1996
DOI: 10.1016/s0014-2999(96)00613-9
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(R,S)-3,4-dichlorobenzoylalanine (FCE 28833A) causes a large and persistent increase in brain kynurenic acid levels in rats

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Cited by 91 publications
(50 citation statements)
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“…It is well known that pharmacological blockade of the enzyme converting KYN to 3-hydroxykynurenine, kynurenine 3-monooxygenase (KMO), results in elevated brain KYNA levels. 19,34,[53][54][55] In addition, we recently reported that a nonsynonymous polymorphism in the KMO gene results in higher CSF KYNA levels in both healthy volunteers and patients with schizophrenia. 56 Also, a postmortem study shows decreased KMO gene expression as well as decreased KMO enzyme activity in individuals with schizophrenia.…”
Section: Discussionmentioning
confidence: 99%
“…It is well known that pharmacological blockade of the enzyme converting KYN to 3-hydroxykynurenine, kynurenine 3-monooxygenase (KMO), results in elevated brain KYNA levels. 19,34,[53][54][55] In addition, we recently reported that a nonsynonymous polymorphism in the KMO gene results in higher CSF KYNA levels in both healthy volunteers and patients with schizophrenia. 56 Also, a postmortem study shows decreased KMO gene expression as well as decreased KMO enzyme activity in individuals with schizophrenia.…”
Section: Discussionmentioning
confidence: 99%
“…The metabolism of kynurenine would thus be shunted toward KYNA, similar to the outcome of administering pharmacologic compounds that block KMO. 36 The availability of kynurenine is suggested to be the determinant of KYNA synthesis. 22 One might speculate that the SNP rs1053230 is affecting the function of the KMO enzyme, as it is associated with CSF concentrations of KYNA.…”
Section: Discussionmentioning
confidence: 99%
“…These findings are in excellent agreement with previous in vivo electrophysiological studies (Gessa et al, 2000;Tung et al, 1991;White and Wang, 1983) and it is generally accepted that antipsychotic drugs increase DA cell firing rate by blockade of somatodendritic DA autoreceptors Grace, 1994, 1996). However, in a situation of hyperdopaminergia induced by elevation of brain KYNA Engberg, 2000, 2002;Erhardt et al, , 2001aErhardt et al, , b, 2002aSpeciale et al, 1996), the excitatory effects of clozapine observed in control rats were converted into pure inhibitory responses by the drug. In contrast, the excitatory action of haloperidol on VTA DA neurons was even more pronounced in rats with elevated levels of endogenous brain KYNA, since administration of the drug in low doses was associated with a depolarization block of all DA neurons recorded.…”
Section: Discussionmentioning
confidence: 99%