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Functional Impairments in Learning and Signal Propagation Following Prenatal Kynurenine Treatment in Mice.

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Title: Functional Impairments in Learning and Signal Propagation Following Prenatal Kynurenine Treatment in Mice.
Authors: Beggiato, Sarah (AUTHOR), Brown, P. Leon (AUTHOR), Milosavljevic, Snezana (AUTHOR), Thomas, Marian A. R. (AUTHOR), Piroli, Maria V. (AUTHOR), Sathyasaikumar, Korrapati V. (AUTHOR), Notarangelo, Francesca M. (AUTHOR), Schwarcz, Robert (AUTHOR), Pocivavsek, Ana (AUTHOR)
Source: European Journal of Neuroscience. Jul2025, Vol. 62 Issue 1, p1-11. 11p.
Subjects: Learning, Kynurenine, Neurophysiology, Cognition disorders, Mice, Schizophrenia
Abstract: The levels of kynurenic acid (KYNA), a metabolite of the kynurenine pathway (KP) of tryptophan degradation, are elevated in the brain of persons with schizophrenia (SZ) and may be linked to cognitive dysfunctions in the disease. Studies in rats indicate that abnormally high fetal brain KYNA may play a pathophysiologically significant role in this context ("EKyn model"). Here, we fed pregnant C57Bl/6J mice with the immediate KYNA precursor kynurenine (10 mg or 30 mg/day; EKyn) or with control chow (ECon) from embryonic day (ED) 11 to ED 18 and assessed offspring postnatally both functionally and biochemically. In adulthood, male, but not female, EKyn mice showed significant impairments in spatial and reversal learning. Moreover, ex vivo recording of evoked local field potentials in coronal brain slices revealed a longer contralateral response latency in EKyn than in ECon animals, suggesting impaired white matter function. However, plasma and brain levels of KYNA and of another KP metabolite, 3‐hydroxykynurenine, did not differ between groups on postnatal day (PD) 21, on PD 35 (adolescence), or in adulthood (PD 56–75). Separate mice were fed prenatally with 4‐chloro‐kynurenine (20 mg/day), which is converted to the selective NMDA receptor antagonist 7‐chloro‐KYNA in vivo. Offspring did not show electrophysiological impairments in adulthood, indicating that NMDA receptors in the fetal brain were not the sole cause of functional deficits of EKyn mice later in life. The implications of these experiments for the study of psychiatric symptoms, as well as the unexpected differences between rats and mice, are discussed. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Label: Title
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  Data: Functional Impairments in Learning and Signal Propagation Following Prenatal Kynurenine Treatment in Mice.
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  Data: <searchLink fieldCode="AR" term="%22Beggiato%2C+Sarah%22">Beggiato, Sarah</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Brown%2C+P%2E Leon%22">Brown, P. Leon</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Milosavljevic%2C+Snezana%22">Milosavljevic, Snezana</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Thomas%2C+Marian A%2E R%2E%22">Thomas, Marian A. R.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Piroli%2C+Maria V%2E%22">Piroli, Maria V.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Sathyasaikumar%2C+Korrapati V%2E%22">Sathyasaikumar, Korrapati V.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Notarangelo%2C+Francesca M%2E%22">Notarangelo, Francesca M.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Schwarcz%2C+Robert%22">Schwarcz, Robert</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Pocivavsek%2C+Ana%22">Pocivavsek, Ana</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Jul2025, Vol. 62 Issue 1, p1-11. 11p.
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  Data: <searchLink fieldCode="DE" term="%22Learning%22">Learning</searchLink><br /><searchLink fieldCode="DE" term="%22Kynurenine%22">Kynurenine</searchLink><br /><searchLink fieldCode="DE" term="%22Neurophysiology%22">Neurophysiology</searchLink><br /><searchLink fieldCode="DE" term="%22Cognition+disorders%22">Cognition disorders</searchLink><br /><searchLink fieldCode="DE" term="%22Mice%22">Mice</searchLink><br /><searchLink fieldCode="DE" term="%22Schizophrenia%22">Schizophrenia</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: The levels of kynurenic acid (KYNA), a metabolite of the kynurenine pathway (KP) of tryptophan degradation, are elevated in the brain of persons with schizophrenia (SZ) and may be linked to cognitive dysfunctions in the disease. Studies in rats indicate that abnormally high fetal brain KYNA may play a pathophysiologically significant role in this context ("EKyn model"). Here, we fed pregnant C57Bl/6J mice with the immediate KYNA precursor kynurenine (10 mg or 30 mg/day; EKyn) or with control chow (ECon) from embryonic day (ED) 11 to ED 18 and assessed offspring postnatally both functionally and biochemically. In adulthood, male, but not female, EKyn mice showed significant impairments in spatial and reversal learning. Moreover, ex vivo recording of evoked local field potentials in coronal brain slices revealed a longer contralateral response latency in EKyn than in ECon animals, suggesting impaired white matter function. However, plasma and brain levels of KYNA and of another KP metabolite, 3‐hydroxykynurenine, did not differ between groups on postnatal day (PD) 21, on PD 35 (adolescence), or in adulthood (PD 56–75). Separate mice were fed prenatally with 4‐chloro‐kynurenine (20 mg/day), which is converted to the selective NMDA receptor antagonist 7‐chloro‐KYNA in vivo. Offspring did not show electrophysiological impairments in adulthood, indicating that NMDA receptors in the fetal brain were not the sole cause of functional deficits of EKyn mice later in life. The implications of these experiments for the study of psychiatric symptoms, as well as the unexpected differences between rats and mice, are discussed. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1111/ejn.70185
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        Text: English
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        PageCount: 11
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    Subjects:
      – SubjectFull: Learning
        Type: general
      – SubjectFull: Kynurenine
        Type: general
      – SubjectFull: Neurophysiology
        Type: general
      – SubjectFull: Cognition disorders
        Type: general
      – SubjectFull: Mice
        Type: general
      – SubjectFull: Schizophrenia
        Type: general
    Titles:
      – TitleFull: Functional Impairments in Learning and Signal Propagation Following Prenatal Kynurenine Treatment in Mice.
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              Text: Jul2025
              Type: published
              Y: 2025
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