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Mice lacking urea transporter UT-B display depression-like behavior.

Xin Li1, Jianhua Ran, Hong Zhou

  • 1Department of Pharmacology, School of Basic Medical Sciences, Peking University, 38 Xueyuan Lu, Haidian District, Beijing, 100191, China.

Journal of Molecular Neuroscience : MN
|July 14, 2011
PubMed
Summary

Urea transporter B (UT-B) deletion in mice causes urea accumulation in the brain, leading to depression-like behaviors. This suggests UT-B plays a crucial role in brain urea transport and function.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Physiology

Background:

  • Urea transporter B (UT-B) facilitates urea transport across membranes and is abundant in the brain.
  • The precise physiological role of UT-B in the brain remains to be fully elucidated.

Purpose of the Study:

  • To investigate the physiological role of UT-B in the brain by examining its localization, urea concentration, tissue morphology, and behavioral phenotypes in UT-B null mice.
  • To determine the impact of UT-B deletion on urea levels, nitric oxide (NO) production, and brain structure.

Main Methods:

  • Studied UT-B mRNA expression in heterozygous mice.
  • Analyzed urea concentration, nitric oxide (NO) levels, and selective neuronal nitric oxide synthase (nNOS) in UT-B null and heterozygous mice.
  • Assessed regional cerebral blood flow and hippocampal morphology, including neuronal integrity and myelin structures.

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  • Conducted in vitro experiments with urea to observe its effect on NO production.

    • Main Results:

    • UT-B mRNA was detected in various brain regions of heterozygous mice.
    • UT-B null mice displayed depression-like behavior, characterized by urea accumulation, reduced NO, and increased nNOS in the hippocampus.
    • Acute urea loading increased urea levels and decreased NO production in the hippocampus of both mouse types.
    • UT-B knockout led to decreased cerebral blood flow, hippocampal neuronal loss (CA3 region), and altered myelin structures.

    Conclusions:

    • Urea accumulation in the hippocampus due to UT-B deletion is linked to depression-like behaviors in mice.
    • The observed behavioral changes may result from disruptions in the nitric oxide synthase/nitric oxide (NOS/NO) system.
    • UT-B plays a significant role in maintaining brain urea homeostasis, cerebral blood flow, and neuronal health.