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Related Experiment Videos

Hypothalamic-pituitary-gonadal axis in the mutant weaver mouse

N B Schwartz1, M Szabo, T Verina

  • 1Department of Neurobiology and Physiology, Northwestern University, Evanston, Ill., 60208-3520, USA.

Neuroendocrinology
|January 5, 1999
PubMed
Summary

The weaver (wv) mutant mouse, with a mutation in the GIRK2 potassium channel, exhibits male infertility due to primary germ cell defects. Hormonal analysis revealed normal pituitary function and testosterone levels.

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Area of Science:

  • Neurogenetics
  • Reproductive Biology
  • Endocrinology

Background:

  • The weaver (wv) mutant mouse displays neurological deficits, including cerebellar granule cell deficiency and midbrain dopaminergic system abnormalities.
  • This phenotype is linked to a missense mutation in the G-protein-gated inwardly rectifying potassium channel, GIRK2.
  • Homozygous male wv mice exhibit infertility, characterized by inadequate sperm production.

Purpose of the Study:

  • To investigate the hypothalamic-pituitary-gonadal (HPG) axis in wv mutant mice.
  • To determine the underlying causes of infertility in homozygous male wv mice.
  • To assess the impact of the GIRK2 mutation on reproductive hormone levels and testicular function.

Main Methods:

  • Evaluation of the HPG axis in heterozygote and homozygote male and female wv mutants compared to wild-type controls.

Related Experiment Videos

  • Measurement of testicular weight, pituitary and serum hormone levels (LH, FSH, prolactin, GH), and serum/testicular testosterone.
  • In situ hybridization to detect GIRK2 mRNA expression in testicular tissue and analysis of hypothalamic monoamine levels.

    • Main Results:

    • Homozygous male wv mice showed significantly reduced testicular weight and degenerative changes in seminiferous epithelium.
    • Pituitary and serum levels of LH, FSH, prolactin, and GH were normal across genotypes, maintaining normal sex differences.
    • Serum and testicular testosterone levels were normal; testicular alpha-inhibin was mildly reduced. Spermatogenesis defects were primarily postmeiotic. GIRK2 mRNA was detected in seminiferous epithelium. Hypothalamic homovanillic acid was reduced in homozygotes.

    Conclusions:

    • Male infertility in wv homozygotes stems from a primary defect within the seminiferous tubules, likely affecting germ cells directly.
    • The HPG axis, including pituitary hormone secretion and Leydig cell function, appears largely intact.
    • The GIRK2 mutation's impact on spermatogenesis is a primary testicular defect, independent of major hormonal imbalances.