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Genetic loss of FAAH compromises male fertility in mice

Academic Article
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Overview

authors

  • Sun, X. F.
  • Wang, H. B.
  • Okabe, M.
  • Mackie, K.
  • Kingsley, P. J.
  • Marnett, L. J.
  • Cravatt, Benjamin
  • Dey, S. K.

publication date

  • February 2009

journal

  • Biology of Reproduction  Journal

abstract

  • Marijuana is the most commonly used illicit drug. Although there is some indication that reproductive functions in males are impaired in chronic marijuana users, the genetic evidence and underlying causes remain largely unknown. Herein we show that genetic loss of Faah, which encodes fatty acid amide hydrolase (FAAH), results in elevated levels of anandamide, an endocannabinoid, in the male reproductive system, leading to compromised fertilizing capacity of sperm. This defect is rescued by superimposing deletion of cannabinoid receptor 1 (Cnr1). Retention of Faah(-/-) sperm on the egg zona pellucida provides evidence that the capacity of sperm to penetrate the zona barrier is hampered by elevated anandamide levels. Collectively, the results show that aberrant endocannabinoid signaling via CNR1 impairs normal sperm function. Besides unveiling a new regulatory mechanism of sperm function, this study has clinical significance in male fertility.

subject areas

  • Amidohydrolases
  • Animals
  • Arachidonic Acids
  • Cannabinoid Receptor Modulators
  • Endocannabinoids
  • Gene Deletion
  • Genetic Complementation Test
  • Infertility, Male
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mutagenesis, Site-Directed
  • Polyunsaturated Alkamides
  • Receptor, Cannabinoid, CB1
  • Signal Transduction
  • Sperm Motility
  • Spermatozoa
  • Urogenital System
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Research

keywords

  • CNR1
  • FAAH
  • anandamide
  • male fertility
  • mouse
  • sperm
  • sperm capacitation
  • sperm motility and transport
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Identity

PubMed Central ID

  • PMC2804815

International Standard Serial Number (ISSN)

  • 0006-3363

Digital Object Identifier (DOI)

  • 10.1095/biolreprod.108.072736

PubMed ID

  • 18987328
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Additional Document Info

start page

  • 235

end page

  • 242

volume

  • 80

issue

  • 2

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