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Related Experiment Video

Updated: Oct 18, 2025

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
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Δ9-Tetrahydrocannabinol inhibits Hedgehog-dependent patterning during development.

Hsiao-Fan Lo1, Mingi Hong1, Henrietta Szutorisz2

  • 1Department of Cell, Developmental, and Regenerative Biology, New York, NY 10029, USA.

Development (Cambridge, England)
|October 5, 2021
PubMed
Summary

Tetrahydrocannabinol (THC) acts as a conditional teratogen, causing developmental defects like holoprosencephaly in mouse models with genetic HH pathway deficits. This occurs independently of the canonical THC receptor.

Keywords:
Birth defectCDONCannabisHedgehogHoloprosencephalyMouseTHC

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Area of Science:

  • Developmental Biology
  • Teratology
  • Molecular Pharmacology

Background:

  • Developmental disorders often result from gene-environment interactions.
  • Hedgehog (HH) signaling is crucial for development; its inhibition causes birth defects like holoprosencephaly (HPE).
  • Cannabinoids, including THC, are known HH pathway inhibitors, but their embryonic effects and mechanisms are poorly understood.

Purpose of the Study:

  • To investigate the effects of the cannabinoid THC on HH-dependent developmental processes in mammalian embryos.
  • To elucidate the mechanism by which THC inhibits the HH signaling pathway.
  • To assess the public health implications of cannabis use during pregnancy concerning developmental risks.

Main Methods:

  • Utilized Cdon mutant mice exhibiting a subthreshold HH signaling deficit.
  • Administered Δ9-tetrahydrocannabinol (THC) to assess teratogenic effects and HH pathway disruption.
  • Performed in vitro experiments to identify the direct molecular target of THC's HH inhibitory action.

Main Results:

  • THC induced hallmark HH loss-of-function phenotypes, including HPE and ventral neural tube defects, in Cdon mutant mice.
  • THC functions as a conditional teratogen, exacerbating pre-existing, subthreshold HH pathway deficits.
  • In vitro studies revealed THC directly inhibits smoothened (SMO), a key HH signal transducer, independent of the cannabinoid receptor type 1 (CB1).

Conclusions:

  • THC can act as a conditional teratogen, posing developmental risks when combined with genetic predispositions.
  • The mechanism of HH inhibition by THC involves direct SMO inhibition, not mediated by CB1.
  • Findings highlight significant public health concerns regarding prenatal cannabis exposure and potential contributions to developmental disorders.