Synthetic Cannabinoid JWH-018 Impairs Sensory Functions Far More Than THC in Mice | Research

The takeaway

The synthetic cannabinoid JWH-018 impaired visual, auditory, and tactile responses at very low doses and caused convulsions at high doses, while equivalent THC doses did not cause these effects.

Read this if you want to understand why synthetic cannabinoids are considered more dangerous than natural cannabis.

Sensory impairment at doses 100x lower than those causing convulsions

What the researchers found

Researchers compared the synthetic cannabinoid JWH-018 (found in "Spice" and "herbal blends") with THC across a battery of sensorimotor tests in mice.

JWH-018 impaired sensorimotor responses (visual, auditory, tactile) at extremely low doses (0.01-0.1 mg/kg), reduced spontaneous movement at intermediate doses, and caused convulsions, myoclonia, and hyperreflexia at high doses (6 mg/kg).

THC at the same doses also reduced some sensorimotor responses but did not inhibit spontaneous locomotion and did not cause any neurological alterations like convulsions. All effects of JWH-018 were blocked by a CB1 receptor antagonist, confirming they work through the same receptor system but with dramatically different intensity.

Why it matters

This study demonstrated that synthetic cannabinoids are not just "stronger weed" but produce qualitatively different and more dangerous effects, including sensory impairment at very low doses and seizures at high doses. This has direct implications for driving and workplace safety.

The numbers in context

JWH-018 impaired sensorimotor function at 0.01-0.1 mg/kg; caused convulsions at 6 mg/kg; THC at same doses did not impair locomotion or cause neurological effects; all JWH-018 effects blocked by AM251

How the study worked

Mouse study comparing JWH-018 and THC at doses from 0.01 to 6 mg/kg. Used a battery of behavioral tests for sensorimotor function (visual, auditory, tactile responses), video-tracking for locomotion, and observation for neurological effects. CB1 antagonist AM251 was used to confirm receptor mechanisms.

What this study cannot tell us

Mouse study with potential species differences in drug sensitivity. Acute dosing only. The numerous synthetic cannabinoids on the market may have different potency and effect profiles than JWH-018 specifically.

How to read the evidence

Controlled animal study with clear dose-response data and receptor mechanism confirmation, but translation to human effects requires caution.

When this study was published

Published in 2015. JWH-018 has been banned in many jurisdictions, but newer synthetic cannabinoids continue to emerge.

The bigger picture

The finding that synthetic cannabinoids impair sensory processing at doses 100 times lower than those causing obvious intoxication raises serious safety concerns. Users may be significantly impaired before they feel notably high.

Questions still open

How does sensorimotor impairment from synthetic cannabinoids translate to human driving performance? Are other synthetic cannabinoids even more potent than JWH-018? Do these effects change with repeated use?

Common questions

Why are synthetic cannabinoids more dangerous than regular cannabis?

Synthetic cannabinoids like JWH-018 are full agonists at CB1 receptors (THC is only a partial agonist), making them more potent. This study showed JWH-018 impaired sensory function at very low doses and caused convulsions at high doses, neither of which occurred with THC at equivalent doses.

Can synthetic cannabinoids cause seizures?

Yes. In this study, JWH-018 at 6 mg/kg caused convulsions, myoclonia (muscle jerks), and hyperreflexia in mice. THC at the same dose did not cause any of these neurological effects.

Read the original research

JWH-018 impairs sensorimotor functions in mice.

Neuroscience, 300, 174-88

View on PubMed ↗Publisher’s paper ↗

Citation

Ossato, A; Vigolo, A; Trapella, C; Seri, C; Rimondo, C; Serpelloni, G; Marti, M. (2015). JWH-018 impairs sensorimotor functions in mice.. Neuroscience, 300, 174-88. https://doi.org/10.1016/j.neuroscience.2015.05.021