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ACS Pharmacology & Translational Science
By Beatriz Carminati dos Santos, Isadora Veiga da Rosa, LAIZE DE FREITAS MAZZARDO and 5 others.
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Abstract Motor impairment in parkinsonism extends beyond the classical triad to weakness and a reduced capacity to sustain motor output, whose neuromodulatory control is poorly resolved. The endocannabinoid system is a candidate regulator, but CB1 and CB2 receptors have not been separated within one preparation. Reserpine-treated adult female Swiss mice received vehicle, the CB1 antagonist AM251, or the CB2 antagonist AM630 into the lateral ventricle; catalepsy was recorded across three trials and neuromuscular performance in a grip force task. Both antagonists increased the force generated at task onset, by amounts these data cannot distinguish: AM630 by 53.9 gf (95% CI 22.5–85.3) and AM251 by 41.2 gf (95% CI 8.8–73.6). They separated on duration. AM251 increased grip time by 619 ms (95% CI 113–1125), whereas AM630 did not (−70 ms, 95% CI −560 to +421). An interaction contrast on the force–time balance followed from that difference: AM630 shifted the balance toward force (−2.03 SD, P = 0.008), AM251 did not (−0.36 SD, P = 0.66), and the two differed from each other by 1.67 SD (P = 0.022). AM251 also reduced the odds of a cataleptic response (OR 0.16, 95% CI 0.03–0.89). Adjusting for body mass left both force effects unchanged. The dissociation is therefore in the duration of effort rather than in its force: both antagonists raise force, and only CB1 blockade also extends the time over which it is maintained. Delivered intracerebroventricularly, these effects are central in origin but not anatomically localized.
Published in ACS Pharmacology & Translational Science. The abstract is shown as published and remains the work of its authors; read the full article at the source.
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