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oai:figshare.com:article/34023313 2026-09-29T11:03:32Z category_7 category_12 category_15 category_16 category_19 category_272 category_122 category_135 portal_63 item_type_6 month_year_09_2026

Central Blockade of Cannabinoid CB1 and CB2 Receptors Increases Force Generation in Reserpine-Treated Mice, but Only CB1 Blockade Extends the Duration of Effort Beatriz Carminati dos Santos (25136719) Izabely Guedes da Rosa (25136722) Laíze de Freitas Mazzardo (25136725) Naiara de Souza Santos (12817042) Izabel Feltrin Fabro (25136728) Tatyana Nery (22641460) Amanda Leite Bastos Pereira (25136731) Aderbal S. Aguiar Jr (25136734) Medicine Cell Biology Neuroscience Physiology Pharmacology Environmental Sciences not elsewhere classified Mental Health Computational Biology whose neuromodulatory control sustain motor output parkinsonism extends beyond data cannot distinguish body mass left 5 – 85 effort motor impairment 8 – 73 67 sd (< ci − 560 am251 also reduced 008 ), am251 (− 70 ms grip force task antagonists raise force cb1 blockade extends cb1 antagonist am251 cb2 antagonist am630 force effects unchanged 03 – 0 03 sd ci 8 task onset reduced capacity effort rather cb2 receptors antagonists increased 66 ), 619 ms force generated 36 sd ci 22 cannabinoid cb1 (− 0 two differed treated mice poorly resolved p </ neuromuscular performance lateral ventricle interaction contrast endocannabinoid system delivered intracerebroventricularly classical triad central blockade cataleptic response candidate regulator anatomically localized 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, <i>P</i> = 0.008), AM251 did not (−0.36 SD, <i>P</i> = 0.66), and the two differed from each other by 1.67 SD (<i>P</i> = 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. 2026-09-29T00:00:00Z Text Journal contribution 10.1021/acsptsci.6c00206.s001 https://figshare.com/articles/journal_contribution/Central_Blockade_of_Cannabinoid_CB1_and_CB2_Receptors_Increases_Force_Generation_in_Reserpine-Treated_Mice_but_Only_CB1_Blockade_Extends_the_Duration_of_Effort/34023313 CC BY-NC 4.0