Central Blockade of Cannabinoid CB1 and CB2 Receptors Increases Force Generation in Reserpine-Treated Mice, but Only CB1 Blockade Extends the Duration of Effort.
- 1Laboratory of Exercise Biology (LABIOEX), Department of Physical Therapy, Centro de Ciências, Tecnologias e Saúde, Federal University of Santa Catarina, Rua Pedro João Pereira 158, Centro Cívico, Araranguá, Santa Catarina 88905-120, Brazil.
- 2Instituto de Ensino e Pesquisa Remederi, Via Anchieta 1616, Vila Moinho Velho, São Paulo, São Paulo 04246-002, Brazil.
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.
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BibTeX
@article{santos2026central,
title = {{Central Blockade of Cannabinoid CB1 and CB2 Receptors Increases Force Generation in Reserpine-Treated Mice, but Only CB1 Blockade Extends the Duration of Effort.}},
author = {Beatriz Carminati Dos Santos and Izabely Guedes da Rosa and Laíze de Freitas Mazzardo and Naiara de Souza Santos and Izabel Feltrin Fabro and Tatyana Nery and Amanda Leite Bastos Pereira and Aderbal S Aguiar},
journal = {ACS pharmacology \& translational science},
year = {2026},
month = sep,
doi = {10.1021/acsptsci.6c00206},
url = {https://europepmc.org/article/MED/42921228},
note = {CC BY},
}
RIS
TY - JOUR
TI - Central Blockade of Cannabinoid CB1 and CB2 Receptors Increases Force Generation in Reserpine-Treated Mice, but Only CB1 Blockade Extends the Duration of Effort.
AU - Beatriz Carminati Dos Santos
AU - Izabely Guedes da Rosa
AU - Laíze de Freitas Mazzardo
AU - Naiara de Souza Santos
AU - Izabel Feltrin Fabro
AU - Tatyana Nery
AU - Amanda Leite Bastos Pereira
AU - Aderbal S Aguiar
PY - 2026
DA - 2026/09/29
JO - ACS pharmacology & translational science
DO - 10.1021/acsptsci.6c00206
UR - https://europepmc.org/article/MED/42921228
AB - 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.
SN - 2575-9108
ER -