The cannabinoid CB agonist LY2828360 suppresses neuropathic pain behavior and attenuates morphine tolerance and conditioned place preference in rats.

Cannabinoid CB agonists show promise as analgesics because they lack unwanted side effects associated with direct activation of CB receptors. CB receptor activation suppresses pathological pain in animal models, but the types of pain that best respond to CB agonists are incompletely understood. This gap in knowledge may contribute to failures in clinical translation.

Cannabinoid CB receptors in primary sensory neurons are implicated in CB agonist-mediated suppression of paclitaxel-induced neuropathic nociception and sexually-dimorphic sparing of morphine tolerance.

Cannabinoid CB agonists show therapeutic efficacy without unwanted CB-mediated side effects. The G protein-biased CB receptor agonist LY2828360 attenuates the maintenance of chemotherapy-induced neuropathic nociception in male mice and blocks development of morphine tolerance in this model. However, the cell types involved in this phenomenon are unknown and whether this therapeutic profile is observed in female mice has never been investigated.

Coming to Terms with the Legacies of the Pound Model in Animal Sheltering in the United States.

This paper examines the legacies of the emergence of the animal control and sheltering industry in the United States and their impact on contemporary public animal shelters. While decades of gradual reform have helped substantially reduce the number of animals entering shelters and being killed there, contemporary animal sheltering largely continues to follow the path set when animal sheltering developed in the late 1800s and early 1900s. Three key interrelated legacies of the pound model of early animal control and sheltering enduringly shape sheltering today: (1) the institutional culture of animal shelters grounded in the logics of caging and killing; (2) the lack of visibility and transparency, especially within government shelters; and (3) the economic logics of the pound model, including the disparities in sheltering resources across communities.

Cannabinoid CB receptors in primary sensory neurons are implicated in CB agonist-mediated suppression of paclitaxel-induced neuropathic nociception and sexually-dimorphic sparing of morphine tolerance.

Cannabinoid CB agonists show therapeutic efficacy without the unwanted side effects commonly associated with direct activation of CB receptors. The G protein-biased CB receptor agonist LY2828360 attenuates the maintenance of chemotherapy-induced neuropathic nociception in male mice and blocks the development of morphine tolerance in this model. However, the specific cell types involved in this phenomenon have never been investigated and whether this therapeutic profile is observed in female mice remains poorly understood.

Conditional deletion of CB2 cannabinoid receptors from peripheral sensory neurons eliminates CB2-mediated antinociceptive efficacy in a mouse model of carrageenan-induced inflammatory pain.

CB cannabinoid receptor agonists suppress pathological pain in animal models and lack unwanted side effects commonly associated with direct activation of CB receptors. However, the types of pain most responsive to CB agonists are incompletely understood and cell types which underlie CB-mediated therapeutic efficacy remain largely unknown. We previously reported that the CB receptor agonist LY2828360 reduced neuropathic nociception induced by toxic challenge with chemotherapeutic and anti-retroviral agents in mice.