In an interprofessional approach to shared decision-making (IP-SDM), an interprofessional team collaborates in identifying best options and helps patients determine their preferences, enabling them to take more control over the treatment plan. However, little is known about fostering IP-SDM in Canada's healthcare system. Therefore, we sought to evaluate health professionals' intentions to engage in IP-SDM in home care and explore the factors associated with this intention. A total of 272 eligible home care providers completed a questionnaire based on the theory of planned behavior. Eight managers and one healthcare team caring for the frail elderly were interviewed about possible barriers and facilitators. Analysis involved descriptive statistics and multivariate analysis of quantitative data and content analysis of qualitative data. On a scale of − 3 (strongly disagree) to +3 (strongly agree), the mean intention to engage in IP-SDM was positive (1.42 ± 1.39). The intention was influenced by the following theory-based determinants (R2 = 57%; p ≤ 0.002), i.e. cognitive attitude (p < 0.001) subjective norm (p < 0.0001) and perceived behavioral control (p < 0.0001), with variations depending on the type of provider. Barriers included lack of time, poor team cohesion and high staff turnover. Facilitators included team cohesion and shared tools. Future programs implementing IP-SDM could address these barriers and facilitators.

The sensory neuron-specific G protein coupled receptors (SNSRs) have been described as a family of receptors whose expression in small diameter sensory neurons in the trigeminal and dorsal root ganglia suggests an implication in nociception. To date, the physiological function(s) of SNSRs remain unknown. Hence, the aim of the present study was to determine the effects of rat SNSR1 activation on nociception in rats. The pharmacological characterization of rat SNSR1 was initially performed in vitro to identify a specific ligand, which could be used subsequently in the rat for physiological testing. Among all ligands tested, ␥2-MSH was the most potent at activating rat SNSR1. Structure-activity relationship studies revealed that the active moiety recognized by rat SNSR1 was the C-terminal part of ␥2-MSH. The radiolabeled C-terminal part of ␥2-MSH, ␥2-MSH-6 -12, bound with high affinity to membranes derived from rat skin and spinal cord, demonstrating the presence of receptor protein at both the proximal and distal terminals of dorsal root ganglia. To investigate the physiological role of SNSR, specific ligands to rat SNSR1 were tested in behavioral assays of pain sensitivity in rats. Selective rat SNSR1 agonists produced spontaneous pain behavior, enhanced heat and mechanical sensitivity when injected intradermally, and heat hypersensitivity when injected centrally, consistent with the localization of rat SNSR1 protein at central and peripheral sites. Together, these results clearly indicate that the SNSR1 plays a role in nociception and may provide novel therapeutic opportunities for analgesia. Gprotein-coupled receptors constitute one of the largest gene family of proteins that have been exploited successfully as drug targets (1). With the near completion of the human genome project, bioinformatic analyses have revealed the existence of Ϸ145 orphan receptors (1, 2). In recent years, the ''reverse pharmacology approach'' has generated Ͼ40 ligand-receptor pairings (1, 3), and the subsequent investigation of these newly discovered ligand-receptor pairings should help in understanding and elucidating their potential physiological and pathophysiological roles.We cloned a previously undescribed family of G protein-coupled receptors that we named the sensory neuron-specific receptors (SNSRs) because of their unique mRNA distribution in small nociceptive sensory neurons in dorsal root (DRG) and trigeminal ganglia (4). The SNSRs are phylogenetically related to the Mas oncogene receptor and belong to the Mas-related genes or Mrg family described for mouse and human by Dong et al. (5). Based on several analyses, this subfamily of receptors is comprised of four to six members in human (MrgX1-4 or SNSR1-6) and 32 receptors in mouse classified into three major subfamilies Mrg A, B, and C (4-7). Initially, only one SNSR gene was identified in rat (4); recently, Zylka et al. (8) have demonstrated that more than one rat SNSR͞ Mrg subtype exists. These receptors have been subclassified in a similar scheme as described for human a...

Cannabinoids are analgesic in man, but their use is limited by their psychoactive properties. One way to avoid cannabinoid receptor subtype 1 (CB1R)-mediated central side-effects is to develop CB1R agonists with limited CNS penetration. Activation of peripheral CB1Rs has been proposed to be analgesic, but the relative contribution of peripheral CB1Rs to the analgesic effects of systemic cannabinoids remains unclear. Here we addressed this by exploring the analgesic properties and site of action of AZ11713908, a peripherally restricted CB1R agonist, in rodent pain models. Systemic administration of AZ11713908 produced robust efficacy in rat pain models, comparable to that produced by WIN 55, 212-2, a CNS-penetrant, mixed CB1R and CB2R agonist, but AZ11713908 generated fewer CNS side-effects than WIN 55, 212-in a rat Irwin test. Since AZ11713908 is also a CB2R inverse agonist in rat and a partial CB2R agonist in mouse, we tested the specificity of the effects in CB1R and CB2R knock-out (KO) mice. Analgesic effects produced by AZ11713908 in wild-type mice with Freund's complete adjuvant-induced inflammation of the tail were completely absent in CB1R KO mice, but fully preserved in CB2R KO mice. An in vivo electrophysiological assay showed that the major site of action of AZ11713908 was peripheral. Similarly, intraplantar AZ11713908 was also sufficient to induce robust analgesia. These results demonstrate that systemic administration of AZ11713908, produced robust analgesia in rodent pain models via peripheral CB1R. Peripherally restricted CB1R agonists provide an interesting novel approach to analgesic therapy for chronic pain.

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