Methylhonokiol attenuates neuroinflammation : a role for cannabinoid receptors?

Acknowledgements We thank Stefanie Hofer-Reyes for proofreading the manuscriptPeer reviewedPublisher PD

Detection of Impending Aggressive Outbursts in Patients with Psychiatric Disorders : Violence Clues from Dogs

Peer reviewedPublisher PD

High fat-fed GPR55 null mice display impaired glucose tolerance without concomitant changes in energy balance or insulin sensitivity but are less responsive to the effects of the cannabinoids rimonabant or Δ(9)-tetrahydrocannabivarin on weight gain

Background The insulin-sensitizing phytocannabinoid, Δ(9)-tetrahydrocannabivarin (THCV) can signal partly via G protein coupled receptor-55 (GPR55 behaving as either an agonist or an antagonist depending on the assay). The cannabinoid receptor type 1 (CB1R) inverse agonist rimonabant is also a GPR55 agonist under some conditions. Previous studies have shown varied effects of deletion of GPR55 on energy balance and glucose homeostasis in mice. The contribution of signalling via GPR55 to the metabolic effects of THCV and rimonabant has been little studied. Methods In a preliminary experiment, energy balance and glucose homeostasis were studied in GPR55 knockout and wild-type mice fed on both standard chow (to 20 weeks of age) and high fat diets (from 6 to 15 weeks of age). In the main experiment, all mice were fed on the high fat diet (from 6 to 14 weeks of age). In addition to replicating the preliminary experiment, the effects of once daily administration of THCV (15 mg.kg-1 po) and rimonabant (10 mg.kg-1 po) were compared in the two genotypes. Results There was no effect of genotype on absolute body weight or weight gain, body composition measured by either dual-energy X-ray absorptiometry or Nuclear Magnetic Resonance (NMR), fat pad weights, food intake, energy expenditure, locomotor activity, glucose tolerance or insulin tolerance in mice fed on chow. When the mice were fed a high fat diet, there was again no effect of genotype on these various aspects of energy balance. However, in both experiments, glucose tolerance was worse in the knockout than the wild-type mice. Genotype did not affect insulin tolerance in either experiment. Weight loss in rimonabant- and THCV-treated mice was lower in knockout than in wild-type mice, but surprisingly there was no detectable effect of genotype on the effects of the drugs on any aspect of glucose homeostasis after taking into account the effect of genotype in vehicle-treated mice. Conclusions Our two experiments differ from those reported by others in finding impaired glucose tolerance in GPR55 knockout mice in the absence of any effect on body weight, body composition, locomotor activity or energy expenditure. Nor could we detect any effect of genotype on insulin tolerance, so the possibility that GPR55 regulates glucose-stimulated insulin secretion merits further investigation. By contrast with the genotype effect in untreated mice, we found that THCV and rimonabant reduced weight gain, and this effect was in part mediated by GPR55

The cellular distribution of cannabinoid and vanilloid type 1 receptors in cultured neurones and the myenteric plexus

This study investigated the distribution of CB1 and VR1 receptors in rat cultured hippocampal and sensory cells and in the myenteric plexus of various rodents. CB1 and VR1 receptor-immunoreactivity was observed in a subset of neurones and their processes.  Primary sensory neurones expressed CB1 receptors on their soma and fibres. The vast majority of CB1 receptor-expressing hippocampal neurones were GABAergic but appeared to be VR1 receptor-immunonegative.  Cannabinoid agonists inhibited the expression of cell surface CB1 receptors in a concentration-dependent, stereoselective manner.  This inhibition of cell surface labelling was maximal at 16 h, did not require the activation of Gi/o-proteins and was abolished in the presence of SR141716A, a selective CB1 receptor antagonist. A new primary antibody pre-labelling protocol demonstrated that this inhibition reflects agonist-induced internalisation and suggests that internalised CB1 receptors are translocated from axons towards somatodentritic regions.  In F-11 cells, shown here to naturally express CB1 receptors on their somatic membrane, cannabinoid-induced internalisation occurred within a relatively short period (30 min). In the guinea-pig and rat myenteric plexus, virtually all CB1 and VR1 receptor-immunopositive cells were cholinergic. Subpopulations of calbindin-, calretinin- and neurofilament protein-immunopositive neurones co-expressed either receptor type. The localisation of VR1 receptors in calcitonin gene-related peptide-positive fibres and the expression of CB1 receptors in their somata implies a role for VR1 receptors in neuropeptide release and identified CB1 receptor-containing secretory neurones. There was also a close association between CB1 and VR1 receptor-immunoreactivity and fibres labelled for synaptic protein, suggesting roles for these receptors in the modulation of neurotransmitter release. These results are consistent with the inhibition of cannabinoids of neurotransmitter release and gastrointestinal transit and peristalsis.  Internalisation of CB1 receptors may be a mechanism by which neurones control sensitivity to endocannabinoids and regulate the development of tolerance to cannabinoid drugs.  The co-localisation studies in the gut identified intrinsic sensory, interneuronal and motor neurones expressing CB1 and VR1 receptors.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Serious Games: Is Your User Playing or Hunting?

Part 3: PostersInternational audienceThere is an increasing demand for entertainment applications developed for pets, in particular for dogs and cats. However, play interaction between animals and technological devices still remains an uncharted territory both for animal behavior and entertainment computing scientific communities. While there is a lot of anecdotal evidence of pets playing digital games, the nature of animal-computer play interactions is still not understood. In this paper we report on empirical findings based on observing and analyzing dog-tablet game interactions. Using categories emerging from our data analysis, we construct an ethogram, a “catalogue” of behavioral patterns typical of dog-tablet interactions. Based on our data analysis, we hypothesize that the nature of the observed interactions is that of predatory behavior, in response to stimuli in the form of “prey-like” virtual objects displayed on the screen. Based on our hypothesis, we further propose some questions for future investigation, and raise some issues that need to be addressed by game developers when targeting dogs as their users

Different responses of repetitive behaviours in juvenile and young adult mice to Δ9-tetrahydrocannabinol and cannabidiol may affect decision making for Tourette syndrome

Funding Information: Our special thanks to Professor Roger G. Pertwee, University of Aberdeen, UK, for critical comments. This study was supported by a Research Grant Award from the Tourette Association of America (S.A.G. and P.M.). V.G. was supported by The Elphinstone Scholarship for Ph.D. students, University of Aberdeen.Peer reviewedPostprin

Motor-like Tics are Mediated by CB2 Cannabinoid Receptor-dependent and Independent Mechanisms Associated with Age and Sex

open access via springer compact agreement Funding This study was supported by the Research Grant Award from the Tourette Association of America (SAG and PM). VG was supported by The Elphinstone Scholarship for Ph.D. students, University of Aberdeen.Peer reviewedPublisher PD