Genetic predisposition, not just intensive management conditions and surroundings, may be a factor in the high crib-biting prevalence in some breeds, and warrants further investigation. Little evidence exists to suggest horses learn the behaviour from other horses, and isolation may cause unnecessary stress.

Object play occurs in diverse animals in addition to birds and mammals. Although many carnivores engage in object play in a predatory context, many non-predators do so also. Conjectures over the years on the motivation to play are reviewed dealing with intrinsic, developmental, and stimulus factors. We then report on quantitative studies of the play of puppies from 6 litters (3 breeds) when given 5 different toys with different sensory and functional properties at half week intervals from 3 to 7 weeks of age. The propensity to engage with objects begins early, play complexity increases rapidly, the structure of the play is similar to adult object play, and breed differences were found. Object play with predatory characteristics appears before weaning, suggesting that hunger is not the primary motivation. Studying the development of object play in different dog breeds may be useful in addressing questions of domestication and play evolution.

Summary A retrospective study of 43 cases of temporohyoid osteoarthropathy was performed to evaluate the epidemiological features and a possible association with crib‐biting. Data collected from records included case details, what diagnostics were utilised, whether medical or surgical treatment was administered, and outcome. Owners were contacted via telephone and asked whether the horse had displayed crib‐biting behaviour. Forty‐three horses were diagnosed with neurological disease associated with temporohyoid osteoarthropathy, 62.8% of which were Quarter Horse‐types. Median age at presentation was 10 years and median duration of neurological signs prior to presentation was 3 days. Skull radiographs and guttural pouch endoscopy were used to definitively diagnose temporohyoid osteoarthropathy in 72% of the cases. Of 43 horses, 21 received medical treatment and 15 surgical treatment, with an overall survival rate of 55.8%. Crib‐biting was observed in 31.3% of cases and there was a significant association between being afflicted with THO and likelihood of possessing the behaviour. Horses with neurological disease associated with THO were 8 times more likely to be crib‐biters compared to the general population.

BackgroundPrevious studies in human patients suggest depth of sedation may be affected by environmental noise or music; however, related data in domestic animals is limited. The objective of the current study was to investigate the effect of noise and music on dexmedetomidine-induced (DM- 10 µg/kg, IM) sedation in 10 dogs.MethodsIn a crossover design, post-DM injection dogs were immediately subjected to recorded human voices at either 55–60 decibel (dB) (Noise 1) or 80–85 dB (Noise 2); classical music at 45–50 dB (Music); or background noise of 40–45 dB (Control+). Control− included IM saline injection and exposure to 40–45 dB background noise. Sedation was assessed via monitoring spontaneous behavior and accelerometry (delta-g) throughout three 20-min evaluation periods: baseline, noise exposure, and post-treatment. Sedation was further assessed during two restraint tests at 30 min (R1) and 40 min (R2) post-injection. A mixed model for crossover design was used to determine the effect of noise exposure and time on either spontaneous behavior scores or delta-g. The restraint scores were analyzed using a two-way repeated measures ANOVA.ResultsSpontaneous behavior scores indicated less sedation during Noise 2 compared to Control+ (P = 0.05). R2 restraint scores for all DM treatments except Noise 2 indicated significantly higher sedation than Control− [C+ (P = 0.003), M (P = 0.014) and N1 (P = 0.044)].DiscussionResults suggest that the quality of sedation is negatively impacted by high-intensity noise conditions (80–85 dB), but exposure to music did not improve sedation in this population of research dogs.

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Shared signaling pathways utilized by melanocytes and neurons result in pleiotropic traits of coat color and behavior in many mammalian species. For example, in humans polymorphisms at MC1R cause red hair, increased heat sensitivity, and lower pain tolerance. In deer mice, rats, and foxes, ASIP polymorphisms causing black coat color lead to more docile demeanors and reduced activity. Horse (Equus caballus) base coat color is primarily determined by polymorphisms at the Melanocortin-1 Receptor (MC1R) and Agouti Signaling Protein (ASIP) loci, creating a black, bay, or chestnut coat. Our goal was to investigate correlations between genetic loci for coat color and temperament traits in the horse. We genotyped a total of 215 North American Tennessee Walking Horses for the 2 most common alleles at the MC1R (E/e) and ASIP (A/a) loci using previously published PCR and RFLP methods. The horses had a mean age of 10.5 years and comprised 83 geldings, 25 stallions, and 107 mares. To assess behavior, we adapted a previously published survey for handlers to score horses from 1 to 9 on 20 questions related to specific aspects of temperament. We utilized principle component analysis to combine the individual survey scores into 4 factors of variation in temperament phenotype. A factor component detailing self-reliance correlated with genotypes at the ASIP locus; black mares (aa) were more independent than bay mares (A_) (P = 0.0063). These findings illuminate a promising and novel animal model for future study of neuroendocrine mechanisms in complex behavioral phenotypes.

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A diagnosis of adverse extrapyramidal symptoms (EPS) was reached in a 14-year-old female blue and gold macaw (Ara ararauna) that presented with disseminated dystonia (manifesting as pacing, head bobbing, and circling), intermittent ataxia, and coarse-muscle tremors of 60 hours duration. The patient had been treated 23 days previously with haloperidol decanoate (1.7 mg/kg IM once), and for 3 days before hospitalization with clomipramine HCl at a prescribed dosage of 3.9 mg/kg PO q12h. The patient was treated with supportive care, a gradual reduction in the clomipramine dose, and intramuscular and oral diphenhydramine (2 mg/kg q12h). As commonly observed in human patients with drug-induced EPS, a dramatic resolution of clinical signs was observed within 2 hours after the first intramuscular administration of diphenhydramine. It is recommended that EPS be considered in macaws experiencing neurologic signs secondary to clomipramine administration and, in particular, in those treated concurrently or previously with haloperidol.