Separation Anxiety in Dogs: The Underlying Causes

A new study into separation anxiety in dogs has found several root causes of the disorder, including: “exit frustration,” “redirected reactive,” “reactive inhibited” and “boredom”.

Abstract -“Diagnoses are widely used in both human and veterinary medicine to describe the nature of a condition; by contrast, syndromes are collections of signs that consistently occur together to form a characteristic presentation. Treatment of syndromes, due to either their lack of a clear biological cause or multiple causes, necessarily remains non-specific. However, the discovery of interventions may help refine the definition of a syndrome into a diagnosis. Within the field of veterinary behavioral medicine, separation related problems (SRPs) provide a good example of a syndrome. We describe here a comprehensive process to develop a diagnostic framework (including quality control assessments), for disambiguating the signs of SRPs as an example of a heterogeneous behavioral syndrome in non-human animals requiring greater diagnostic and treatment precision. To do this we developed an online questionnaire (243 items) that covered the full spectrum of theoretical bases to the syndrome and undertook a large-scale survey of the presenting signs of dogs with one or more of the signs of SRPs (n = 2,757). Principal components analysis (n1 = 345), replicated in a second sample (n2 = 417; total n = 762), was used to define the structure of variation in behavioral presentation, while hierarchical agglomerative cluster analysis cross checked with the partitioned around medoids method was used to determine sub-populations. A total of 54 signs were of value in defining a latent structure consisting of seven principal components (termed “exit frustration,” “social panic,” “elimination,” “redirected frustration,” “reactive communication,” “immediate frustration,” “noise sensitivity”), which divided the population in four clusters (termed “exit frustration,” “redirected reactive,” “reactive inhibited” and “boredom” related SRPs) with 11 sub-clusters (3, 3, 3, and 2, respectively). We used a bottom-up data-driven approach with numerous quality checks for the definition of robust clusters to provide a robust methodology for nosological studies in veterinary behavioral medicine, that can extend our understanding of the nature of problems beyond SRPs. This provides a solid foundation for future work examining aetiological, and differential treatment outcomes, that will allow both more effective treatment and prevention programmes, based on a fully appreciation of the nature of the problem of concern.”

The original paper

Associative Fear Learning in the Brain

An interesting article came out in Nature (abstract and link below) providing more evidence that neural links between the hippocampus and amygdala are necessary for associative fear learning. This evidence reinforces the idea that to reduce / undo fear association learning, we need to focus on amygdala activity reducing training techniques and environmental constructs, such as:

  • Training using positive reinforcement and pleasant stimuli, rather than aversives that may further activate the amygdala-hippocampus network.
  • Deconditioning fear through methods less likely to trigger fear/panic: such as systematic desensitisation, cognitive activation and counter conditioning.
  • Watching the animals body language to make sure you are not near the fear/panic threshold for the fear triggering stimuli while training so that the amgdala -hippocampal pathways are not activated and the associative memory strengthened.
  • Increase oxytocin through stable, social interactions allowing supportive attachments to form
  • Reduce overall environmental stress

Abstract

In contextual fear conditioning, experimental subjects learn to associate a neutral context with an aversive stimulus and display fear responses to a context that predicts danger. Although the hippocampal–amygdala pathway has been implicated in the retrieval of contextual fear memory, the mechanism by which fear memory is encoded in this circuit has not been investigated. Here, we show that activity in the ventral CA1 (vCA1) hippocampal projections to the basal amygdala (BA), paired with aversive stimuli, contributes to encoding conditioned fear memory. Contextual fear conditioning induced selective strengthening of a subset of vCA1–BA synapses, which was prevented under anisomycin-induced retrograde amnesia. Moreover, a subpopulation of BA neurons receives stronger monosynaptic inputs from context-responding vCA1 neurons, whose activity was required for contextual fear learning and synaptic potentiation in the vCA1–BA pathway. Our study suggests that synaptic strengthening of vCA1 inputs conveying contextual information to a subset of BA neurons contributes to encoding adaptive fear memory for the threat-predictive context.”

 

https://www.nature.com/articles/s41467-020-15121-2