As a cynologist, I have dedicated my life to understanding canine behavior, not just the surface-level actions we observe but the intricate neurological and genetic mechanisms that drive those behaviors. Every bark, every growl, every anxious glance stems from a complex interplay of brain structures, neurochemical processes, and evolutionary history. Today, I want to address a topic that is often overlooked or misunderstood: the hidden costs of miniaturizing dog breeds.
While many people are drawn to these smaller companions because they fit seamlessly into modern urban lifestyle's requiring less space, less food, and often seen as easier to manage, there is an unseen complexity beneath their adorable appearances. This complexity is not limited to physical traits like smaller bodies or rounder faces; it extends deep into their neurological architecture, affecting their brains, behaviors, emotional stability, and overall well-being.
Take Tater Tot, for example, a two-year-old Miniature Australian Shepherd currently enrolled in a behavior modification program designed to increase his cognitive abilities. Despite his playful demeanor and undeniable charm, Tater Tot faces daily challenges rooted not in poor training or a difficult temperament, but in the very genetics that shaped his miniature stature. His struggles with impulse control, heightened reactivity, and anxiety are symptoms of deeper neurological imbalances tied directly to the process of miniaturization.
Tater Tot's journey is not unique. Many miniature breeds experience similar behavioral challenges, yet the root causes are rarely acknowledged. This article aims to pull back the curtain on these hidden factors, explaining the underlying genetic, neurological, and evolutionary issues that contribute to dogs like Tater Tot facing difficulties that go far beyond simple training problems.
In this article I will guide you through the scientific landscape of canine miniaturization. We will explore how selective breeding for smaller sizes has far-reaching consequences on neuroanatomy, behavior, and cognitive function. We will dive deep into the roles of the amygdala, prefrontal cortex, and neurochemical imbalances that create a brain more prone to anxiety, impulsivity, and reactivity.
But this isn't just an academic exercise. Understanding these principles can empower breeders to make more ethical choices, help veterinarians recognize the biological roots of behavioral issues, and, most importantly, provide dog owners with the tools and knowledge needed to support their dogs effectively. Tater Tot's story, and the science behind it, illustrates a critical lesson: when we alter a dog' s size, we are not just changing how they look, we are reshaping their minds..
The Evolutionary and Anthropogenic Forces Behind Miniaturization
Throughout history, humans have shaped dog breeds to suit specific role's herding livestock, guarding property, hunting game, pulling sleds, and providing companionship. This process of selective breeding has been one of the most influential forces in canine evolution, with humans acting as both architects and gatekeepers of genetic traits. Every breed, from the towering Great Dane to the agile Border Collie, reflects generations of human intervention, tailored to meet the demands of specific environments, tasks, or cultural preferences.
Initially, dogs were bred with functional purposes in mind. Their physical traits, temperaments, and even cognitive abilities were selected to enhance their performance in particular roles. A herding dog needed agility, problem-solving skills, and a strong prey drive tempered by control. A guardian dog required size, strength, and protective instincts. In all these cases, form followed function; a dog's value was intrinsically tied to its ability to perform tasks essential for human survival and prosperity.
However, as human societies evolved, particularly with the rise of urbanization, so too did our relationship with dogs. The Industrial Revolution marked a pivotal shift as people moved from rural, agrarian lifestyles to densely populated cities. In these urban environments, the traditional working roles of dogs diminished. No longer needed to herd livestock or guard large properties, dogs transitioned primarily into companions, their value increasingly rooted in emotional support, companionship, and aesthetic appeal rather than functional utility.
With this shift came new breeding priorities. Smaller dogs became highly desirable because they fit neatly into compact living spaces, required less food, and were perceived as easier to manage in crowded city environments. Breeds like the Pomeranian, once larger sled dogs, were selectively bred down to toy sizes, catering to the tastes of royalty and, eventually, the broader public. Similarly, the Dachshund, originally bred for hunting badgers, was miniaturized to become more suitable as a household pet.
This trend toward miniaturization accelerated rapidly in the 20th and 21st centuries. Today, the popularity of toy and teacup breeds reflects not just a preference for small dogs but a broader cultural phenomenon where dogs are seen as lifestyle accessories, symbols of status, fashion, and personal identity. Social media has further fueled this trend, with images of tiny, "pocket-sized" dogs becoming viral sensations, reinforcing the appeal of extreme miniaturization.
But unlike functional traits that evolve under natural selection, miniaturization is an artificial construct, achieved through intense selective breeding practices that often prioritize appearance over health, behavior, or well-being. The genetic manipulation required to achieve such drastic size reductions affects far more than just the dog' s stature. It influences every aspect of the dog's biology, bone density, organ development, hormonal regulation, and, critically, brain structure and neurochemistry.
Miniaturization is not as simple as scaling down an existing blueprint. Biological systems do not shrink uniformly. A smaller body does not automatically equate to a proportionally smaller brain, heart, or other organs. This disproportion can create a cascade of health issues, including respiratory problems, skeletal deformities, and neurological disorders. Conditions like syringomyelia, hydrocephalus, and brachycephalic obstructive airway syndrome are alarmingly common in miniature and brachycephalic breeds, directly linked to the physical changes imposed by selective breeding.
Beyond the physical implications, there are profound behavioral and psychological consequences. The brain' s architecture, particularly regions responsible for emotion regulation, impulse control, and stress responses, can be significantly altered through miniaturization. Neurochemical imbalances, heightened anxiety, increased reactivity, and even aggression are common behavioral issues observed in many miniature breeds. These are not merely quirks or signs of poor training; they are rooted in the dog's altered biology, a direct result of breeding decisions focused on aesthetics rather than function.
The ethical considerations of this trend cannot be ignored. When we breed for extreme traits, whether it is size, coat color, or facial structure, we risk compromising the dog's quality of life. The health issues, shortened lifespans, and behavioral struggles faced by many miniature breeds raise critical questions about our responsibilities as breeders, owners, and stewards of canine evolution.
Which leads us to the pivotal question: but what happens when we prioritize size over function in breeding?
The Neurological Architecture of Miniaturization
One of the most profound and often overlooked consequences of miniaturization in canine breeds is its impact on the dog's brain. It is easy to assume that shrinking a dog's body simply results in a proportionally smaller brain, with all regions scaling down uniformly. However, the biological reality is far more complex. Miniaturization disrupts the intricate balance of brain structures, neurochemistry, and neural pathways, leading to significant changes in cognitive function, emotional regulation, and overall behavior.
In biology, allometric scaling refers to how the size of one part of an organism changes relative to another as the organism grows or evolves. Not all organs shrink uniformly during miniaturization. For example, while the body may become significantly smaller, certain internal organs, such as the heart or brain, do not reduce in size at the same rate. This disproportionate scaling can have profound physiological consequences, particularly when it comes to the brain.
The canine brain is a highly specialized organ composed of interconnected regions that manage different functions, from basic survival instincts to complex problem-solving abilities. When miniaturization occurs, some areas of the brain shrink more than others, leading to imbalances that disrupt the normal flow of information. This results in alterations in emotional regulation, cognitive flexibility, and behavioral responses, often manifesting as heightened anxiety, impulsivity, and reactivity.
The Amygdala: The Fear and Aggression Center
One of the most affected areas of the miniature dog's brain is the amygdala, a small, almond-shaped cluster of neurons located deep within the brain's limbic system. The amygdala plays a critical role in processing emotions, particularly those related to survival, such as fear and aggression. It acts as the brain's alarm system, rapidly assessing threats and triggering appropriate responses, fight, flight, or freeze.
In many miniature breeds, neuroimaging studies, including MRI (Magnetic Resonance Imaging) and fMRI (functional MRI) scans, have shown that the amygdala is disproportionately large relative to the overall brain volume. This enlargement is not just a structural anomaly; it has profound functional consequences. A larger, hyperactive amygdala means these dogs are neurologically wired to have an exaggerated fear response. They are more likely to overreact to environmental stimuli that larger dogs might perceive as non-threatening, such as sudden noises, unfamiliar people, or minor changes in their environment.
Why is this significant? Because fear-based behavior is at the root of many canine behavioral issues. When the amygdala dominates the brain's activity, the dog's response to stress is immediate and intense, often bypassing more thoughtful, regulated reactions. This is why many miniature breeds are prone to what owners describe as "overreacting", barking excessively at visitors, snapping when startled, or showing signs of anxiety even in seemingly safe situations.
Moreover, the amygdala does not work in isolation. It communicates constantly with other parts of the brain, particularly the prefrontal cortex, which helps regulate and moderate emotional responses. When the amygdala is hyperactive, it overwhelms these regulatory systems, making it difficult for the dog to "calm down" once aroused. This leads to prolonged periods of stress, chronic anxiety, and even aggression rooted in fear.
The Prefrontal Cortex: The Seat of Self-Control
While the amygdala governs primal, instinctive emotions, the prefrontal cortex is responsible for higher-order cognitive functions such as decision-making, impulse control, problem-solving, and behavioral inhibition. It is essentially the brain's executive center, helping the dog assess situations, weigh options, and regulate its emotional and behavioral responses.
In miniature breeds, the prefrontal cortex is often underdeveloped compared to their larger counterparts. Neuroimaging studies reveal several key differences:
1. Reduced Gray Matter Density: Gray matter consists of neuronal cell bodies responsible for processing information. A reduction in gray matter density means there are fewer neurons available for critical thinking, emotional regulation, and impulse control.
2. Weaker Neural Connectivity: The brain's ability to function efficiently depends on strong connections between different regions. In miniature breeds, these connections are often weaker, leading to poor communication between the prefrontal cortex and other areas like the amygdala.
3. Decreased Myelination: Myelin is a fatty substance that insulates nerve fibers, allowing electrical signals to travel quickly and efficiently. In miniature dogs, reduced myelination slows down neural processing, affecting reaction times and cognitive flexibility.
This underdevelopment of the prefrontal cortex has profound behavioral implications. Dogs with compromised prefrontal functions struggle with impulse control, making them prone to sudden outbursts of aggression, hyperactivity, and poor frustration tolerance. They find it difficult to pause, assess a situation, and choose an appropriate response. Instead, they react instinctively, driven by the more primitive parts of their brain.
For example, consider a miniature dog that reacts aggressively when another dog approaches its food bowl. In larger, well-balanced breeds, the prefrontal cortex might help the dog assess the situation: This dog isn' t a threat; there is plenty of food. However, in miniature breeds with an underdeveloped prefrontal cortex, the fear of resource loss triggers an immediate, unfiltered aggressive response, even if the perceived threat is minimal.
The Primal vs. Cognitive Mind: A Critical Framework
My work revolves around dissecting the complexities of canine behavior, peeling back the layers of what we see on the surface to reveal the intricate neurological and biological mechanisms underneath. One of the most critical concepts I teach is the distinction between the primal mind and the cognitive mind. This framework is key to understanding not just isolated behaviors, but the very way a dog processes the world around them, how they perceive threats, manage stress, regulate emotions, and make decisions. The dominance of the primal mind over the cognitive mind in miniature breeds isn't a coincidence; it is the direct result of the neurological imbalances we have already discussed. This dominance shapes their emotional responses, decision-making capabilities, and even their baseline state of arousal.
The Primal Mind: Instincts and Survival
The primal mind is the most ancient part of the canine brain, rooted in the limbic system, which includes structures like the amygdala, hypothalamus, and brainstem. This system governs instinctual, survival-driven behaviors that have been hardwired into mammals through millions of years of evolution. The primal mind is responsible for:
Fight: Defensive aggression as a response to threats.
Flight: The instinct to flee from danger.
Freeze: A survival mechanism where immobility can help an animal avoid detection.
Fawn (appeasement behaviors): Submissive gestures to diffuse conflict.
These responses occur automatically and rapidly, often before the dog has consciously processed the situation. The primal mind does not "think”, it reacts. This is why a dog will jump at a sudden noise, snap at a perceived threat, or bolt when frightened without apparent forethought.
In miniature breeds, the primal mind tends to dominate because of the hyperactivity of the amygdala ”the brain' s emotional alarm system”and the underdevelopment of the prefrontal cortex, which would normally help regulate these instinctual responses. As discussed earlier, neuroimaging studies have shown that miniature breeds often have a disproportionately large amygdala relative to their brain size. This hyperactive amygdala acts like an over-sensitive smoke detector, triggering fear, anxiety, and defensive behaviors even in situations that are objectively safe.
Imagine living in a world where every shadow might be a predator, every loud noise a potential threat. This is the reality for many miniature dogs. They are neurologically wired to exist in a state of hyper-vigilance, where their primal mind is constantly scanning for danger, and their ability to "turn off" that alert system is compromised.
This is why miniature breeds often exhibit behaviors such as:
Excessive barking: A common fear-based alert behavior.
Resource guarding: Defensive aggression over food, toys, or even people.
Leash reactivity: Lunging and barking at other dogs or strangers during walks.
Separation anxiety: Inability to self-soothe when left alone, driven by primal attachment instincts.
These are not signs of stubbornness or poor training; they are the visible symptoms of an overactive primal mind that is stuck in survival mode.
The Cognitive Mind: Learning, Adaptation, and Emotional Regulation
In contrast to the primal mind, the cognitive mind is centered in the prefrontal cortex, the brain's executive control center. This region, along with its associated neural pathways, is responsible for higher-order cognitive functions, including:
Decision-making: Evaluating situations and choosing appropriate responses.
Impulse control: Inhibiting instinctual reactions when they are unnecessary or counterproductive.
Emotional regulation: Managing feelings like fear, frustration, or excitement.
Learning and memory: Processing new information, problem-solving, and adapting to changing environments.
The cognitive mind allows dogs to move beyond reflexive, instinctual behavior. It enables them to pause, assess, and respond rather than simply react. This is the part of the brain engaged when a dog learns that the vacuum cleaner isn't actually a monster, or when it resists the urge to chase a squirrel because it has been trained to stay by its owner's side.
In larger or neurologically balanced breeds, there is a fluid transition between the primal and cognitive minds. A dog might initially startle at a loud noise (primal response) but quickly shift into a cognitive state to evaluate whether the noise was truly threatening. This dynamic interplay between instinct and reason is what allows for adaptive, flexible behavior.
However, in miniature breeds, this transition is often impaired. Due to the structural imbalances we explored earlier ”specifically the underdeveloped prefrontal cortex”, these dogs struggle to engage their cognitive mind effectively. They become "stuck" in the primal mode, unable to process new information or regulate their emotions once they have been triggered.
This explains why miniature breeds often have difficulty "calming down" after becoming aroused or why they seem to overreact to minor stimuli. Their neurological wiring traps them in a loop of reactivity with limited access to the cognitive tools needed to break free from that cycle.
The Primal-Cognitive Imbalance: A Neurological Tug-of-War
The interaction between the primal and cognitive minds is critical for healthy emotional and behavioral functioning. In a well-balanced brain, the amygdala (primal mind) quickly alerts the organism to potential threats, while the prefrontal cortex (cognitive mind) evaluates the situation and modulates the response. This dynamic balance allows for both quick reactions when necessary and thoughtful, measured behavior when appropriate.
In miniature breeds, this balance is disrupted. The hyperactive amygdala sends constant danger signals, while the underdeveloped prefrontal cortex lacks the capacity to regulate these signals effectively. The result is a dog that lives in a perpetual state of heightened arousal, where even mundane experiences are processed as potential threats.
This neurological tug-of-war manifests as:
Chronic anxiety: A baseline state of fearfulness, even in familiar environments.
Hyper-reactivity: Exaggerated responses to minor stimuli, such as sudden noises or strangers.
Aggression: Often fear-based, driven by the inability to regulate emotional arousal.
Compulsive behaviors: Repetitive actions like tail-chasing, excessive licking, or pacing, as the dog attempts to self-soothe.
Neurochemical Imbalances: The Chemistry of Behavior
While structural differences in the brain explain much of the primal-cognitive imbalance, the neurochemical environment within the brain adds another layer of complexity. Neurotransmitters like serotonin, dopamine, norepinephrine, and hormones like cortisol play pivotal roles in mood regulation, impulse control, and stress responses.
Cortisol: The Stress Hormone: Cortisol is the body's primary stress hormone, released by the adrenal glands as part of the hypothalamic-pituitary-adrenal (HPA) axis. It helps the body respond to stress by increasing alertness, mobilizing energy reserves, and preparing for fight or flight.
Research shows that miniature breeds often have elevated baseline cortisol levels, even in low-stress environments. This is not just a reaction to specific event's, it is a chronic state, indicating that their bodies are perpetually on high alert.
Prolonged high cortisol levels can lead to:
Immune suppression: Increased susceptibility to illness.
Digestive issues: Such as irritable bowel syndrome, common in anxious dogs.
Increased anxiety: High cortisol levels sensitize the amygdala, reinforcing fear-based behaviors.
Aggression: Lowering the threshold for aggressive responses due to heightened arousal.
Chronic stress also has a neurotoxic effect, damaging brain regions like the hippocampus (involved in learning and memory) and further impairing the prefrontal cortex, creating a vicious cycle where stress begets more stress.
Serotonin: The Mood Stabilizer: Serotonin is a key neurotransmitter involved in regulating mood, anxiety, aggression, and impulse control. Low serotonin levels are associated with:
Anxiety disorders: Including generalized anxiety, phobias, and separation anxiety.
Impulsive aggression: Difficulty inhibiting aggressive responses.
Compulsive behaviors: Such as repetitive licking, chewing, or pacing.
In miniature breeds, studies suggest there is often reduced serotonin receptor density and impaired serotonin signaling. This deficiency makes it harder for these dogs to regulate their emotions, increasing the likelihood of anxiety and aggression.
Norepinephrine and Dopamine: The Arousal Regulators
Norepinephrine regulates arousal, attention, and the body's response to stress. In miniature breeds, excess norepinephrine activity contributes to hyper-vigilance, poor stress recovery, and reactivity.
Dopamine influences motivation, reward processing, and focus. Dysregulated dopamine can lead to compulsive behaviors and poor frustration tolerance, common issues in anxious, reactive dogs.
When these neurotransmitters are out of balance, the dog' s ability to shift from the primal mind to the cognitive mind is further compromised. The result is a brain that is chemically primed for constant arousal, with limited capacity for calm, focused behavior.
The Self-Reinforcing Nature of the Primal Mind
One of the most challenging aspects of this neurological imbalance is its self-reinforcing nature. Each time a dog experiences a stress response, whether it is a burst of anxiety, aggression, or compulsive behavior, it strengthens the neural pathways associated with that response. This phenomenon, known as experience-dependent plasticity, means that the more often a behavior is repeated, the more deeply it becomes ingrained in the brain.
In miniature breeds:
Chronic stress rewires the brain: Prolonged activation of stress circuits leads to further amygdala hypertrophy (enlargement) and prefrontal cortex atrophy (shrinkage).
Behavioral reinforcement: Owners often inadvertently reinforce maladaptive behaviors through inconsistent responses, punishment, or unintentional rewards.
Reduced cognitive flexibility: The underdeveloped prefrontal cortex limits the dog's ability to adapt to new situations or learn alternative coping strategies.
This creates a vicious cycle where the brain's architecture, neurochemistry, and behavior continually feed into each other, making it increasingly difficult for the dog to break free from the dominance of the primal mind.
The Vicious Cycle: Reinforcing the Primal State
One of the most challenging aspects of working with miniature breeds is not just addressing the initial behavioral problems, but breaking the self-reinforcing cycle that keeps these issues entrenched. This cycle is rooted in both the dog' s neurological architecture and the way human responses, often driven by frustration or misunderstanding, can unintentionally perpetuate the very behaviors we are trying to change. This creates a stress feedback loop that operates on both biological and behavioral levels.
At the heart of this vicious cycle is the dog' s primal mind ,overactive, hyper-vigilant, and constantly on high alert. This is compounded by the structural and neurochemical imbalances we have discussed, particularly the hyperactive amygdala, underdeveloped prefrontal cortex, and chronic dysregulation of stress hormones like cortisol. When these neurological factors interact with environmental stressors and inconsistent human handling, the result is a feedback loop that is incredibly difficult to break.
Let's unpack how this cycle works:
1. Stress Leads to Reactivity: Miniature breeds often operate from a baseline of chronic stress due to their heightened sensitivity to environmental stimuli and poor emotional regulation. Even minor triggers, such as a doorbell ringing, encountering another dog, or being left alone, can push them into a reactive state. This reactivity may manifest as barking, lunging, growling, or destructive behavior, all of which are primal responses rooted in the dog' s survival instincts.
2. Reactivity Leads to Owner Frustration: When a dog' s behavior seems "out of control", it naturally leads to frustration for the owner. They may feel embarrassed by their dog' s outbursts in public, exhausted by constant barking at home, or even fearful if the behavior escalates to aggression. This emotional response is understandable, but it often leads to reactive human behavior, yelling, inconsistent corrections, or, in some cases, punitive training methods.
3. Frustration Leads to Inconsistent Training or Punishment: Frustrated owners may switch between different training techniques, trying to find a quick fix. One day they might ignore the behavior, the next day they might scold or physically correct the dog, and the day after that, they might overcompensate with excessive affection to "calm" the dog. This inconsistency confuses the dog, making it harder for them to predict outcomes and feel secure. Punishment, in particular, increases the dog's stress levels, reinforcing the primal mind's dominance and making future reactions even more intense.
4. Inconsistent Responses Increase the Dog's Stress: The dog learns that their environment and the humans within is unpredictable. This lack of predictability is a major stressor for animals, as it signals that they have little control over their surroundings. In response, the dog's stress hormones remain elevated, their amygdala stays hyperactive, and their behaviors become more entrenched. The more the dog reacts, the more the owner reacts, and the cycle continues.
Breaking this cycle requires a fundamental shift in how we view and respond to these dogs. Rather than labeling them as "stubborn, spoiled, or untrainable," we need to recognize them as dogs with unique neurological needs. Their behavior is not a conscious choice but a biological response rooted in brain structure and chemistry.
This paradigm shift involves:
Understanding the Root Causes: Recognizing that behaviors like reactivity, anxiety, and aggression are symptoms of neurological imbalances, not personality flaws.
Managing Expectations: Accepting that progress will most likely be very slow and that setbacks are part of the process when working with a dog whose brain is hardwired for stress and reactivity.
Consistency and Predictability: Providing a stable, predictable environment that reduces stress and helps the dog feel secure.
Addressing Neurochemical Imbalances: In some cases, veterinary support (such as medication to regulate serotonin or cortisol levels) may be necessary to create a neurological environment conducive to learning and behavior change.
Ultimately, breaking this cycle is not just about modifying the dog' s behavior, it is about changing our behavior as humans. When we respond with patience, consistency, and compassion, we create the conditions necessary for the dog's cognitive mind to engage, allowing for true learning and emotional growth.
Conclusion:
Throughout this article, we have explored the hidden costs of miniaturization, costs that extend far beyond the superficial appeal of tiny, portable, "cute" dogs. Miniaturization is not just a physical transformation; it is a profound biological alteration that affects the dog's neurology, behavior, and quality of life.
I have explained how selective breeding for size disrupts the brain's architecture, leading to an overdeveloped amygdala (the fear and aggression center) and an underdeveloped prefrontal cortex (the seat of self-control). This imbalance leaves miniature breeds neurologically predisposed to chronic stress, anxiety, and reactivity. Compounding these structural issues are neurochemical imbalances elevated cortisol levels, reduced serotonin function, and dysregulated dopamine and norepinephrine activity that further entrench maladaptive behaviors.
The distinction between the primal mind and the cognitive mind is central to understanding these behaviors. While all dogs rely on both systems to navigate their world, miniature breeds often get "stuck" in the primal state, unable to transition into cognitive processing due to their neurological limitations. This dominance of the primal mind drives behaviors that are frequently misunderstood dismissed as "Small Dog Syndrome", blamed on poor training, or punished as disobedience.
But the reality is far more complex. These dogs are not choosing to be anxious, reactive, or aggressive. They are living in bodies and with brains that have been biologically altered by human-driven breeding practices. Their behaviors are not character flaws; they are the inevitable outcomes of selective pressures that prioritized aesthetics and convenience over neurological health and emotional well-being.
Breaking the vicious cycle of stress and reactivity requires more than just behavior modification techniques. It demands a shift in perspective, a recognition that these dogs need more than obedience training. They need environments that reduce stress, consistent and predictable human interactions, and, in some cases, medical interventions to address underlying neurochemical imbalances.
As breeders, trainers, veterinarians, and dog owners, we have a responsibility to acknowledge these hidden costs. The choices we make about breeding practices, the standards we set for canine health, and the ways we interpret and respond to canine behavior all have ripple effects that shape not just individual dogs but the future of entire breeds.
Miniature dogs may be small in stature, but the challenges they face and the lessons they teach us are monumental. By approaching these challenges with compassion, scientific understanding, and a commitment to ethical practices, we can create a world where these dogs are not just surviving, but truly thriving.
In the end, the question we must all ask ourselves is this: Is the cost of convenience worth the price these dogs pay?
Bart de Gols - Copyright 2025
References
1. Hecht, E. E., & Smaers, J. B. (2015). Insights into the evolution of the human brain from neuroimaging studies of nonhuman primates. Current Opinion in Neurobiology, 35, 34-42.
2. Neill, D. G., Church, D. B., McGreevy, P. D., Thomson, P. C., & Brodbelt, D. C. (2013). Longevity and mortality of owned dogs in England. The Veterinary Journal, 198(3), 638-643.
3. Berns, G. S., Brooks, A. M., & Spivak, M. (2012). Functional MRI in awake unrestrained dogs. PLOS ONE, 7(5), e38027.
4. Tiira, K., & Lohi, H. (2014). Early life experiences and exercise associate with canine anxieties. PLOS ONE, 9(11), e97670.
5. Serpell, J., Duffy, D. L., & Jagoe, J. A. (2016). Becoming a dog: Early experience and the development of behavior. In The Domestic Dog: Its Evolution, Behavior and Interactions with People (2nd ed., pp. 93 - 117). Cambridge University Press.
6. Ostrander, E. A., & Kruglyak, L. (2000). Unleashing the canine genome. Genome Research, 10(9), 1271 - 1274.
7. McGreevy, P. D., & Nicholas, F. W. (1999). Some practical solutions to welfare problems in dog breeding. Animal Welfare, 8(4), 329 - 341.
8. Starling, M. J., Branson, N., Thomson, P. C., & McGreevy, P. D. (2013). Age, sex, and reproductive status affect boldness in dogs. Journal of Veterinary Behavior, 8(6), 334 -340.
9. Riemer, S., Müller, C., Virányi, Z., Huber, L., & Range, F. (2016). Individual and group level predictors of fear-related behaviors in companion dogs. Applied Animal Behaviour Science, 171, 152 -160.
10. Dodman, N. H., Shuster, L., Seim, H., & Moon-Fanelli, A. (1996). Use of fluoxetine to treat dominance aggression in dogs. Journal of the American Veterinary Medical Association, 209(9), 1585 -1587.
11. Breed, M. D., & Moore, J. (2015). Animal Behavior (2nd ed.). Academic Press.
12. Hopkins, W. D., & Vauclair, J. (2002). Handedness and brain asymmetry in nonhuman primates. In Comparative Vertebrate Cognition: Are Primates Superior to Non-Primates? Springer, Boston, MA.
13. Miklósi,2009 . Dog Behaviour, Evolution, and Cognition. Oxford University Press.
14. Overall, K. L. (2013). Manual of Clinical Behavioral Medicine for Dogs and Cats. Elsevier Health Sciences.
15. Sundman, A. S., Van Poucke, E., Holm, A. C., Faresj Ã…., Theodorsson, E., Jensen, P., & Roth, L. S. V. (2019). Long-term stress levels are synchronized in dogs and their owners. Scientific Reports, 9(1), 7391.
16. Boyko, A. R., Boyko, R. H., Boyko, C. M., Parker, H. G., Castelhano, M., Corey, L., & Ostrander, E. A. (2010). Complex population structure in African village dogs and its implications for inferring dog domestication history. Proceedings of the National Academy of Sciences, 106(33), 13903 - 13908.
17. Sutter, N. B., Bustamante, C. D., Chase, K., Gray, M. M., Zhao, K., Zhu, L., & Ostrander, E. A. (2007). A single IGF1 allele is a major determinant of small size in dogs. Science, 316(5821), 112 - 115.
18. Axelsson, E., Ratnakumar, A., Arendt, M. L., Maqbool, K., Webster, M. T., Perloski, M., & Lindblad-Toh, K. (2013). The genomic signature of dog domestication reveals adaptation to a starch-rich diet. Nature, 495(7441), 360 - 364.
19. Wayne, R. K., & vonHoldt, B. M. (2012). Evolutionary genomics of dog domestication. Mammalian Genome, 23(1–2), 3 - 18.
20. Horwitz, D. F., & Mills, D. S. (2009). BSAVA Manual of Canine and Feline Behavioural Medicine (2nd ed.). British Small Animal Veterinary Association.
21. de Souza, J. C., & Salum, F. G. (2012). Neuroendocrine regulation of stress response in animals. Journal of Applied Animal Research, 40(3), 195 -202.