
Emotional pain in non-human mammals: from neural circuitry and opioid signaling to dysthymia-like states, grief-like behaviors, and physiological dysregulation
Front Vet Sci. 2026 Jul 29;13:1878991. doi: 10.3389/fvets.2026.1878991. eCollection 2026.
ABSTRACT
This review aims to analyze the neurobiological, pathophysiological, and ethological foundations of emotional pain in non-human mammals, with particular emphasis on the transition from adaptive responses to pathological states such as animal dysthymia and Takotsubo syndrome. In the review, four conditions that can activate emotional systems will be discussed, such as pain derived from surgery or injury, stressful conditions that do not cause pain (e.g., unknown noises or smells), separation stress where an animal is isolated from the group (e.g., dam-calf separation), and death of a familiar animal or conspecific. The review will examine the role of subcortical brain regions, highlighting the amygdala-particularly the basolateral complex and central nucleus-as key integrators of negative affect and stress responses. In addition, it will address the contribution of cortical regions, such as the anterior cingulate cortex, and their interaction with the endogenous opioid system in the processing of affective suffering. The review will also incorporate evidence of thanatological behaviors and mourning-like responses, suggesting a degree of death awareness and social sensitivity to loss across multiple species. While the function of these neural circuits is fundamentally adaptive, chronic activation may induce neuroplastic changes and neurotransmitter dysregulation, leading to maladaptive outcomes. These include persistent anxiety, depression-like states, thanatological behaviors, and stress-related cardiac conditions such as Takotsubo syndrome, all of which may compromise animal welfare. Finally, further comparative research is needed to deepen our understanding of emotional pain in non-human animals.
PMID:42591201 | PMC:PMC13461465 | DOI:10.3389/fvets.2026.1878991
