RESUMEN
Stress is a complex and multifaceted phenomenon that can significantly influence both aggressive behavior and sexual function. This review explores the intricate relationship between stress, neuromodulator pathways, and epigenetics, shedding light on the various mechanisms that underlie these connections. While the role of stress in both aggression and sexual behavior is well-documented, the mechanisms through which it exerts its effects are multifarious and not yet fully understood. The review begins by delving into the potential influence of stress on the Hypothalamic-Pituitary-Adrenal (HPA) axis, glucocorticoids, and the neuromodulators involved in the stress response. The intricate interplay between these systems, which encompasses the regulation of stress hormones, is central to understanding how stress may contribute to aggressive behavior and sexual function. Several neuromodulator pathways are implicated in both stress and behavior regulation. We explore the roles of norepinephrine, serotonin, oxytocin, and androgens in mediating the effects of stress on aggression and sexual function. It is important to distinguish between general sexual behavior, sexual motivation, and the distinct category of "sexual aggression" as separate constructs, each necessitating specific examination. Additionally, epigenetic mechanisms emerge as crucial factors that link stress to changes in gene expression patterns and, subsequently, to behavior. We then discuss how epigenetic modifications can occur in response to stress exposure, altering the regulation of genes associated with stress, aggression, and sexual function. While numerous studies support the association between epigenetic changes and stress-induced behavior, more research is necessary to establish definitive links. Throughout this exploration, it becomes increasingly clear that the relationship between stress, neuromodulator pathways, and epigenetics is intricate and multifaceted. The review emphasizes the need for further research, particularly in the context of human studies, to provide clinical significance and to validate the existing findings from animal models. By better understanding how stress influences aggressive behavior and sexual function through neuromodulator pathways and epigenetic modifications, this research aims to contribute to the development of innovative protocols of precision medicine and more effective strategies for managing the consequences of stress on human behavior. This may also pave way for further research into risk factors and underlying mechanisms that may associate stress with sexual aggression which finds application not only in neuroscience, but also law, ethics, and the humanities in general.
RESUMEN
The piriform cortex (PC) is a major cortical processing center for the sense of smell that receives direct inputs from the olfactory bulb. In mice, the PC consists of three neuronal layers, which are populated by cells with distinct developmental origins. One origin of PC neurons is the pool of Dbx1-expressing neural progenitors located in the ventral pallium at the pallial-subpallial boundary. Since the precise mechanisms of PC neuron development are largely unknown, we sought to define the distribution, timing of neurogenesis, morphology and projection patterns of PC neurons from the Dbx1 lineage. We found that Dbx1-lineage neurons are preferentially distributed in layer 2 and enriched in the ventral portion of the PC. Further, Dbx1 neurons are early-born neurons and contribute to most neuronal subtypes in the PC. Our data also revealed an enrichment of Dbx1-lineage neurons in the ventral anterior PC that project to the orbitofrontal cortex. These findings suggest a specific association between the developmental origin of PC neurons and their neuronal properties.