In mammals, parental care is essential for the survival of the young; therefore, it is vitally important to the propagation of the species. These behaviors, differing between the two sexes, are innate, stereotyped, and are also modified by an individual's reproductive experience. These characteristics suggest that neural mechanisms underlying parental behaviors are genetically hardwired, evolutionarily conserved as well as sexually differentiated and malleable to experiential changes. Classical lesion studies on neural control of parental behaviors, mostly done in rats, date back to the 1950s. Recent developments of new methods and tools in neuroscience, which allow precise targeting and activation/inhibition of specific populations of neurons and their projections to different brain structures, have afforded fresh opportunities to dissect and delineate the detailed neural circuit mechanisms that govern distinct components of parental behaviors in the genetically tractably organism, the laboratory mouse (Mus musculus). In this review, we summarize recent discoveries using modern neurobiological tools within the context of traditional lesion studies. In addition, we discuss interesting cross talk between neural circuits that govern parent care with those that regulate other innate behaviors such as feeding and mating.Social behavior is a complex behavior that requires processing of sensory cues and integration of internal states. Social interaction involves two or more individuals to approach each other and engage communications. Although sensory, motivational, emotional, or reward cues may all play roles in directing the sociability and social preference during social interaction, how neural activities from different brain regions are modulated during the behavioral process of social interaction are only beginning to be studied. Multiple brain regions including prefrontal cortex, hippocampus, and amygdala contain active neurons during social interaction. This review examines the neural responses in behaving rodents during social behavior and discusses how manipulation of specific neural pathways can modulate social behavior. Neural activities during social interaction provide direct measurements about how social information is coded and are beneficial in understanding the neural mechanisms underlying social behavior.Innate behaviors often viewed as genetically predetermined behaviors. However, in the environment animals often are subjected to external stimuli conflicting with those. Thus, animals subsequently need to change those behaviors to survive and reproduce. In the brain, the reward pathway is well-known for its role to adjust behaviors according to external stimuli, or rewards. However, only recently the relationship between reward pathway and innate behavior begins to be explored. In this review, we summarize the recent data on this subject from rodent studies which suggest an important role of this crosstalk between circuits involved in reward pathway and innate behaviors. We also discuss some of the neurotransmitters and neuromodulators underlying this crosstalk and the related mechanisms.Food intake and energy homeostasis determine survival of the organism and species. Information on total energy levels and metabolic state are sensed in the periphery and transmitted to the brain, where it is integrated and triggers the animal to forage, prey, and consume food. Investigating circuitry and cellular mechanisms coordinating energy balance and feeding behaviors has drawn on many state-of-the-art techniques, including gene manipulation, optogenetics, virus tracing, and single-cell sequencing. These new findings provide novel insights into how the central nervous system regulates food intake, and shed the light on potential therapeutic interventions for eating-related disorders such as obesity and anorexia.Aggression takes several forms and can be offensive or defensive. Aggression between animals of the same species or society aims to inflict harm upon another for the purpose of protecting a resource such as food, reproductive partners, territory, or status. This chapter explores the neurobiology of aggression. We summarize the behavior of aggression, rodent models of aggression, and the correlates of aggressive behavior in the context of neuroendocrinology, neurotransmitter systems, and neurocircuitry. Translational implications of rodent studies are briefly discussed, applying basic research to brain imaging data and therapeutic approaches to conditions where aggression is problematic.Fear is defined as a fundamental emotion promptly arising in the context of threat and when danger is perceived. Fear can be innate or learned. Examples of innate fear include fears that are triggered by predators, pain, heights, rapidly approaching objects, and ancestral threats such as snakes and spiders. Animals and humans detect and respond more rapidly to threatening stimuli than to nonthreatening stimuli in the natural world. The threatening stimuli for most animals are predators, and most predators are themselves prey to other animals. Predatory avoidance is of crucial importance for survival of animals. Although humans are rarely affected by predators, we are constantly challenged by social threats such as a fearful or angry facial expression. This chapter will summarize the current knowledge on brain circuits processing innate fear responses to visual stimuli derived from studies conducted in mice and humans.Protocadherin-19 (PCDH19) pathogenic variants cause an infantile onset epilepsy syndrome called Girls Clustering Epilepsy due to the vast majority of affected individuals being female. This syndromic name was developed to foster early recognition and diagnosis in infancy. It has, however, sparked debate, as, there are rare males with postzygotic somatic, and therefore, mosaic, PCDH19 pathogenic variants with similar clinical features to females. Conversely, "transmitting" males with germline inherited PCDH19 variants are considered asymptomatic.  https://www.selleckchem.com/products/bexotegrast.html  To date, there has been no standardized neuropsychiatric assessment of males with PCDH19 pathogenic variants. Here, we studied 15 males with PCDH19 pathogenic variants (nine mosaic and six transmitting) aged 2 to 70 years. Our families completed a survey including standardized clinical assessments Social Responsiveness Scale, Strengths and Difficulties Questionnaire, Behavior Rating Inventory of Executive Function, and Dimensional Obsessive-Compulsive Scale. We identified neuropsychiatric abnormalities in two males with germline PCDH19 possibly pathogenic variants.