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The acquisition and use of social information are integral to social behaviour and parasite/pathogen avoidance. This involves social cognition which encompasses mechanisms for acquiring, processing, retaining and acting on social information. Social cognition entails the acquisition of social information about others (i.e. social recognition) and from others (i.e. social learning). Social cognition involves assessing other individuals and their infection status and the pathogen and parasite threat they pose and deciding about when and how to interact with them. Social cognition provides a framework for examining pathogen and parasite avoidance behaviours and their associated neurobiological mechanisms. Here, we briefly consider the relationships between social cognition and olfactory-mediated pathogen and parasite avoidance behaviours. We briefly discuss aspects of (i) social recognition of actual and potentially infected individuals and the impact of parasite/pathogen threat on mate and social partner choice; (ii) the roles of ‘out-groups’ (strangers, unfamiliar individuals) and ‘in-groups’ (familiar individuals) in the expression of parasite/pathogen avoidance behaviours; (iii) individual and social learning, i.e. the utilization of the pathogen recognition and avoidance responses of others; and (iv) the neurobiological mechanisms, in particular the roles of the nonapeptide, oxytocin and steroid hormones (oestrogens) associated with social cognition and parasite/pathogen avoidance. This article is part of the Theo Murphy meeting issue ‘Evolution of pathogen and parasite avoidance behaviours'.

Various aspects of sociality, including mate choice, are dependent on social information. Mate choice is a social cognitive process that encompasses mechanisms for acquiring, processing, retaining and acting on social information. Social cognition includes the acquisition of social information about others (i.e., social recognition) and social information from others (i.e., social learning). Social cognition involves both assessing other individuals and their condition (e.g., health, infection status) and deciding about when and how to interact with them, thus, providing a frame-work for examining mate choice and its associated neurobiological mechanisms. In vertebrates, and in particular rodents, odors are an essential source of direct and indirect social information not only from others but also for others. Here, we briefly consider the relations between social cognition and olfactory-mediated mate choice in rodents. We briefly discuss aspects of: (1) social recognition of potential mates and the impact of infection threat on mate choice; (2) social learning and the utilization of the mate choices of others (“mate-choice copying”) including in the context of infection; and (3) the neurobiological mechanisms, with particular focus on particular the roles of the nonapeptide, oxytocin and the steroid hormones, estrogens, associated with social cognition and mate choice.

It is well established that estrogens affect neuroplasticity in a number of brain regions. In particular, estrogens modulate and mediate spine and synapse formation as well as neurogenesis in the hippocampal formation. In this review, we discuss current research exploring the effects of estrogens on dendritic spine plasticity and neurogenesis with a focus on the modulating factors of sex, age, and pregnancy. Hormone levels, including those of estrogens, fluctuate widely across the lifespan from early life to puberty, through adulthood and into old age, as well as with pregnancy and parturition. Dendritic spine formation and modulation are altered both by rapid (likely non-genomic) and classical (genomic) actions of estrogens and have been suggested to play a role in the effects of estrogens on learning and memory. Neurogenesis in the hippocampus is influenced by age, the estrous cycle, pregnancy, and parity in female rodents. Furthermore, sex differences exist in hippocampal cellular and molecular responses to estrogens and are briefly discussed throughout. Understanding how structural plasticity in the hippocampus is affected by estrogens and how these effects can influence function and be influenced by other factors, such as experience and sex, is critical and can inform future treatments in conditions involving the hippocampus.

The neurobiological mechanisms underlying social learning (ie, in which an animal's learning is influenced by another) are slowly being unraveled. Previous work with systemic treatments shows that dopamine (DA) D1-type receptors mediate social learning in the social transmission of food preferences (STFP) in mice. This study examines the involvement of one brain region underlying this effect. The ventral tegmental area has dopaminergic projections to many limbic structures, including the hippocampus-a site important for social learning in the STFP in rodents. In this study, adult male and female CD-1 mice received a dorsal hippocampal microinfusion of the D1-like receptor antagonist SCH23390 at 1, 2, 4, or 6 μg/μl 15 min before a 30 min social interaction with a same-sex conspecific, in which mice had the opportunity to learn a socially transmitted food preference. Results show that social learning was blocked in female mice microinfused with 6 μg/μl, and in males infused with 1, 4, or 6 μg/μl of SCH23390. This social learning impairment could not be explained by changes in total food intake, or olfactory discrimination. A detailed analysis of the social interactions also revealed that although SCH23390 did not affect oronasal investigation for either sex, drug treatments affected other social behaviors in a sex-specific manner; there was primarily a reduction in agonistic-related behaviors among males, and social investigatory-related behaviors among females. Thus, this study shows that dorsal hippocampal D1-type receptors mediate social learning and social behaviors in male and female mice.

Animals are under constant threat of parasitic infection. This has influenced the evolution of social behaviour and has strong implications for sexual selection and mate choice. Animals assess the infection status of conspecifics based on various sensory cues, with odours/chemical signals and the olfactory system playing a particularly important role. The detection of chemical cues and subsequent processing of the infection threat that they pose facilitates the expression of disgust, fear, anxiety, and adaptive avoidance behaviours. In this selective review, drawing primarily from rodent studies, the neurobiological mechanisms underlying the detection and assessment of infection status and their relations to mate choice are briefly considered. Firstly, we offer a brief overview of the aspects of mate choice that are relevant to pathogen avoidance. Then, we specifically focus on the olfactory detection of and responses to conspecific cues of parasitic infection, followed by a brief overview of the neurobiological systems underlying the elicitation of disgust and the expression of avoidance of the pathogen threat. Throughout, we focus on current findings and provide suggestions for future directions and research.

Dramatic increases in hippocampal spine synapse density are known to occur within minutes of estrogen exposure. Until now, it has been assumed that enhanced spinogenesis increased excitatory input received by the CA1 pyramidal neurons, but how this facilitated learning and memory was unclear. Delivery of 17β-estradiol or an estrogen receptor (ER)-α (but not ER-β) agonist into the dorsal hippocampus rapidly improved general discrimination learning in female mice. The same treatments increased CA1 dendritic spines in hippocampal sections over a time course consistent with the learning acquisition phase. Surprisingly, estrogen-activated spinogenesis was associated with a decrease in CA1 hippocampal excitatory input, rapidly and transiently reducing CA1 AMPA activity via a mechanism likely reflecting AMPA receptor internalization and creation of silent or immature synapses. We propose that estrogens promote hippocampally mediated learning via a mechanism resembling some of the broad features of normal development, an initial overproduction of functionally immature connections being subsequently “pruned” by experience.

The challenges and threats posed by out-groups have major effects on human social behavior and how individuals interact with one another. We briefly review evidence here that out-group threat similarly affects nonhuman animal behavior. Actual and potential threats posed by out-group individuals (unfamiliar and genetically nonrelated individuals of the same species) affect social behavior promoting “out-group” avoidance and “in-group” bias and enhancing in-group (familiar and/or genetically related individuals) affiliation and interactions. Individuals from out-groups present risks of pathogen exposure as well as being threats to resources, territory, and offspring. All of these threats function to promote in-group bias in humans and nonhumans. There are also striking similarities in the underlying neurobiological mechanisms mediating the responses to out-group threat and the expression of in-group bias. In particular, the evolutionarily conserved, hormone-regulated nonapeptide systems (oxytocin, arginine-vasopressin, and homologous neuropeptides and their receptors) are involved in the mediation of the detection and avoidance of out-groups and response to in-groups and facilitation of in-group responses across multiple vertebrate species. Consequently, comparative investigations of both the behavioral expression of and the mechanism underlying out-group avoidance and in-group bias are necessary for a full understanding of the evolution of social behavior and responses to in- and out-groups.

The neurotransmitter acetylcholine supports goal-directed cognitive functions via activation of its nicotinic and muscarinic classes of receptors within the prefrontal cortex. These receptors are expressed on pyramidal neurons located within layer V of the prefrontal cortex, which integrate afferent signals and contribute toward cognitive circuits via efferent projections to cortical and subcortical targets. Using whole-cell electrophysiology, retrograde labelling, and neuron reconstruction in the juvenile mouse prefrontal cortex, we identified three unique nicotinic receptor responses that are present in distinct subtypes of layer V pyramidal neurons. Broadly, we observed responses mediated by (i) postsynaptic α7 nicotinic receptors in burst-firing neurons that project to the contralateral cortex, (ii) a combination of postsynaptic α7 and presynaptic β2* nicotinic receptors in burst-firing neurons that project to the nucleus accumbens, and (iii) postsynaptic β2* nicotinic receptors in regular-firing neurons that project to the ventromedial thalamus. These findings provide insight into a mechanism by which nicotinic acetylcholine neurotransmission may support cognitive functions via the unique receptor isoform responses found in distinct efferent projections from this brain region.

The mammalian neurohypophyseal peptide hormones oxytocin and vasopressin act to mediate human social behavior - they affect trust and social relationships and have an influence on avoidance responses. Describing the evolutionary roots of the effects that these neuropeptides have on behavior, this book examines remarkable parallel findings in both humans and non-human animals. The chapters are structured around three key issues: the molecular and neurohormonal mechanisms of peptides; phylogenetic considerations of their role in vertebrates; and their related effects on human behavior, social cognition and clinical applications involving psychiatric disorders such as autism. A final chapter summarizes current research perspectives and reflects on the outlook for future developments. Providing a comparative overview and featuring contributions from leading researchers, this is a valuable resource for graduate students, researchers and clinicians in this rapidly developing field.

Estrogens control many physiological and behavioral processes, some of which are connected to reproduction. These include sexual and other social behaviors. Here we implicate four gene products in a micronet required for mammalian social recognition, through which an individual learns to recognize other individuals. Female mice whose genes for the neuropeptide oxytocin (OT) or the estrogen receptor (ER)-β or ER-α had been selectively \"knocked out\" were deficient specifically in social recognition and social anxiety. There was a remarkable parallelism among results from three separate gene knockouts. The data strongly suggest the involvement in social recognition of the four genes coding for ER-α, ER-β, OT, and the OT receptor. We thus propose here a four-gene micronet, which links hypothalamic and limbic forebrain neurons in the estrogen control over the OT regulation of social recognition. In our model, estrogens act on the OT system at two levels: through ER-β, they regulate the production of OT in the hypothalamic paraventricular nucleus, and through ER-α, they drive the transcription of the OT receptor in the amygdala. The proper operation of a social recognition mechanism allows for the expression of appropriate social behaviors, aggressive or affiliative.