Well-studied physiological mechanisms for relatively simple instinctive behaviors like sex and aggression are unlikely to have secondary roles, subservient to affect systems. Adding psychoanalytic ideation does not advance their understanding. However, concepts of the dynamic unconscious may find parallels in current day neuroscience.

The ability to silence the expression of gene products in a chemically, spatially, and temporally specific manner in the brains of animals has enabled key breakthroughs in the field of behavioral neuroscience. Using this technique, estrogen receptor alpha (ERα) has been specifically implicated in a multitude of behaviors in mice, including sexual, aggressive, locomotor, and maternal behaviors, in a variety of brain regions, including the medial preoptic area, ventromedial hypothalamus, and amygdala. In this chapter, we describe the techniques involved in the generation of the small hairpin RNAs (shRNAs) specifically designed to silence ERα, the construction of the adeno-associated viral (AAV) vector for delivery of the shRNA, the procedures to confirm the silencing of ERα (in vitro and in vivo) and in vivo delivery of the shRNAs to the brains of animals.

Good sleepers and patients with insomnia symptoms (poor sleepers) were tracked with two measures of arousal; conventional polysomnography (PSG) for electroencephalogram (EEG) assessed cortical arousals, and a peripheral arterial tonometry device was used for the detection of peripheral nervous system (PNS) arousals associated with vasoconstrictions. The relationship between central (cortical) and peripheral (autonomic) arousals was examined by evaluating their close temporal dynamics. Cortical arousals almost invariably were preceded and followed by peripheral activations, while large peripheral autonomic arousals were followed by cortical arousals only half of the time. The temporal contiguity of these two types of arousals was altered in poor sleepers, and poor sleepers displayed a higher number of cortical and peripheral arousals compared with good sleepers. Given the difference in the number of peripheral autonomic arousals between good and poor sleepers, an evaluation of such arousals could become a means of physiologically distinguishing poor sleepers.

Mechanisms for fish social behaviours involve a social brain network (SBN) which is evolutionarily conserved among vertebrates. However, considerable diversity is observed in the actual behaviour patterns amongst nearly 30000 fish species. The huge variation found in socio-sexual behaviours and strategies is likely generated by a morphologically and genetically well-conserved small forebrain system. Hence, teleost fish provide a useful model to study the fundamental mechanisms underlying social brain functions. Herein we review the foundations underlying fish social behaviours including sensory, hormonal, molecular and neuroanatomical features. Gonadotropin-releasing hormone neurons clearly play important roles, but the participation of vasotocin and isotocin is also highlighted. Genetic investigations of developing fish brain have revealed the molecular complexity of neural development of the SBN. In addition to straightforward social behaviours such as sex and aggression, new experiments have revealed higher order and unique phenomena such as social eavesdropping and social buffering in fish. Finally, observations interpreted as 'collective cognition' in fish can likely be explained by careful observation of sensory determinants and analyses using the dynamics of quantitative scaling. Understanding of the functions of the SBN in fish provide clues for understanding the origin and evolution of higher social functions in vertebrates.

Social encounters often start with speech: a question, a call, a familiar greeting. Unlike a baby's cry, which is at once universal but vague in meaning, speech is culture-bound but immediately intelligible. Hearers know what the initiator meant virtually at the speed of sound; they can respond with equal speed, or as quickly as they can formulate a desired response. Speech is a highly effective means of inviting a social approach. If we respond to what someone says, we usually do so with more conversation, employing speech that is apprehensible to whomever began the exchange. Speech is efficient because language can be so precise, and our hearing—at least at close range—creates so little distortion.

When we see a friend and get a warm feeling, how does that work? What is the pathway from the eye to areas of the brain that register "friend" and then happiness? The serial, split-second steps are an important substrate of the social impulse which, in part, depends on facial recognition. To understand the process, we must first trace visual signals from the eye to the mid- and forebrain. For the neuroscientist, this is business as usual. Then, surprisingly, evidence suggests that nerve cells in the cerebral cortex participate actively in "top-down" control of visual perception, i.e., they interpret the image: "Okay, that's my friend!" The last step—that of actually triggering the social impulse—is somewhat trickier, but there is exciting evidence from both human and non-human primate brains of neurons specialized for prosocial behaviors.

In Social, I have sought to understand the first spark of human attraction towards another human, i.e., the instinct towards social contact. Data relevant to the time scales underlying this impulse are measured in milliseconds, as in neurophysiology; in months, as in babies' development; and in the eons over which Homo sapiens evolved, measured to the extent that it can be by paleoanthropology. Accordingly, my book scales across time-frames appropriate to its subjects.

Fish present complex resource management problems that continue to raise tough biological, economic, and political concerns. The U.N.'s Food and Agriculture Organization has initiated an array of treaties that govern world fisheries. The U.S. participates in bi- and multi-lateral conventions concerning sea life of all sorts—not just fish, but whales and turtles. The issues are invariably sensitive. Where can the British trawl, the French, the Canadians? What can they catch, how much, and when? What do we do about climate change, the destruction of spawning grounds, and the effects of toxic waste? What is the effect of fish farming, building dams, and run-off from power-plants? How do we stop invasive species, introduced when the bilges of cruise ships are emptied? How do we save the dolphins? What type of markets should be permitted in light of health scares from the sale of raw food? We want to maintain stocks but we need to feed people. We think about the balance between finite—even shrinking—aquatic resources and the world's demand for protein.

Yesterday, it happened again. A man leapt onto the track to save another man who was stuck there, "staring ahead absently." As an example of such positive human social behavior, my New York ideal from years ago is Wesley Aubrey, a Black construction worker who left his own child on a subway platform to jump on the tracks, cover a trapped epileptic, a young white man, with his own body, and save him from an oncoming train. Afterwards and to great fanfare, Aubrey said that he never gave his act a second thought—it just came naturally. He was no neuroscientist, but he was right. Altruism, the willingness to give without any expectation of reward, is an extreme but also utterly commonplace human social impulse. We do not give because we think it's "right," but because we do not think. We just do it. As I will show, our brains are designed so that—should the need arise—we put ourselves in other people's places and act empathetically.

The most obvious social approach behaviors are those necessary for survival of the species. Sex, without which no vertebrate species can survive, is by definition social. In this chapter, I will look at sex, among other social behaviors that are so basic to a species' survival that the species would disappear were these behaviors to decline significantly.

Previous experiments charted the development of behavioral arousal in postnatal mice. From Postnatal Day 3 (P3) to Postnatal Day 6 (P6) mice (a) become significantly more active, "arousable"; and (b) in large reticular neurons, nucleus gigantocellularis (NGC), patch clamp recordings reveal a significantly increased ability to fire high frequency trains of action potentials as are associated with elevated cortical arousal. These action potential trains depend on delayed rectifiers such as Kv2.1. Here we report tracking the development of expression of a delayed rectifier, Kv2.1 in NGC neurons crucial for initiating CNS arousal. In tissue sections, light microscope immunohistochemistry revealed that expression of Kv2.1 in NGC neurons is greater at day P6 than at P3. Electron microscope immunohistochemistry revealed Kv2.1 labeling on the plasmalemmal surface of soma and dendrites, greater on P6 than P3. In brainstem reticular neuron cell culture, Kv2.1 immunocytochemistry increased monotonically from Days-In-Vitro 3-10, paralleling the ability of such neurons to fire action potential trains. The increase of Kv2.1 expression from P3 to P6, perhaps in conjunction with other delayed rectifier currents, could permit the ability to fire action potential trains in NGC neurons. Further work with genetically identified NGC neurons is indicated.

Neurons in nucleus gigantocellularis (NGC) have been shown by many lines of evidence to be important for regulating generalized CNS arousal. Our previous study on mouse pups suggested that the development of NGC neurons' capability to fire action potential (AP) trains may both lead to the development of behavioral arousal and may itself depend on an increase in delayed rectifier currents. Here with whole-cell patch clamp we studied delayed rectifier currents in two stages. First, primary cultured neurons isolated from E12.5 embryonic hindbrain (HB), a dissection which contains all of NGC, were used to take advantage of studying neurons in vitro over using neurons in situ or in brain slices. HB neurons were tested with Guangxitoxin-1E and Resveratrol, two inhibitors of Kv2 channels which mediate the main bulk of delayed rectifier currents. Both inhibitors depressed delayed rectifier currents, but differentially: Resveratrol, but not Guangxitoxin-1E, reduced or abolished action potentials in AP trains. Since Resveratrol affects the Kv2.2 subtype, the development of the delayed rectifier mediated through Kv2.2 channels may lead to the development of HB neurons' capability to generate AP trains. Stage Two in this work found that electrophysiological properties of the primary HB neurons recorded are essentially the same as those of NGC neurons. Thus, from the two stages combined, we propose that currents mediated through Kv2.2 are crucial for generating AP trains which, in turn, lead to the development of mouse pup behavioral arousal.

If altruism represents a high point in human social relations, then the failures of social approach in autism represent something that is not just "different," but worthy medical and scientific attention. With autism, not socially engaging is a defining characteristic. Autistic children often do not exhibit an ordinary interest in other people, or may act in ways that keep other people at a distance.

The activation of behaviour in a daily rhythm governed by the light cycle is a universal phenomenon among humans, laboratory mammals and other vertebrates. For mice, the active period is during the dark. We have quantified the increase in activity when the lights shut off (Light to Dark, L to D) using a generalized CNS arousal assay with 20 ms resolution, rather than traditional running wheels. Data analysis yielded the rare demonstration of an equation which precisely tracks this behavioural transition and, surprisingly, its reverse during D to L. This behavioural dynamic survives in constant darkness (experiment 2) and is hormone-sensitive (experiment 3). Finally (experiment 4), mice on a light schedule analogous to one which proved troublesome for U.S. Navy sailors, had dysregulated activity bursts which did not conform to the transitions between D and L. These experiments show the lawfulness of a behavioural phase transition and the consequence of deviating from that dynamic pattern. And, in a new way, they bring mathematics to the realm of behavioural neuroscience.

Concerns have been raised over the neurotoxicity of triphenyl phosphate (TPP), but there have been few studies of the neurotoxic effects of TPP on mammals and the underlying mechanisms. In this study, weaned male mice (C57/BL6) were used and exposed to 0, 50, or 150 mg/kg TPP daily by oral gavage for 30 days. The blood brain barrier (BBB) permeability of TPP and its metabolite diphenyl phosphate (DPP) in the brain, and TPP induced metabolomic and transcriptomic changes of the brain were investigated. The results showed that TPP and DPP can cross the BBB of mice. Histopathological examination of the brain revealed abnormalities in the hippocampus, cortex and thalamus, and mice treated with high doses showed a potential inflammation in the thalamus and hippocampus. Untargeted metabolomic results revealed that the changed level of glutamic acid, N-acetyl CoA metabolites, and organic acid in the brain of treated mice, suggest that amino acid and lipid metabolism was interfered. RNA-seq data indicated that neuronal transcription processes and cell apoptosis pathway (forkhead box (FOXO), and mitogen-activated protein kinase (MAPK) signaling pathways) were significantly affected by TPP exposure. RT-PCR showed proinflammation cytokine tumor necrosis factor alpha (TNIF-alpha) and interleukin-6 (IL-6)) levels were increased, while antioxidant genes including nuclear factor-E2-related factor 2 (Nrf2), heme oxygenase1 (HO-1) and superoxide dismutase (SOD1) decreased. These results suggest that TPP could cause a degree of neurotoxicity by inducing neuroinflammation and neuronal apoptosis, which are related to oxidative stress. The potential implications for neurophysiology and behavioral regulation cannot be ignored. (C) 2020 Elsevier Ltd. All rights reserved.

Background During the past 50 years, motivational studies have evolved from the logical inference of logically required “intervening variables” to explain behavioral change, to electrophysiological and molecular analyses of the mechanisms causing such changes. Aim The purpose of this review article is two-fold: first to describe the logic of sexual motivation in a way that applies to laboratory animals as well as humans, and the second is to address some of the problems of sexual motivation experienced by men. Results When problems of motivational mechanisms are stripped down to their essentials, as performed in the laboratory animal models and are available for reductionistic studies, then the problems can be solved with certainty, as illustrated in the first part of this review. However, with respect to human sexual motivation, the various determinants which include so many behavioral routes and so many brain states come into play, that definite conclusions are harder to come by, as illustrated in the second part of this review. Conclusions This review highlights a number of key questions that merit further investigation. These include (a) What mechanisms do cultural and experiential influences interact with androgenic hormone influences on human sexual motivation? (b) How would epigenetic effects in the human brain related to changes in motivation be investigated? (c) What are the effects of unpredictable traumatic and stressful human experiences on sexual motivation; (d) How such mechanisms are activated upon unpredictable traumatic and stressful insults? (e) What are the outstanding differences between sexual motivational drive and motivations driven by homeostatic systems such as hunger and thirst?