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This chapter presents the views of the other hemisphere by describing and discussing the various theoretical approaches which have been taken by Western psychologists studying meditation. Attention is a central component in descriptions of the mechanics of meditation and emphasis is placed upon the potential value of studying meditation from an information-processing orientation. Interest in bilateral brain explanations of experience and abilities is reflected in the discussion of consciousness and meditation. The psychoanalytic orientations described in this chapter suggests that meditation induces regression in the service of the ego to preverbal levels of experience and facilitates primary process mentation. Behavioural orientations, in contrast, see meditation as a form of systematic desensitization, involving reciprocal inhibition and counter-conditioning.

This chapter takes a look at the possible future of privacy. It considers the views of privacy defenders, and examines the judgments on where and how to draw a line against the endless erosion of privacy. It looks at the official responses to privacy protection and tries to balance the various privacy codes. It then identifies the roots of the conflict in privacy and the type of world that is emerging from the growth of surveillance systems. Finally, the chapter discusses the apparent desensitization of publics to the daily demands on privacy and draws some positive and negative conclusions.

Both kainate receptors and AMPA receptors mediate fast excitatory synaptic transmission and are associated primarily with voltage-independent channels that gate a depolarizing current mainly carried by an influx of sodium ions. Two compounds—the natural plant product kainic acid, which was isolated from Digenea simplex and is used in traditional medicine for the treatment of diseases caused by parasites, and a synthetic analogue of quisqualic acid, α-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionate (AMPA)—have played pivotal roles in the characterization of the non-N-methyl-D-aspartate (NMDA) glutamate receptor (GluR) subclass. The question of whether functional kainate receptors exist in the human central nervous system remained unresolved for a long time. This situation changed signiticantly with the cloning of GluR subunits. Cloning of additional GluR subunits firmly established the existence of genuine kainate receptors. This chapter discusses the molecular structure and subunit composition of kainate receptors, along with their single-channel conductance and desensitization, alternative splicing, messenger RNA editing, distribution, pharmacology, role in synaptic plasticity, and therapeutic applications.

Ionotropic glutamate receptors, including NMDA receptors, mediate most of the excitatory synaptic transmission in the mammalian central nervous system. When NMDA receptors are activated by membrane depolarization, a relatively slow-rising, long-lasting current develops, which allows the summation of responses to stimuli for a relatively long periods (tens of milliseconds). In addition to their role in synaptic transmission, NMDA receptors affect functions that are critical for the survival and differentiation of cells and for synaptic plasticity, in part through Ca²⁺-dependent signal transduction. In addition, receptor activation elicits long-term changes in cellular functions, mediated through interactions (either directly or via scaffolding proteins) with signaling systems, including protein kinase cascades that lead to modulation of gene transcription. This chapter discusses the unique role of NMDA receptors in excitatory transmission, their molecular structure, posttranslational modifications (phosphorylation and dephosphorylation), molecular interactions relevant for signal transduction, desensitization, anatomical distribution, pharmacology, modulation of expression in transgenic mice, and therapeutic applications.

Metabotropic glutamate receptors (mGluRs) are a distinct family of excitatory amino acid receptors. Unlike the ionotropic glutamate receptors (iGluRs), which constitute cation-specific ion channels and mediate fast excitatory synaptic responses, the more recently characterized mGluRs are coupled to a variety of signal transduction pathways via guanine nucleotide binding proteins (G proteins), They produce alterations in intracellular second messengers, affect ion channels, generate relatively slow synaptic responses, and modulate synaptic transmission. In addition, recent observations indicate that G protein-coupled receptors, including mGluRs, are key components in multiprotein signaling assemblies that facilitate interactions with iGluRs and protein kinase cascades, such as the mitogen-activated protein kinase (MAPK) pathway. The prevalence of glutamate as a neurotransmitter, in combination with the widespread distribution of mGluRs, points to this system as a major modulator of second messengers in the mammalian central nervous system. This chapter discusses the molecular structure of mGluRs, along with their distribution, desensitization, effects on neurotransmission and ion channels, regulation of plasma membrane ion channels and intracellular calcium stores by Group I mGluRs, and pharmacology.

What causes paranoia? That’s a tough question to answer, and for at least a couple of reasons. For one thing, there’s no simple explanation. Paranoia, like so many psychological experiences, is the result of a complex interaction of numerous factors—as we’ll see over the course of the next three chapters. But there’s a bigger, more fundamental problem. How can we accurately and scientifically observe paranoid thinking? Paranoid thoughts don’t pop into our heads out of the blue. They’re generally our attempt to make sense of something we’ve experienced—perhaps a colleague ignored us at lunch or someone looked at us oddly on the bus. We can ask people about their paranoid thoughts, but how do we get at the truth of the situation? How do we even know for sure whether their thoughts are genuinely paranoid? Perhaps the colleague ignored us because our existing paranoia makes us reluctant to socialize. Or perhaps our fears are a legitimate response to a threatening situation. Maybe the guy on the bus really was looking for trouble. Any rigorous, scientific study of paranoia would need to expose a statistically significant number of people to exactly the same experience to see which of them reacted in a paranoid way. Once you had these data, you could start probing to see whether there was anything distinctive about the paranoid group. But how on earth can we arrange for hundreds of people to experience exactly the same everyday event in laboratory conditions? It’s impossible, right? Actually, there is a way, and it’s one we used in a groundbreaking recent experiment. That way is virtual reality. In the summer of 2006, we sent a leaflet to all households local to King’s College London. The leaflet announced a study of virtual reality at the college and invited people to participate. In the end we recruited 100 men and 100women of varying ages from 18 to 77, and from very diverse socioeconomic backgrounds. The mix, in fact, was pretty representative of the UK as a whole. We didn’t tell the volunteers that we were researching into paranoia until we’d completed the experiment.

This chapter describes changes and developments experimental psychopathology and psychological treatment during the past fifty years. Since the first emergence of psychology as an experimental science in the late 19th century and early 20th century, its application to psychological disorders had been a prominent goal. Two key developments during the 1950s were Hans Eysenck's review of the efficacy of psychological treatment and Joseph Wolpe's book on the use of systematic desensitization in psychotherapy.

Wherever there is a military establishment, men and women must be recruited into it and conditioned to be effective war-fighters. Whether or not they are ever deployed, there is a respect in which this conditioning is morally damaging to those involved. Combat training is geared towards making soldiers more comfortable with killing, so that they can do it repeatedly and efficiently in battle, without thinking too much or feeling too deeply. One of its aims is to enable recruits to use lethal violence without suffering emotional distress. But a morally decent person would experience distress in these circumstances. The upshot is that military conditioning is (or tries to be) morally damaging, or corrosive of virtue. It is morally injurious not by accident, but by design.

This chapter extends arguments that Eisenman has made elsewhere regarding the “Abu Ghraib effect,” which is the public’s desensitization to images of torture because of the long history of artistic representations of it. In particular, it explains the American public’s seeming acceptance of the use of waterboarding in the struggle against terrorism by both highlighting how visual representations of torture across the centuries depict torture victims as accepting, even participating in, their denigration and by suggesting that longstanding depictions of the “water cure” evoke images of religious sanctification that make waterboarding appear no more threatening than full immersion adult baptism. A concluding section considers practices of art that resist or otherwise seek to undo this desensitization to images of torture.

“Docile Bodies” focuses on behavioral sex therapists who were contemporaries of Masters and Johnson, including Joseph Wolpe, Arnold A. Lazarus, William Hartman, and Marilyn Fithian. This chapter shows how they valued intercourse for women partnered with men, much as Masters and Johnson did, not for what it means to women, but as a behavior that is intrinsically natural and healthful. This chapter shows that for Masters and Johnson’s contemporaries, intercourse was not only mandatory for heterosexuals; it was the unstated, unrecognized foundation of sexuality and sex therapy. Topics covered include systematic desensitization, typical hierarchies of sex scenes, and when sex therapists prescribe intercourse.

Pharmacology is defined as the study of the effects of drugs on the function of a living organism. It is an inte­grative discipline that tackles drug/ compound behaviours in varied physiological systems and links these to cellular and molecular mechanisms of action. As a scientific endeavour, pharmacology evolved from the early identification of therapeutic properties of nat­ural compounds, with herbal medicines and relatively complex pharmacopoeias widely used in early cultures. Despite this, lack of understanding of the physio­logical, pathological, and chemical processes governing the human body prevented the early establishment of pharmacology as a scientific discipline. Since then, pharmacology has progressed to be considered a fully developed integrative science that employs techniques and theories from various disciplines, such as chemistry, biochemistry, genomics, medicinal chemistry, physi­ology, and cellular and molecular biology. Collectively, these are applied to study disease causality and the rele­vant mechanistic action of compounds, to establish new treatments. In the last 100 years, the importance of clinical pharmacology has increased in line with the scientific and technological advances in biomedical research. Benefits gained from molecular and cellular approaches have enabled a more comprehensive analysis of drugs and their actions in functional context. Now, clinical pharmacology and therapeutics encompass the dis­covery, development, regulation, and application of drugs in a process that integrates scientific research with clinical practice to better treat illness and preserve health. Within this textbook the principles of pharmacology are discussed by therapeutic area so that the reader can link disease pathophysiology, drug mechanism, and modern prescribing behaviours for conditions commonly seen in clinical practice. There are, however, fundamental concepts that are universal in understanding the interaction between drugs and their ‘targets’, including receptor pharmacology, genomic pharmacology, and pharmacokinetics. The pharmacological receptor models preceded by many years the knowledge of the receptor as an entity. It was not until the last 150 years that a series of contributions from many notable biologists and chemists established the principles that founded modern day pharmacology. They produced a significant paradigm shift in therapeutics, where empirical descriptors of the activities observed (heating, cooling, moistening, emetic, etc.) were replaced by the concept of a ‘target’. After more than a century, the basic receptor concept is still the foundation of biomed­ical research and drug discovery.