When the stored representation of the meaning of a stimulus is accessed through the processing of a sensory input it is maintained in an activated state for a certain amount of time that allows for further processing. This semantic activation is generally accompanied by conscious identification, which can be demonstrated by the ability of a person to perform discriminations on the basis of the meaning of the stimulus. The idea that a sensory input can give rise to semantic activation without concomitant conscious identification was the central thesis of the controversial research in subliminal perception. Recently, new claims for the existence of such phenomena have arisen from studies in dichotic listening, parafoveal vision, and visual pattern masking. Because of the fundamental role played by these types of experiments in cognitive psychology, the new assertions have raised widespread interest.

The purpose of this paper is to show that this enthusiasm may be premature. Analysis of the three new lines of evidence for semantic activation without conscious identification leads to the following conclusions. (1) Dichotic listening cannot provide the conditions needed to demonstrate the phenomenon. These conditions are better fulfilled in parafoveal vision and are realized ideally in pattern masking. (2) Evidence for the phenomenon is very scanty for parafoveal vision, but several tentative demonstrations have been reported for pattern masking. It can be shown, however, that none of these studies has included the requisite controls to ensure that semantic activation was not accompanied by conscious identification of the stimulus at the time of presentation. (3) On the basis of current evidence it is most likely that these stimuli were indeed consciously identified.

As neurophysiological investigations of sleep cycle control have provided an increasingly detailed picture of events at the cellular level, the concept that the sleep cycle is generated by the interaction of multiple, anatomically distributed sets of neurons has gradually replaced the hypothesis that sleep is generated by a single, highly localized neuronal oscillator.

Cell groups that discharge during rapid-eye-movement (REM) sleep (REM-on) and neurons that slow or cease firing during REM sleep (REM-off) have long been thought to comprise at least two neurochemically distinct populations. The fact that putatively cholinoceptive and/or cholinergic (REM-on) and putatively aminergic (REM-off) cell populations discharge reciprocally over the sleep cycle suggests a causal interdependence.

In some brain stem areas these cell groups are not anatomically segregated and may instead be neurochemically mixed (interpenetrated). This finding raises important theoretical and practical issues not anticipated in the original reciprocal-interaction model. The electrophysiological evidence concerning the REM-on and REM-off cell groups suggests a gradient of sleep-dependent membrane excitability changes that may be a function of the connectivity strength within an anatomically distributed neuronal network. The connectivity strength may be influenced by the degree of neurochemical interpenetration between the REM-on and REM-offcells. Recognition of these complexities forces us to revise the reciprocal-interaction model and to seek new methods to test its tenets.

Cholinergic microinjection experiments indicate that some populations of REM-on cells can execute specific portions of the REM sleep syndrome or block the generation of REM sleep. This observation suggests that the order of activation within the anatomically distributed generator populations may be critical in determining behavioral outcome. Support for the cholinergic tenets of the reciprocal-interaction model has been reinforced by observations from sleep-disorders medicine.

Specific predictions of the reciprocal-interaction model and suggestions for testing these predictions are enumerated for future experimental programs that aim to understand the cellular and molecular basis of the mammalian sleep cycle.

The following factors underlying behavioral plasticity are discussed: (1) reflex adaptability and its role in the voluntary control of movement, (2) degrees of freedom and motor equivalence, and (3) the problem of the discrete organization of motor behavior. Our discussion concerns a variety of innate motor patterns, with emphasis on the wiping reflex in the frog.

It is proposed that central regulation of stretch reflex thresholds governs voluntary control over muscle force and length. This suggestion is an integral part of the equilibrium-point hypothesis, two versions of which are compared.

Kinematic analysis of the wiping reflex in the spinal frog has shown that each stimulated skin site is associated with a group of different but equally effective trajectories directed to the target site. Such phenomena reflect the principle of motor equivalence -the capacity of the neuronal structures responsible for movement to select one or another of a set of possible trajectories leading to the goal. Redundancy of degrees of freedom at the neuronal level as well as at the mechanical level of the body's joints makes motor equivalence possible. This sort of equivalence accommodates the overall flexibility of motor behavior.

An integrated behavioral act or a single movement consists of dynamic components. We distinguish six components for the wiping reflex, each associated with a certain functional goal, specific body positions, and motor-equivalent movement patterns. The nervous system can combine the available components in various ways in forming integrated behavioral sequences. The significance of command neuronal organization is discussed with respect to (1) the combinatory strategy of the nervous system and (2) the relation between continuous and discrete forms of motor control. We conclude that voluntary movements are effected by the central nervous system with the help of the mechanisms that underlie the variability and modifiability of innate motor patterns.

This book critically examines Freud's own detailed arguments for his major explanatory and therapeutic principles, the current neorevisionist versions of psychoanalysis, and the hermeneuticists' reconstruction of Freud's theory and therapy as an alternative to what they claim was a “scientistic” misconstrual of the psychoanalytic enterprise. The clinical case for Freud's cornerstone theory of repression – the claim that psychic conflict plays a causal role in producing neuroses, dreams, and bungled actions – turns out to be ill-founded for two main reasons: (a) Even if clinical data were valid, the method of free association has failed to support the psychoanalytic theory of unconscious motivation; (b) Clinical data tend in any case to be artifacts of the analyst's self-fulfilling expectations, thus losing much of their evidential value. The hypothesis that psychoanalytic treatment is in reality a placebo poses a serious challenge to the assumption that insight is a key causal factor when therapy is successful. This challenge has yet to be met by psychoanalysts. Similar conclusions undermine the neorevisionist versions of psychoanalysis. The most influential hermeneuticists, on the other hand, are shown to have imposed an alien philosophy on psychoanalysis, partly through their reliance on gross misconceptions of the natural sciences. Karl Popper's criticism of the Freudian corpus as empirically untestable has misjudged its evidential weaknesses, which are more subtle. If there exists empirical evidence for the principal psychoanalytic doctrines, it cannot be obtained without well-designed extraclinical studies of a kind that have for the most part yet to be attempted.