Animal research suggests that central serotonergic neurons are involved in behavioral suppression, particularly anxiety-related inhibition. The hypothesis linking decreased serotonin transmission to reduced anxiety as the mechanism in the anxiolytic activity of benzodiazepines conflicts with most clinical observations. Serotonin antagonists show no marked capacity to alleviate anxiety. On the other hand, clinical signs of reduced serotonergic transmission (low 5-HIAA levels in the cerebrospinal fluid) are frequently associated with aggressiveness, suicide attempts, and increased anxiety. The target article attempts to reconcile such (...) human and animal findings by investigating whether anxiety reduction or increased impulsivity is more Likely to account for animal behavioral changes associated with decreased serotonergic transmission. The effects of manipulating central serotonin in experimental anxiety paradigms in animals (punishment, extinction, novelty) are reviewed and compared with the effects of antianxiety drugs. Anxiety seems neither necessary nor sufficient to induce control by serotonergic neurons on behavior. Further evidence suggests that behavioral effects of anxiolytics thought to be mediated by decreases in anxiety are not caused by the ability of these drugs to reduce serotonin transmission. Blockade of serotonin transmission, especially at the level of the substantia nigra, results in a shift of behavior toward facilitation of responding. This behavioral shift is particularly marked when there is competition between acting and restraining response tendencies and when obstacles prevent the immediate attainment of an anticipated reward. It is proposed that serotonergic neurons are involved not only in behavioral arousal but also in enabling the organism to arrange or tolerate delay before acting. Decreases in serotonin transmission seem to be associated with the increased performance of behaviors that are usually suppressed, though not necessarily because of the alleviation of anxiety, which might contribute to the suppression. (shrink)

The Strange Situation procedure was developed by Ainsworth two decades agoas a means of assessing the security of infant-parent attachment. Users of the procedureclaim that it provides a way of determining whether the infant has developed species-appropriate adaptive behavior as a result of rearing in an evolutionary appropriate context, characterized by a sensitively responsive parent. Only when the parent behaves in the sensitive, species-appropriate fashion is the baby said to behave in the adaptive or secure fashion. Furthermore, when infants are (...) observed repeatedly in the Strange Situation,the pattern of behavior is said to be highly similar, and this pattern is said to predict the infants' future behavior in a diverse array of contexts. After an exhaustive review of the literature, it is shown that these popular claims are empirically unsupported in their strong form, and that the interpretations in terms of biological adaptationare misguided. There is little reliable evidence about the specific dimensions of parental behavior that affect Strange Situation behavior, although there does appear to be some relationship between these constructs. Temporal stability in security of attachment ishigh only when there is stability in family and caretaking circumstances. Likewise, patterns of Strange Situation behavior only have substantial predictive validity in similarly stable families. Implications for future research and theorizing — particularly as they relate to the use of evolutionary biology in psychological theory — are discussed. (shrink)

One of 15 volumes in this series, this title is part of a plan to generate non-specialist Freud titles for a wide readership - beyond the institutional/clinical ...

This is a unique book. It is excellently written, crammed with information, wise and a pleasure to read.' ---Daniel C. Dennett, Tufts University.

A Neurocomputationial Perspective illustrates the fertility of the concepts and data drawn from the study of the brain and of artificial networks that model the...

Aversive experiences have been thought to provoke or exacerbate clinical depression. The present review provides a brief survey of the stress-depression literature and suggests that the effects of stressful experiences on affective state may be related to depletion of several neurotransmitters, including norepinephrine, dopamine, and serotonin. A major element in determining the neurochemical changes is the organism's ability to cope with the aversive stimuli through behavioral means. Aversive experiences give rise to behavioral attempts to cope with the stressor, coupled with (...) increased utilization and synthesis of brain amines to contend with environmental demands. When behavioral coping is possible, neurochemical systems are not overly taxed, and behavioral pathology will not ensue. However, when there can be no behavioral control over the stressful stimuli, or when the aversive experience is perceived as uncontrollable, increased emphasis is placed on coping through endogenous neurochemical mechanisms. Amine utilization increases appreciably and may exceed synthesis, resulting in a net reduction of amine stores, which in turn promotes or exacerbates affective disorder. The processes governing the depletions may be subject to sensitization or conditioning, such that exposure to traumatic experiences may have long-term repercussions when the organism subsequently encounters related stressful stimuli. With continued uncontrollable stimulation, adaptation occurs in the form of increased activity of synthetic enzymes, and levels of amines approach basal values. It is suggested that either the initial amine depletion provoked by aversive experiences or a dysfunction of the adaptive processes, resulting in persistent amine depletion, contributes to behavioral depression. Aside from the contribution of behavioral coping, several organismic, experiential, and environmental variables will influence the effects of aversive experiences on neurochemical activity, and may thus influence vulnerability to depression. (shrink)

This paper and its subsequent parts (Part II and Part III) build on an earlier publication (McKenna 1986). They suggest that important clinical data on the relationship between infantile constitutional deficits and microenvironmental factors relevant to SIDS can be acquired by examining the physiological regulatory effects (well documented among nonhuman primates) that parents assert on their infants when they sleep together.I attempt to show why access to parental sensory cues (movement, touch, smell, sound) that induce arousals in infants while they (...) sleep could possibly help one of many different subclasses of infants either to override certain kinds of sleep-induced breathing control errors suspected to be involved in SIDS or to avoid them altogether. I do not suggest that solitary nocturnal sleep “causes” SIDS, that all parents should sleep with their infants, or that traditional SIDS research strategies should be abandoned. However, using evolutionary data, I do suggest that an adaptive fit exists between parent-infant sleep contact and the natural physiological vulnerabilities of the neurologically immature human infant, whose breathing system is more complex than that of other mammals owing to its speech-breathing abilities. This “fit” is best understood, it is argued, in terms of the 4–5 million years of human evolution in which parent-infant contact was almost certainly continuous during at least the first year of an infant’s life. Thus, to dismiss the idea that solitary sleep has no physiological consequences for infants does not accord with scientific facts. (shrink)

Postnatal parent-infant physiological regulatory effects described in the previous paper (Part I) are viewed here as being biologically contiguous with events that occur prenatally, preparing and sensitizing the fetus to the average microenvironment into which the infant is expected, based on its evolutionary past, to be born. Following McKenna (1986), evidence (some of which is circumstantial) is presented concerning fetal hearing and fetal amniotic liquid breathing as they are affected both by maternal cardiovascular blood flow sounds in the uterus and (...) by fluctuating maternal blood sugar levels. These data are linked in turn to the infant’s postulated postnatal responsivity to parental sensory cues, including auditory and vestibular respiratory cues that may assist infants as they “learn” to breathe and, for some, to resist a SIDS event. Data on the respiratory and vocalizing behavior of normal and hearing-impaired persons are used to show that not all forms of human breathing are innate; some forms develop with experience. These data reveal how human infants learn, for example, to coordinate higher and lower brain respiratory nuclei in the context of learning initially to cry with intent and purpose and later to speak. Voluntary, cortex-based breathing emerges at the same time that infants are most likely to die from SIDS, between 2 and 4 months of age. This switch between voluntary and involuntary breathing during both sleep (while dreaming) and wake cycles, which depends on the integration of higher cortical and lower brain stem nuclei, is complex and is possibly the basis of the human species’ unique susceptibility to SIDS—a syndrome as yet unrecognized in other species. These human infant vulnerabilities, including delayed maturity, can explain in part why natural selection ought to favor increased infant sensitivity to parental sensory cues provided by a caregiver—stimuli available in the evolving parental care environment that included parent-infant co-sleeping for more than 4–5 million years of human evolution. (shrink)