of the original article: 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 368 THE BEHAVIORAL AND BRAIN SCIENCES (1985) 8:2 Continuing Commentary stimuli, or when the aversive experience is perceived as uncontrollable, increased emphasis is placed on coping through endogenous neuroehemical 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 process 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 neuroehemical activity, and may thus influence vulnerability to depression. Learned helplessness, human depression, and perhaps endorphins?

In a previous study we showed that prenatal neuroleptic drug exposure has postnatal effects on children's growth (Platt et al., 1988). In the present study the effect of prenatal exposure to neuroleptic drugs on motor performance at birth, 8 months, 4 years and 7 years of age was examined in children of psychiatrically normal parents, and of parents with a history of psychiatric treatment, using‐data from the Collaborative Perinatal Project of the National Institute of Neurological Diseases, Communicative Disorders and Stroke. The majority of the analyses were done using multiple logistic regression to control for possible confounding factors and to derive risk ratios. Some negative effects on motor behaviour were present in all groups at birth, most noticeably in the group of children who had been exposed to dopamine (DA)‐depleting drugs. Negative effects were less prevalent at later ages, but were still present. The results are discussed in terms of possible mechanisms and methodological limitations.

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The present studies examined the effect of restraint stress on the sensitivity of the catecholamine-cAMP generating system in the rat cerebral cortex. Restraint was found to cause a persistent reduction in the magnitude of the cAMP response to catecholamines. This effect occurred after repeated but not acute stress and was more marked with twice-daily as compared to once-daily treatment. The reduction in response was more marked with norepinephrine than with isoproterenol, indicating a selective action of stress on the non-β component of the noradrenergic response. The findings suggest that subsensitivity of the cAMP response to norepinephrine is a general response to chronic stressful stimuli and may be related to the action of certain antidepressant agents.