Neurophysiological Responses to Stressful Motion and Anti-motion Sickness Drugs as Mediated by the Limbic System

TECHNICAL) This report has characterized performance in terms of attention and memory, categorizing extrinsic mechanisms mediated by ACTH, norepinephrine and dopamine, and intrinsic mechanisms as cholinergic. The cholinergic role in memory and performance has been viewed from within the limbic system and related to volitional influences of frontal cortical afferents and behavioral responses of hypothalamic and reticular system efferents. The inhibitory influence of the hippocampus on the autonomic and hormonal responses mediated through the hypothalamus, pituitary, and brain stem are correlated with the actions of such anti-motion sickness drugs as scopolamine and amphetamine. These drugs appear to exert their effects on motion sickness symptomatology through diverse though synergistic neurochemical mechanisms involving the septohippocampal pathway and other limbic system structures. The particular impact of the limbic system on an animal's behavioral and hormonal responses to stress is influenced by ACTH, cortisol, scopolamine, and amphetamine. These agents share a number of neurochemical actions which can be regarded as neurophysiologically equivalent, differing mainly in a temporal sense and in terms of the scope of their metabolic influence. A neurophysiologically defined neural mismatch theory is defined that integrates preceding discussion on memory, attention, stress, the neurochetitistry of anti-motion sickness drugs, perTormance behavior and the iimbic system. A parallel is drawn between the ability of scopolamine and stress hormones to modulate attention, reinforcement, memory and the psychological stress of neural mismatch that leads to motion sickness. Essentially, neural mismatch is characterized as a process by which ongoing sensory experience is associated with a neural store of reality that cannot be satisfactorily reconciled or habituated, thus causing excessive psychological stress and eventual sickness and vomiting. Drugs like scopolamine which interfere with memory and learning are conceptualized to exert part of their therapeutic action through disruption of necessary associative mechanisms of learning and memory. Without the association of present sensory experience with past experience, the psychological impact of the neural mismatch is not as readily appreciated or channeled into a stress response. Summarizing, drugs like scopolamine may be of therapeutic benefit to motion sickness because of sedative or hypnotic properties through which conscious awareness of stressful novelty is subjectively impaired. Manipulation of the body's stress hormone system may instead be therapeutically valuable due to an enhancement of adaptive capabilities that allow novelty to be recognized with greater perspective. This occurs without the disorientation and sickness that attends excessive efforts at neural mismatch in intensely i;ovel environments. The value of pharmacological manipulation of the stress hormone system can not be overemphasized in our quest to prophylactically treat motion sickness, after all, this system is designed to serve an adaptive role in stress situations in the first place.