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Slow brain potentials

Otto D, Benignus V, Muller K, et al Event-related slow brain potential changes in asymptomatic children with secondary exposure to lead, in Neurobehavioral Methods in Occupational Health. Edited by Gilioli R, Cassitto MG, Foa V. Oxford, UK, Pergamon, 1983b, pp 295-300... [Pg.144]

Slow Brain Potentials As Index of Mental Effort... [Pg.258]

Bauer, H., Nimberger, G. (1981). Concept identification as a function of preceding negative or positive spontaneous shifts in slow brain potentials. Psychophysiology, 18, 466 69. [Pg.265]

Freude, G., Ullsperger, P., Erdmann, U. (in press). Slow brain potentials in a visual monitoring task-timing accuracy and pre-movement negativity. International Journal of Psychophysiology. [Pg.266]

Slow Brain Potentials as a Measure of Effort Applications in Mental Workload Studies in Laboratory Settings Gabriele Freude and Peter Ullsperger... [Pg.390]

Sensory evoked and event-related slow brain potentials have been used to study the effects of lead exposure on central nervous system function in man and animals. Most human data derive from a series of studies carried out in North Carolina (Otto et al, 1981, 1982, 1985 Hawk et al, 1986 Robinson et al, 1985 Schroeder et al, 1985). Electro-physiological results have been reviewed previously (Otto, 1987). An updated review with some previously unreported observations is presented below. [Pg.279]

Winneke, G., G.Fodor, and H.Schlipkoter. 1978. Carbon monoxide, trichloroethylene, and alcohol reliability and validity of neurobehavioral effects. Pp. 461-469 in Multidisciplinary Perspectives in Even-Related brain Potential Research, Proceedings of the Fourth International Congress on Event-Related Slow Potentials of the Brain (EPICIV), Univ. of NC and U.S. EPA, Hendersonville, NC, April 4—10, 1976, D.P.Otto, ed. EPA-600/9-77-043. Research Triangle Park, NC U.S. Environmental Protection Agency. [Pg.117]

I There are also GAB Ab receptors in the brain found at both pre- and postsynaptic sites. These receptors increase conductance and produce slow inhibitory potentials through inhibition of cAMP. The physiologic and behavioural significance of these receptors is not well understood but they... [Pg.29]

Rosier, F., Heil, M., Glowalla, U. (1993). Monitoring retrieval fiom long-term memory by slow event-related brain potentials. Psychophysiology, 39,170-182. Sanders, A. F. (1983). Toward a model of stress and human performance. ctaP. c/20/ogzca, 53, 61-97. [Pg.267]

The slow local potentials of 10-20 msec duration accompanying synaptic transmission or gradual changes in the excitability of the dendrites. These potentials seem to be the basis of the electroencephalographic rhythms of the brain. [Pg.121]

The mechanism of genesis of steady and infra-slow rhythmic potentials is not yet clear A change in these potentials is believed to accompany the slow regulation of the excitability of central neurons when a large number of units are transferred to a new level of activity. The source of these potentials may be either the above-motioned polarization of similarly oriented neurons or a possible ionic imbalance across the blood-brain barrier. This method is commonly used in studying drug effects on the cerebral cortex. [Pg.123]

Cholecystokinin (CCK) is produced in the intestine and the brain. It appears to be an important mediator of anxiety. It also stimulates vasopressin secretion and slows gastric emptying. In addition, it is an important humoral satiety signal (appetite control). Various antagonists have been developed and are currently being investigated with regard to their therapeutic potential. [Pg.356]

With disruption of this barrier, molecules such as albumin freely enter the brain and ions and water follow. Because the brain lacks a well-developed lymphatic system, clearance of plasma constituents is slow, edema occurs, and intracranial pressure rises. At lower levels of exposure, subtle dysfunction of the blood-brain barrier may contribute to neurobehavioral deficits in children (Bressler and Goldstein 1991 Goldstein 1993). The particular vulnerability of the fetus and infant to the neurotoxicity of lead may be due in part to immaturity of the blood-brain barrier and to the lack of the high-affinity leadbinding protein in astroglia, which is discussed later in this section. Results of measurements of transendothelial electrical resistance across the blood-brain barrier from mice of various ages showed that lead potentiates cytokines-induced increase in ion permeability of the blood-brain barrier (Dyatlov et al. [Pg.270]


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