Cortical Mechanisms that Augment or Reduce Evoked Potentials in Cats

Abstract

The augmenting or reducing of flash-evoked potentials in paralyzed cats was significantly correlated with their previously videotaped behaviors. Augmenting reducing was due to alterations in cortical rather than subcortical responsiveness, and was duplicated by increasing cortical arousal by means of reticular stimulation while the animal was exposed to visual stimuli of constant intensity. Brainstem activation of cortical inhibition may underlie the behavioral results as well as the results obtained with the evoked potentials.

Evidence for disturbed cortical signal processing and altered serotonergic neurotransmission in generalized anxiety disorder

“…Following this concept, the shallow LD in patients with GAD would indicate an overactivity of this regulating mechanism. Several authors have suggested that such a mechanism acts at the level of the brainstem (Bruneau et al 1993;Lukas and Siegel 1977;Zuckerman et al 1974) and is most likely represented by the 5-HT system. Serotonin has a homeostatic function in the central nervous system Jacobs 1990) and acts to adjust and control gain factors and excitability levels of cortical neurons (Jacobs and Azmitia 1992).…”

Loudness Dependence of Auditory Evoked Potentials as Indicator of Central Serotonergic Neurotransmission: Simultaneous Electrophysiological Recordings and In Vivo Microdialysis in the Rat Primary Auditory Cortex

“…The LDAEP is very suitable for monitoring central serotonergic activity as individual differences in LDAEP result from variations in the cortical mechanisms involved in the generation of these waves because they do not covary with peripheral or subcortical changes of neuronal activity caused by increases in stimulus intensity (Lukas and Siegel, 1977;Lukas, 1987a, b). Such nonspecific modulation of the LDAEP is considered to be dependent on extrathalamic LDAEP and 5-HT in auditory cortex A Wutzler et al monaminergic systems projecting from the brainstem to the cortex (Foote and Morrison, 1987;Morrison and Hof, 1992), especially the serotonergic system (Hegerl and Juckel, 1993).…”

A Functional Disturbance in the Auditory Cortex Related to a Low Serotonergic Neurotransmission in Women with Type 2 Diabetes

“…Habituation is primarily considered to be a protective mechanism against central nervous system overstimulation [39], but also an elementary form of learning [40] and a model for studying cognitive behavior [41]. Habituation and potentiation of evoked potentials are cortical phenomena [42] most likely modulated by central monoamines, in particular by serotonin neurotransmission [43]. The raphe serotonergic neurons innervate layer IV pyramidal cells and GABAergic inhibiting interneurons and are thus ideally organized to modulate the thalamocortical input [43, 44].…”