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Results for “Subliminal Stimulation”

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At least 469 records · Page 26Linked to original sources
PubMed1987

[Neurologic mechanism of the unconscious craving for alcohol in chronic alcoholic patients].

The author studied cortical mechanisms of the perception of subconscious motivationally meaningful word "vodka" in patients with chronic alcoholism. Clear-cut diffuse activation of the cerebral cortex in response to a subconscious verbal stimulus was identified through recording evoked cortical potentials which are a sensitive indicator of reactivity of the cerebral structures to alcohol. The elucidated cortical activation may be one of the nervous mechanisms of stable craving for alcohol which is poorly controlled by the patient's conscious experience.

Adult↗
PubMed1986

[Changes in the dehydrogenase and GABA transaminase activity in the cerebral cortex during corazol kindling].

The experiments on (CBA X C57BL/6)F1 mice have shown that regular corazol injections in subliminal doses stimulated seizure susceptibility (pharmacological kindling). Cytophotometric assay of the activity of oxidative metabolism enzymes (glutamate dehydrogenase, malate dehydrogenase, succinate dehydrogenase, alpha-oxoglutarate dehydrogenase, lactate dehydrogenase) and GABA-transaminase in the sensorimotor cortex of kindled mice in post-convulsive period, and 24 hours or 30 days after corazol injections were discontinued, has revealed some specific alterations of the enzymes under study, that suggest the existence of two phases of energy metabolism disturbances. The first phase (24 hours after corazol injections were discontinued) is characterized by intensified succinic acid oxidation, while the second phase (30 days after the last injection) is characterized by anaerobic glycolysis in neuronal and glial cells. Inhibition of GABA-transaminase activity was particularly marked in postconvulsive period. From a molecular point of view these data may be considered as enzyme disturbances during stimulation of seizure susceptability or seizure activity and as a compensation component ensuring anticonvulsive mechanisms and reparative processes (antagonistic principle of molecular mechanism regulation) during activation of antiepileptic system.

4-Aminobutyrate Transaminase↗