The inositol lipid system (polyphosphoinositides and inositol phosphates) represents an important component of the cell signal transduction. Electroconvulsive shock (ECS) is known to activate cell signaling and lead to the release of second messengers. We tested the effects of daily ECS on the inositol lipid system and the generation of second messengers in vivo, by prelabeling the components of the system with [H-3]myo inositol. The response to ECS was greater 30 sec after the sixth ECS, as compared to that obtained 30 sec after the first one. Also, rats killed 24h after the fifth ECS exhibited an increased PI labeling, as compared to rats handled for 6 days without receiving ECS. These results show that daily seizures (ECS-evoked) deeply modify the neuronal response to the stimulus, thus providing new information on the biochemical events involved in cell signal transduction during seizures.

DAILY ELECTROCONVULSIVE SHOCK-TREATMENT ALTERS THE INOSITOL LIPID SYSTEM RESPONSE IN THE RAT HIPPOCAMPUS

VISIOLI, FRANCESCO;
1994

Abstract

The inositol lipid system (polyphosphoinositides and inositol phosphates) represents an important component of the cell signal transduction. Electroconvulsive shock (ECS) is known to activate cell signaling and lead to the release of second messengers. We tested the effects of daily ECS on the inositol lipid system and the generation of second messengers in vivo, by prelabeling the components of the system with [H-3]myo inositol. The response to ECS was greater 30 sec after the sixth ECS, as compared to that obtained 30 sec after the first one. Also, rats killed 24h after the fifth ECS exhibited an increased PI labeling, as compared to rats handled for 6 days without receiving ECS. These results show that daily seizures (ECS-evoked) deeply modify the neuronal response to the stimulus, thus providing new information on the biochemical events involved in cell signal transduction during seizures.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/3174738
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