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EN
The selected lines of rats WHP (Warsaw High Preferring) and WLP (Warsaw Low Preferring) determine the animal model to investigate neurobiological mechanism of ethanol action. WHP rats drink excessive amounts of alcohol whereas WLP rats drink only small amounts. Patterns of ethanol consumption in WHP and WLP lines are constant. Due to cessation of alcohol intake the WHP rats have developed features of withdrawing signs. Level of dopamine and serotonine is lower in some brain regions of the WHP rats. WHP rats show an increased responsiveness to the stimulatory effects of low dose of ethanol.It has been suggested that acquisition of acute tolerance to ethanol may promote increased ethanol consumption. The effects of acute administration of ethanol (dose – 2.3 g/kg i.p.) were established by assessing ethanol-induced motor impairment, hypothermia and blood ethanol level in WHP and WLP rats. The rotarod model was used to measure motor impairment. Results have been revealed that WHP rats recovered motor activity and normal temperature when blood ethanol was at the highest level, indicating the development of acute tolerance to ethanol. The WLP rats showed similar recovery to WHP rats but at the lower blood ethanol level.Tolerance to ethanol may have a great value as a predictor of susceptibility to alcoholism therefore may signifi cant means in the relation to alcohol consumption and dependence. Generally tolerance is thought as the neuroadaptive processes to intoxicate effect of ethanol.
EN
In the present study, the c-Fos expression was used to map brain structures recruited during the evolution of seizures after repeated, administration of pentylenetetrazol at the subconvlusive dose (35 mg/kg, i.p.), in rats. It has been found that the earliest expression of cFos, at the stage 1,2 of kindling, appeared in the nucleus accumbensshell, the piriform cortex, the prefrontal cortex and striatum. On the 3rd stage of kindling, the central amygdala nucleus, the entorhinal cortex, and the lateral septal nucleus (LSV), showed an enhanced expression of c-Fos. On the 4th stage of kindling, c-Fos was increased in the basolateral amygdala, and CA1 area of the hippocampus. Finally, c-Fos labelling was enhanced in the dentate gyrus of the hippocampus, only when the stage 5 of kindling, i.e. the clonic-tonic convulsions, appeared. The most potent changes in c-Fos (in a descending order) were shown in the dentate gyrus, piriform cortex, CA1 area, the LSV, basolateral amygdala, central amygdala nuclei, and prefrontal cortex. It appeared, that there are important similarities in the structures recruited at the beginning and at the end of electrically and chemically-induced kindling, i.e. the piriform cortex and the hippocampal dentate gyrus, respectively. On the other hand, the differences gradually disappear at the later stages of kindling, followed by the symmetrical propagation of epileptic activity from the limbic system to the neocortex, during the generalized seizures.
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