摘要
We have previously shown that both acute and chronic ethanol treatment depresses neural activity, specifically in the cingulate cortex. Minor influences were found in the motor cortex. The acute effect of ethanol in the hippocampus was intermediate to those in the cingulate and motor cortices. In the present study, we concentrate on the chronic effects of ethanol on the hippocampus. We demonstrate how the neuronal activity underlying food-acquisition behavior is modified after chronic ethanol treatment, and how the hippocampus subserves formation of newly-formed alcohol-acquisition behavior. Neuronal activity in CA1 was more sensitive to chronic ethanol than the Dg area. Acute administration of ethanol had a normalizing effect on the chronically-treated animals: their performance and the hippocampal neural activity approached a normal range. The sets of neurons involved in food-acquisition behavior formed before chronic ethanol treatment, and those involved in alcohol-acquisition behavior formed after treatment significantly overlapped supporting the view that the neuronal mechanisms of pre-existing behavior provide the basis for the formation of new behavior. Additionally, we also discovered alcohol-acquisition selective neurons. Assuming that the formation of new neuronal specializations underlies learning, we believe that alcohol-selective neurons are specialized during the formation of alcohol-acquisition behavior. Our data demonstrate several new findings on the effect of acute and chronic ethanol on hippocampus activity, and how the neuronal activity relates to behavior before and after ethanol treatment.
We have previously shown that both acute and chronic ethanol treatment depresses neural activity, specifically in the cingulate cortex. Minor influences were found in the motor cortex. The acute effect of ethanol in the hippocampus was intermediate to those in the cingulate and motor cortices. In the present study, we concentrate on the chronic effects of ethanol on the hippocampus. We demonstrate how the neuronal activity underlying food-acquisition behavior is modified after chronic ethanol treatment, and how the hippocampus subserves formation of newly-formed alcohol-acquisition behavior. Neuronal activity in CA1 was more sensitive to chronic ethanol than the Dg area. Acute administration of ethanol had a normalizing effect on the chronically-treated animals: their performance and the hippocampal neural activity approached a normal range. The sets of neurons involved in food-acquisition behavior formed before chronic ethanol treatment, and those involved in alcohol-acquisition behavior formed after treatment significantly overlapped supporting the view that the neuronal mechanisms of pre-existing behavior provide the basis for the formation of new behavior. Additionally, we also discovered alcohol-acquisition selective neurons. Assuming that the formation of new neuronal specializations underlies learning, we believe that alcohol-selective neurons are specialized during the formation of alcohol-acquisition behavior. Our data demonstrate several new findings on the effect of acute and chronic ethanol on hippocampus activity, and how the neuronal activity relates to behavior before and after ethanol treatment.
