Brain damage is caused by many different things, but one of the most common is substance abuse. Drug and alcohol use cause neuropathological damage in individuals, and after deciding to discontinue substance abuse, many individuals may benefit from assistance in healing that damage.
Animals are often used to replicate the effects of drugs and alcohol on the human body. A recent study looked at the effects of medication on mediating the damage caused by alcohol consumption in rats. Jian Hu, Yan Xia, Zheng Wu, Leu Liu and Chunling Tang examined how fluoxetine might alleviate brain damage and hypercortisolemia due to alcohol consumption in rats.
The researchers wanted to investigate the neuropathological damage and changes of corticosteroid concentrations relating to chronic alcohol consumption. They also wanted to see how Fluoxetine (Prozac) might affect neuropathological damage and corticosteroid levels and to evaluate any possible association between neuropathological damage and changes in corticosteroid levels.
Rats were randomly divided into two groups, which were alcohol and control groups. The alcohol group rats were given ethanol intraperitoneally for 8 weeks. Corticosterone levels were measured in both groups, and then fluoxetine hydrochloride or saline was injected into the animals.
The rats were killed and the number of neurons in five regions of the cerebral cortex was determined.
The results of the study showed that the number of neurons on the frontal cortex, parietal cortex, and CA3 regions of the hippocampus were significantly reduced in the group of rats that was given alcohol and then saline when compared with the results of the control group that was treated with saline.
The alcoholic group that was treated with fluoxetine showed an increased number of neurons in the CA3 regions of the hippocampal cortex when compared with the group treated with saline.
In addition, corticosteroid levels were significantly increased in the alcohol group treated with saline, when compared with the control group. Corticosteroid levels were reduced in the group of rats given alcohol and then treated with fluoxetine, when compared with the alcoholic group treated with saline.
The neuron numbers seen in the CA3 region showed a negative association with the levels of corticosteroids.
The results of the study indicate that chronic alcohol consumption causes significant loss of neurons in rats’ brain regions and increased levels of corticosteroid concentration. The use of fluoxetine in rats may have offset the loss of neurons in the hippocampus and affected levels of corticosteroids related to alcohol consumption.
