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= C57 Mice =

C57 mice are a common strain of laboratory mice because they are genetically bred to be ideal for experimentation, are used quite frequently because of the research done on their genome, and because of their translational value as an animal model. Mice in general have enormous research value because they are able to be bred quickly, are relatively inexpensive, and are often readily able to have their genome modified for knock out and knock in experiments. C57 mice have had extensive research done on them, making their background information readily accessible to researchers.

Model of Alcoholism
C57 mice are good models to study chronic ethanol consumption. They often times display depressive and anxious behaviors post chronic ethanol consumption (Abreu-Villaça). These behaviors are relatable to common withdrawal behaviors exhibited in humans, making these rodents the ideal model to study possible metabolic pathways that are affected, as well as possible treatments for withdrawal. In a study, Yael Abreu-Villaça, an esteemed researcher, found that the C57 mice would readily consume many addictive substances, including ethanol and nicotine. This makes them ideal because it closely resembles the manner in which a human would consume ethanol. It has been noted that the anxiogenic affects were noted more profoundly in the female rodents, showing a sex-dependent difference.

Withdrawal Symptoms
It has been observed that the C57 mice exhibit withdrawal symptoms, many of which show translational value to human symptoms. Withdrawal from ethanol produces anxiety-like behaviors as well as depressive-like behaviors. Anxiety behaviors were noted mostly as a change in the patterns of the rodents in various assays while the depressive behaviors were noted only in some feeding and behavioral assays. The depressive behaviors manifested as lethargy, reluctance to move, or general changes in behavioral patterns. Because the withdrawal symptoms in the C57 mice have translational value, and are easily measured using standard assays, this rodent model has high validity for a scientific model of human chronic ethanol consumption and the withdrawal that can follow. The behaviors of this model furthermore provide insight into why relapse during withdrawal is common. Whilst relapse was not something studied in these experiments, the severity and type of withdrawal symptoms gave the researchers reason to believe that relapse may go beyond a neurological craving to a more physical manifestation of symptoms.

Wheel Running Behavior
Pang, among other researchers, with funding from an internationally recognized institute of research, explored the positive effects of wheel-running with mice post chronic alcohol consumption. It was found that wheel-running after 8 weeks of chronic alcohol consumption, in which the rodent has essentially free access to the ethanol, alleviated some of the depressive symptoms that were noted in the control group. Many different assays were used, including a light-dark box, a forced swim test, and the elevated plus maze. These various assays were chosen because they provide a good way to measure the withdrawal symptoms that were being highlighted. Additionally, these assays have high validity in that they show reproducibility with this strain of mice. These assays have had extensive research done on them, and therefore, a normal behavior with these assays have been established with C57 mice.

Anxiety Regulation
Studies on regulation of anxiety at the protein level in C57 mice have allowed scientist to implicated certain proteins as integral parts of the functional mechanisms behind anxiety. Beyond this, these regulatory proteins have began to become important in the mechanistic study of autism. Seungmin Ha, among other researchers, identified the specific protein Shank2 as an important part of repetitive motion as it releates to anxiety. This research on anxiety without a cause ties into the research done on the anxiety from withdrawal, and ultimately, how that anxiety plays into relapse. Strains of C57 mice had the protein Shank2 completely knocked out from their genome, and the results were increased presynaptic and postsynaptic dysfunction as well as motor issues.