Sample Article Review On Basic Mechanism Of Alcohol Addiction
Alcoholism is a major disorder that is characterized by chronic relapses and a lifelong loss of control over intake of the substance. The (Funk et al.) titled “Corticotropin-Releasing Factor within the Central Nucleus of the Amygdala Mediates Enhanced Ethanol Self-administration in withdrawn, Ethanol-dependent Rats” Hypothesized that similar to humans, animal subjects will also show a higher amount of self-administration while experiencing anxiety states under withdrawal conditions. The study was aimed to show the relationship between certain brain regions such as the central nucleus and the amygdala which have significant numbers of CRF receptors that are responsible for increased alcohol self-administration in withdrawn alcohol dependent rats.
The figure 1. of the article depicts the basic concept of the study thereby being the most important figure of the article. This figure shows the ethanol lever presses in dependent and non-dependent rats facing withdrawal as the Corticotropin releasing factor receptor antagonist D-Phe-CRF 12-41 dosage is increased. The figure clearly shows that the number of lever presses in dependent rats decrease as the receptor antagonist dosage is increased. Which means that as the amount of free CRF in amygdala is decreased, dependent rats no longer binge drink ethanol.
The figure 3. Depicts the difference in water and ethanol responses in dependent and non-dependent rats during acute withdrawal. While the ethanol responses show that the dependent rats have a clear preference for ethanol, the reaction to increased dosage of the Corticotropin releasing factor receptor antagonist D-Phe-CRF 12-41 is mixed and similar in both dependent and non-dependent rats.
The figure 5 is very important as it depicts the differences in CRF immunereactivity in the CeA of ethanol dependent vs non-dependent rats after a 2h withdrawal time. The rats were killed, their brains were extracted and frozen, CRF immune expression was measured in the central nucleus of the amygdala and the CRF immunereactivity in section -2.80, and -3.14 showed a significant decrease in withdrawn and dependent rats (p<0.01). This figure clearly shows a decrease in CRF immunereactivity in the CeA of the dependent rats, which could be caused by the decrease of CRF in the nerve fibers.
The researchers hypothesized at the beginning of the article that the extra hypothalamic CRF may be responsible for relapse in animals showing withdrawal symptoms. Primarily, this study corroborates the long held belief that binge drinking following a long period of abstinence during a negative emotional state may be caused by the CRF acting in the hypothalamus and amygdala. Through an elaborate experimental setup Funk and associates proved that ethanol dependent rats when exposed to a stressful situation while under a withdrawal state crave ethanol more than non-dependent rats. The subjects of this study were two groups of rats, one which was addicted to alcohol, and another (control) that was recently exposed to alcohol vapours and was not addicted to it. Both the groups were not exposed to alcohol for 2 hrs and then were provided with an opportunity to consume alcohol. When the CRF receptor antagonist dosage was increased the number of ethanol acquiring behaviors also reduced in dependent animals. This effectively proves that anxiety caused due to withdrawal was forcing animals to binge drink to get rid of the anxiety which was done by the CRF receptor antagonist. The authors also showed through immunohistochemistry that the central nucleus of the amygdala was responsible for the CRF activity causing binge drinking in withdrawn rats. Therefore the funk and associates effectively proved their hypotheses that extra hypothalamic CRF is responsible for binge drinking in alcohol dependent rats facing withdrawal symptoms.
Funk, Cindy K et al. “Corticotropin-Releasing Factor within the Central Nucleus of the Amygdala Mediates Enhanced Ethanol Self- Administration in Withdrawn, Ethanol-Dependent Rats.” The Journal of Neuroscience 26.44 (2006): 11324–11332.
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