Wednesday, April 15, 2015

Vassoler et. al (2012)

Vassoler et. al explored the effect of paternal cocaine use on male and female progeny. This study found that male progeny of cocaine using sires were more resilient to cocaine use (by reduced cocaine infusions at high and low doses, decreased cocaine administration after reaching a breakpoint at high cocaine doses). This study furthered their research by examining changes in the brain, and the study found that there was an increase in BDNF expression in the male progeny of cocaine sires, which they did further studies to show the mechanisms behind this increase in BDNF expression in the medial prefrontal cortex. Vassoler et. al (2012) showed that increasing acetylation of histones in the sperm and testes may account for the increased BDNF expression in the brain resulting in this cocaine resilient phenotype in the male progeny of cocaine using sires. While reading this article, I kept comparing it to the Holly et. al paper that we read last week. The increased susceptibility of females using cocaine seems a lot more convincing than a gender-specific phenotype induced by a cocaine-using sire. Even though the sperm and testes of the cocaine-using sires showed an increased in the acetylation of histones, I believe this would affect the male and female progeny, not just the males. The Holly et. al paper from last week even mimicked the data about the breakpoints where males stopped cocaine administration before the female rats. There were a couple of different points in this paper where they "threw out" data also. For example, there was not a difference between the DSMO and saline control groups, so they combined these groups for analysis. However, what about the difference between DSMO and the cocaine sired male progeny or the cocaine sired female progeny? I would have liked them to address and include this data even if it was in a supplementary figure, because even though they didn't find significant differences between the two control groups does not necessarily mean that there wouldn't be a significant difference between one of the controls and an experimental group. They also noted that some of the rats needed to meet a threshold of lever presses in order to be included in the data for the pretreatment with TrkB, and some rats were excluded from the data set since they didn't reach the lever presses threshold. Again, I still would've liked this data to be included, because this could have skewed the results.

I appreciate this paper, because it did take a unique approach looking at cocaine administration in regards to the paternal influences. I thought it had the potential to be a really interesting paper, but it fell short for me after reading the paper last week. I thought the mechanisms of the paper last week were much more convincing than showing an epigenetic cause for cocaine administration. I know they showed differences with BDNF in the male progeny as well as the paternal sperm and testes, but I think BDNF's role in cocaine administration is probably a lot more complicated than this article portrays it. I would've liked for Vassoler et. al to control for gender differences in cocaine administration before introducing the cocaine-administered sire.

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