Writing in Biology

This article is titled “Inhibition of the substantia nigra pars reticulata produces divergent effects on sensorimotor gating in rats and monkeys.”  It piqued my interest because I am a part of Karine Fenelon’s lab here on campus, in which we investigate the neural circuits that modulate sensorimotor gating.  In the study, the GABA_A receptor agonist muscimol was used to test the role of the SNpr in auditory pre-pulse inhibition (PPI), a key component of sensorimotor gating.  From class, we know that GABA is the major inhibitory amino acid neurotransmitter, so muscimol must mimic its inhibitory effects on target neurons.  In the study, it was found that the inhibition of the SNpr using muscimol disrupted PPI in rats, while facilitated PPI in rhesus macaques.  This study discovered these divergent effects.  I wonder what differences in neuron connections contribute to this divergence, because there must be a difference either upstream or downstream of the point of innervation of the SNpr.  I also wonder what the effect of muscimol on the SNpr in mice is, since this is the model organism we use in lab.

https://www.nature.com/articles/s41598-018-27577-w.pdf

There are many ways that this data could be analyzed and classified. Some options being:

• Create a plot such as a stacked bar graph to visualize and compare data side by side
• Find averages for each set of data for each gender to compare
• Create a scatter plot of all data

With the data we could find the weight by sex, balloon length by sex, baloon length compared to weight. We could also calculate the average, standard deviation or mode for the given data set. Constructing a graph or chart based upon the data to show a comparison of the variables would make the data visually easier to analyze.

The purpose of this experiment is to assess the effect of caffeine on the development of sea urchins. The gametes of sea urchins were collected and added to different concentrations of caffeine. The rate of development was measured by the fraction of eggs fertilized and cleaved under a microscope over the span of 40 minutes at intervals of 10, 25, and 40 minutes. Results show that sea urchins treated with 0.25 mg of caffeine have faster development than the control. On the other hand, sea urchins treated with 0.5 mg of caffeine have slower development than the control. These results indicate that small amounts of caffeine increase the rate of development, however, excessive amounts of caffeine lower the rate of development.

            Patient 3 has Fibrodysplasia Ossificans Progressiva. Patients with this disease have abnormal development of bone in parts of the body where bone is not typically present. The mode of inheritance is autosomal dominant. It is caused by a gene called ACVR1. The ACVR1 protein receptor is found in skeletal muscle and cartilage and regulates ossification. In this disease, the mutated ACVR1 protein is constitutively activated, which causes excessive proliferation of bone.

Patient 2 has Pierre Robin Syndrome, which is a disease that results in facial abnormalities. It is inherited in an autosomal recessive fashion. This disease is caused by rearrangements or deletions on the SOX9 gene or the KCNJ2 gene. SOX9 is a transcription factor that turns on other genes involved in skeletal development and embryogenesis. A mutation in this protein is one of the reasons for abnormal ossification. Mutations upstream or downstream of SOX9 can also cause Pierre Robin Syndrome. These mutations produce proteins that are unable to interact with MSX1, a transcription factor that controls formation of structures in the mouth. This causes a fixed jaw and other oral abnormalities characteristic of Pierre Robin Syndrome.

Patient 1 has Brachydactyly type A1, which causes the middle fingers of fingers and toes to be reduced or absent. Short stature and malformed epiphyses is also common in patients with this disease. Brachydactyly type A1 is usually caused by a mutation on the BDA1B gene or on the IHH (Indian Hedgehog gene). It is inherited in an autosomal dominant fashion. While there are different types of mutations on BDA1B or IHH that can lead to the disease, missense mutations on IHH are a common pathological cause. The mutant Hedgehog protein encoded by IHH is unable to bind to a receptor called Patched-1, which is responsible for differentiation. This mutation along with others on BDA1 and IHH have the potential to prevent cellular growth, condensation and differentiation, which can lead to abnormal bone development.

Amyotrophic Lateral Sclerosis is a neurodegenerative disease that affects nerve cells in both the brain and spinal cord. These neurons are interconnected from the brain to the spinal cord and the spinal cord to our muscles. As these motor neurons progressively die, the ability of our brain to control muscle movement is diminished. With voluntary muscle movement being affected, many patients lose the ability to control simple everyday actions. Scientists around the world have been completing studies towards discovering various treatments for this disease. ALS affects both patients neurologically and physically and that is where my interest in the disease stems from. As I have been completing research regarding muscle function and muscle fatigue, I would love nothing more than to develop a better understanding of ALS and gain first-hand experience in the clinical research and care of the disease in relation to muscle function. 

A control treatment is a baseline treatment against which one or more other treatments will be compared. Depending on your question, this can be an untreated treatment, a procedural treatment, or a different treatment to that of the treatment group. Determining the appropriate control can be difficult. In an experiment done by researchers to examine how foxes and wolves affect plant communities, they set up fenced plots to exclude predators and outsiders. The hypothesis was the excluding predators in fenced plots will cause higher rodent populations, leading to greater seed predation and dispersal since rodents consume them. But, the result of this was that fenced plots had lower rodent populations because hawks would perch themselves on the fence posts and prey on the rodents. The fence posts unintentionally caused a higher predation rate inside the predator-excluded plots. A better control for this treatment would be to put posts all round the area that is being examined so that they mimic the real fence posts and all hawks don't perch solely on the posts put in for the fences.