Are Ticks Venomous?

Hi everyone,

Here's the citation to the paper I discussed during today's presentation in case anyone is interested :)

Citation:

Cabezas-Cruz, A., & Valdés, J. J. (2014). Are ticks venomous animals?. Frontiers in zoology, 11, 47. https://doi.org/10.1186/1742-9994-11-47

The Discovery of Feature Detectors

I recently read a classic neuroscience paper from 1959 entitled "What the frog's eye tells the frog's brain," describing the discovery of what we now call "feature detectors," or visual receptors within the retina that are sensitive only to certain kinds of visual stimuli within their receptive field. For example, one kind of feature detector could be sensitive only to moving parallel lines, while another is only sensitive to curvature through color contrast. By encoding their excitement through different patterns of action potentials, these different feature detectors enable images to be relayed to the brain through a universal language of neuronal firing -- and without the discovery of feature detectors, we may have gone on for awhile yet believing that the retina was just an amorphous conglomeration of random receptors that all fired at once, and seemingly at random. 

While this paper relates more to our week about the nervous system than this past week's lectures, I greatly enjoyed delving into this publication. If you have any interest in brain science, I would highly recommend giving it a moment of your time, because it really is an entertaining read. Though the paper's findings are fascinating within themselves (I mean, the scientists mounted frogs on corkboard, conducted neurosurgery to reveal their optic nerve, successfully recorded individual action potentials from both myelinated and unmyelinated axons, concluded that feature detectors existed, and then patched up the frogs for release into the wild), the way the paper is written is also quite marvelous from a literary standpoint. Lettvin, the first author, began his early career as a poet, then became an electrical engineer, and then turned to neuroscience to make one of the most quintessential discoveries to our understanding of the visual system to date. His background as a poet really shines through in the stylistic aspects of this paper, and I think that's perhaps what makes it so entertaining. Lettvin brings the frog to life, as if he were studying some divine being, and cracks intellectual jokes throughout the paper. Again, really worth a read! Sometimes I wonder why that sense of humor has slowly crept out of science as we read more contemporary papers. I had more fun reading this paper than most any other paper in my undergraduate career thus far, and I retained more from it due to my interest in the narrative it creates. Maybe, as the next generation of scientists and authors of scientific publications, this aspect of playfulness and engaging with readers might be something to think about. 

Here's a link to the paper pdf: What the frog's eye tells the frog's brain

Muscle Damage

After John's brief introduction of muscular functions this week, I wanted to take a bit of time to look into muscle damage, and why we get so sore after working out!

Now, it's firstly important to understand that the main perpetrator of our muscle damage and subsequent soreness is eccentric muscle action, aka movements that lengthen the muscle while applying force to them. John briefly mentioned a great example of this- running downhill. As you extend your leg forward, your quadriceps lengthen as you apply force. As he also mentioned, this is one of the times you are most injury-prone. However, the force applied to the muscle isn't the only potential cause for muscle damage. Other factors like metabolic depletion, calcium influx, or musculotendinous stiffness can contribute to or cause muscle damage during eccentric movements (Bryne et al., 2004). 

One general effect of muscle damage is a loss in isometric strength (Byrne et al., 2004). Isometric strength is required during static exercises, like planks or wall squats. It's particularly important because it also represents the strength required by your body to simply fight gravity while you're standing up. Additionally, studies have shown a decrease in dynamic strength (Byrne et al., 2004). Dynamic strength is required when a force is repeatedly applied for a period of time and is used during exercises like sprinting. 

Overall, it is important to recognize your limits and prepare yourself as best as possible to avoid muscle damage. Pay attention to your body's limits, avoid over-exercising, and give your body time to recover (also in general, stretching is great). Whether you plan on becoming an elite athlete or you just enjoy running on the weekends, just remember to stretch out and take care of your body!

Byrne, C., Twist, C., & Eston, R. (2004). Neuromuscular Function After Exercise-Induced Muscle Damage: Theoretical and Applied Implications. Sports Medicine, 34(1), 49–69. https://doi.org/10.2165/00007256-200434010-00005

Preventing Osteoporosis in Space with Melatonin

Osteoporosis is a big problem for astronauts and the future of space exploration and space missions. Instead of exercise, this research team turned to preventative medicine. They found that melatonin can be used to prevent osteoporosis in microgravity.



Melatonin was found to stimulate the mRNA expression of Calcitonin, which inhibits osteoclasts, and also decrease the mRNA expression of kB ligand, which promotes osteoclastogenesis. Osteoclasts are bone cells that absorb bone tissue during growth and healing.



My favorite part of this study lies in their creative methods. Obviously they couldn’t test on human astronauts, so they instead used the next best thing: goldfish scales. The goldfish scales spent time on the International Space Station, before returning to Florida’s Kennedy Space Center lab on Earth for analysis.



Citation:Ikegame, M, Hattori, A, Tabata, MJ, et al. 2019. Melatonin is a potential drug for the prevention of bone loss during space flight. J Pineal Res. 67(3). https://doi.org/10.1111/jpi.12594

Cocaine

Hey everyone! Since middle school I've always been a little frightened about the effects of drugs so, today I wanted to talk about the effects chronic cocaine use has on the brain.

As some background, when cocaine is snorted, smoked, or injected, it enters our bloodstream and passes through the blood brain barrier. The high from cocaine comes from the buildup of dopamine within our brains once cocaine is ingested. Dopamine is a neurotransmitter that attaches to a receptor of another cell. This all takes place in the synapse. Dopamine is responsible for the pacing of our cells, making cells work harder during periods of stress. The transfer of dopamine from neuron to neuron is regulated by receptors on the initiating neuron that pick up dopamine, preventing it from binding to the active site of neurons. Cocaine binds to these dopamine inhibitors preventing them from picking up excess dopamine. This causes more dopamine than is needed to be transmitted across the synapse to our receiving neuron.

One of the most notable effects of extended cocaine use is the alteration of gene expression in brain cells. This paper focuses on the change of expression of the protein FosB. FosB is a protein that is found in the cells of the nucleus accumbens. Interestingly, FosB plays a similar role to dopamine in that it acts as a pacer. It does this by acting as a transcription factor in the cell, controlling the expression of certain genes. Chronic cocaine use causes an increase in the amount of FosB found in the cell. Unfortunately, FosB can live up to 6-8 weeks, which means chronic cocaine use only exacerbates the high levels of FosB found in the nucleus accumbens. Furthermore, mice with increased expression of FosB exhibit addictive behavior while those that have a normal amount of FosB expression do not. This suggests that FosB plays some part from drug abuse to full blown addiction in humans.

With all this in mind, it is important to remember that reformed addicts still receive cravings for drug abuse years after their sobriety started. FosB only lasts for up to 2 months, so the likelihood of FosB to be involved in these cravings is believed to be low. There are some hypothesis as to why these cravings last for so long. One important detail is that chronic cocaine use causes nerve cells to extend and grow more offshoots in their dendrites. This could cause an increase in signals, specifically from the amygdala, hippocampus, and frontal cortex. This causes the aforementioned regions of the brain to have more influence over the nucleus accumbens. As drug associated memories are induced, the influx of messaging from the amygdala and hippocampus could be responsible for the intense cravings.

 Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2851032/

Citation: Nestler E. J. (2005). The neurobiology of cocaine addiction. Science & practice perspectives, 3(1), 4–10. https://doi.org/10.1151/spp05314

Donut Brains?

We all know that octopuses and other cephalopods are among the smartest animals on the planet. My question for the week is why did their brains and nervous systems develop the way they did?

These creatures have always been some of my favorites, since they have really interesting adaptations and special features. Since we were talking about the nervous system this week, and I remembered that octopuses have donut shaped brains, I wanted to look more in depth on it.

As it turns out, the donut shaped brain is not exclusive to octopuses. It was also found that the colossal squid has a donut shaped brain, too. Why would an animal have a donut shaped brain? Great! I'm glad you asked. 

About 1/3 of the "brain" is in the donut shaped mass. The rest are distributed in ganglion throughout the octopus' arms, so technically they have nine brains. One "mini brain" (aka a large ganglion) is in each arm, and then plus the donut shaped brain in the head makes 9 brains. Another fun fact that I found was that the cephalopod's esophagus runs directly through the center of their donut shaped brain. The hole in the center isn't large, but is large enough so that the esophagus can run through it. Because of this, certain species of colossal squid are known to break their food up into tiny bits to avoid hurting their brains.

Overall, I could not find anything that says why a cephalopod may have developed this way, but I still thought it was a cool fun fact, so I kept looking into it.

After looking into cephalopod brain development a bit more, I found that the development is very complex (as to be expected) with various developmental genes and molecular processes. I have attached an article below that goes in depth on cephalopod nervous system development, and it is surprisingly well organized and not terrible to try to comprehend.

http://www.todayifoundout.com/index.php/2012/10/the-colossal-squid-has-a-doughnut-shaped-brain-with-their-esophagus-running-through-the-hole/

https://www.nhm.ac.uk/discover/octopuses-keep-surprising-us-here-are-eight-examples-how.html

https://www.frontiersin.org/articles/10.3389/fphys.2018.00952/full (article for nervous system development)

Also: my knowledge from working at an aquarium for 3 years... I'm not sure how to cite that.

Remapping The Mind: Real-Life Neuromods

Prey was an old video game that I used to play, and in it there were many sci-fi tools that could help the player progress.  The main tool of the game was called the "Neuromod", a device that injected a serum into the brain via the optic nerve and had the ability to remap someone's brain to match that of someone with a certain skill.  According to the game's lore, this Neuromod would grant the user the template organism's skill as well. Although this idea, and the subsequent abilities "learned", are outlandish and fictional, I wondered if there was any research being done in the field of remapping the brain for therapeutic purposes. I found that this idea seems to not be as outlandish as I originally thought. 
According to two papers I read, the brain is not only always changing, but these changes can be observed in different physical changes in the brain like changes in the dendritic lengths, the number of connections, and other physical changes (1).  In one experiment, monkey brains were analyzed after localized damage. It was found that, although the brain naturally starts to create new dendritic connections with time and even faster after learning a challenging new skill, localized brain damage was found to also increase new connections (1). Now, although this offers a novel way to stimulate growth and diversification of new neural connections in the brain, it does come at the cost of brain damage and the high possibility of permanent disability. However, a second paper on the neural interfaces used in high-tech prosthetics seems to offer some ways to potentially fix this issue. In this paper, BMI (brain-machine interfaces) and BoMI (body-machine interfaces) can be used to improve connections in the brain after damages to the brain and spinal cord(2). These neural interfaces allow people to recover motor skills after accidents and other cases of brain/spinal cord injuries. Now, if a way to direct and specify the fixes the brain makes was found, then these three procedures could lead to the development of something very similar to a Neuromod.

1.) Johansen-Berg, H., Structural Plasticity: Rewiring the Brain (February 2007), Current Biology (17-4), 141-144, https://doi.org/10.1016/j.cub.2006.12.022
2.)Pierella, C., et al, Remapping residual coordination for controlling assistive devices and recovering motor functions (December 2015), Neuropsychologia (79-B), 364-376, https://doi.org/10.1016/j.neuropsychologia.2015.08.024