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Synaptic Plasticity PP

Submitted by zalam on Fri, 09/20/2019 - 00:52

Synaptic plasticity is a concept that had always seemed interesting to me. Even after birth, your brain is capable of changing its connections and wiring. It best described by Donald Hebb's words on long-term potentiation: "Neurons that wire together, fire together". The concept of long-term potentiation involves three stages: input, induction and expression. During the input period, the presynaptic neuron fires a single action potential. This causes a small post-synaptic potential. During induction, multiple action potentials are fired repeatedly along the presynaptic neuron, leaving very little time for the postsynaptic neuron to fire a small action potential and then die down. As a result, the postsynaptic potentials keep bulidng up and reach a threshhold where the neuron is depolarized, leading to an action potential to be fired. This event of accumulation of potentials over a brief period of time is called temporal summation. Finally in the last stage, we see that a single action potential, like the one in the first stage, is able to cause a full action potential called the excitatory postsynaptic potential. This is essentially how we learn. If we keep introducing the same stimulus over and over again, the wiring in our brain adjusts to fire a strong action potential. However, our brain does have a capacity for how much we can learn. The neurons can get too saturated with new wirings if there is no way to reverse this process. Thus, certain wirings start getting weaker by time and this is called long term depression. This would be another way of saying that we are slowly forgetting what we had learned. 

Digestion Draft

Submitted by zalam on Tue, 09/17/2019 - 13:50

As soon we take one look at food, our salivary glands are at work to produce saliva mixed with enzymes to start breaking down carbohydrates. Our teeth play a major role in mechanical digestion to form a paste out of the food we are chewing, making it easier for us to swallow the food bolus down our esophagus. Due to peristalsis, the food bolus keeps moving down to the stomach, where gastric acid kills any bacteria or germs and the food is churned to make it more liquid. The food passes down to the duodenum. Pancreatic enzymes further break down carbohydrates, proteins and fats. The fat gets emulsified by the bile from the gall bladder to help in digestion. The smaller molecules move down to the small ileum and get absorbed by the blood vessels and sent to the liver to get sorted. Water is absorbed by the colon and the undigested food is egested through large intestine. 

Synaptic Plasticity Draft

Submitted by zalam on Mon, 09/16/2019 - 11:06

Synaptic plasticity is something that always seemed very interesting to me. Even after birth, your brain is capable of changing it's connections and wiring. It best described by Santiago Cajal's words on long-term potentiation: "Neurons that wire together, fire together". The concept of long-term potentiation involves three stages: input, induction and expression. During the input period, the presynaptic neuron fires a single action potential. This causes a small post-synaptic potential. During induction, multiple action potentials are fired repeatedly along the presynaptic potential, leaving very little time for the postsynaptic neuron to fire a small action potential and then die down. As a result, the postsynaptic potentials keep bulidng up and reach a threshhold where the neuron is depolarized, leading to an action potential to be fired. This event of accumulation of potentials over a brief period of time is called temporal summation. Finally in the last stage, we see that a single action potential, like the one in the first stage, is able to cause a full action potential called the excitatory postsynaptic potential. This is essentially how we learn. If we keep introducing the same stimulus over and over again, the wiring in our brain adjusts to fire a strong action potential and so we can learn events. However, our brain does have a capacity for how much we can learn. The neurons can get too saturated with new wirings if there is no way to reverse this process. Thus certain wirings start getting weaker by time and this is called long term depression. This would be another way of saying that we are slowly forgetting what we had learned. 

Day's activities

Submitted by zalam on Fri, 09/13/2019 - 15:27

Activities

I woke up at 7AM and brushed my teeth, after which I picked an outfit and changed. I met my friends outside of my dorm and we walked to class together. I had a granola bar on the way. The first class was a 50 minute Psychology lecture. At the end of it I walked over to Tobin for my neurobiology research lab and Nisl stained microscope slides for 2 hours. Then I went to my second class of the day for another 50 minutes - History lecture. I had some time at hand, so I had lunch and did some homework at the Campus Center. Finally I went to the last class of the day – Biochemistry and at the end of it, walked over to a lab meeting for my psychology lab, which had lasted for 1 hour. I had dinner at Frank and then went back to my room. 

Categories

Food/Meals - Granola bar, Lunch, Dinner

Labs - Neurobiology lab; Psychology lab

Academics/classes - Biochemistry, History, Psychology

 

Food/Meals

On my way to class, I had a chocolate Cliff bar to avoid missing breakfast. Around 1:10pm, I had a longer break than usual, so I first walked over to the library to get food. However, they were almost out and there was a long line of people waiting. Then I decided to go to Blue Wall and get a rice bowl from Tamales. After my lab meeting ended around 6PM, I decided to meet up with my friends for dinner at Franklin dining hall. It took us a while to find a table and settle down. Then I went to the sandwich station to get a tuna sandwich. 

Drosophila formation PP

Submitted by zalam on Thu, 09/12/2019 - 23:22

How does the body at an embryonic stage even know where to place all the organs in such perfect order? The drosophila's dorsoventral axis formation is a good model system to give us a general idea. At an early stage, the drosophila undergoes syncytial specification – in short, it is one cell full of nuclei in the same cytoplasm and they signal each other. Along the cytoplasm, there are genes creating proteins in different concentrations to establish different axes, including the dorsoventral axis. Gurken is a protein that starts off a signaling cascade that leads to the determination of the ventral identity. Dorsal protein controls the ventral identity of the embryo. Toll protein assists in transporting dorsal into the nucleus of the ventral side, where it acts a transcription factor to establish the identity. Another protein called cactus helps by preventing dorsal from entering and hence dorsalizing that end. To prove this theory, Roth et al had performed immunolocalization and Western blots to find location of the proteins in the wildtype, dorsalized and ventralized embryo. In short, it is the difference in concentrations of dorsal in the cytoplasm and the nucleus that creates the morphogenic gradient, which leads to the embryo to have a dorsoventral axis. In fact, the morphogenic gradient is a concept that can be seen in other settings too. For example, when our hands our forming, the the placement of our fingers from our thumb down to our little finger depends upon morphogenic gradient of a certain protein. 

Drosophila formation

Submitted by zalam on Wed, 09/11/2019 - 14:04

How does the body at an embryonic stage even know where to place all the organs in such perfect order? The drosophila's dorsoventral axis formation is a good model system to give us a general idea. At a very early stage, the drosophila undergoes syncytial specification – in short, it is one cell full of nuclei in the same cytoplasm and they signal each other. Along the cytoplasm, there are genes creating proteins in different concentrations to establish different axes, including the dorsoventral axis. Gurken is a protein that starts off a signaling cascade that leads to the determination of the ventral identity. Dorsal protein controls the ventral identity of the embryo. Toll protein assists in transporting dorsal into the nucleus of the ventral side, where it acts a transcription factor to establish the identity. Another protein called cactus helps by preventing dorsal from entering and hence dorsalizing that end. To prove this theory, Roth et al had performed immunolocalization and Western blots to find location of the proteins in the wildtype, dorsalized and ventralized embryo. In short it is the difference in concentrations of dorsal in the cytoplasm and the nucleus that creates the morphogenic gradient, which leads to the embryo to have a dorsoventral axis. In fact, the morphogenic gradient is a concept that can be seen in other settings too. For example, when our hands our forming, the the placement of our fingers from our thumb down to our little finger depends upon morphogenic gradient of a certain protein. 

Draft 2

Submitted by zalam on Mon, 09/09/2019 - 18:59

Today I was reading a neuroscience paper on the zona incerta of the brain. This paper was the first time I had ever heard about this incredibly underrated brain region. The ZI is a subthalamic region that has proven to be of great importance in terms of treatment for various psychological issues tested in mice model. The paper that I had read shed light on the activation of the ZI leading to the attenuation of fear, but only maladaptive fear. The mice were classically conditioned into being fearful of a certain stimulus. Upon trigger of the stimulus, they had tried to escape. When the ZI was activated using viral injections, the rate of expressing fear had significantly gone down. To further confirm their results, they used viral injections to inhibit the ZI, and as expected, the mice had a higher rate of exhibiting fear. They even tried to activate the GABAergic neurons to the ZI, which lead to the decrease in fear generalization. This had confused me slightly as GABAergic neurons are responsible for inhibitory responses. However, my professor later explained that it worked as a double negative - the GABAergic neurons inhibited possibly another set of neurons which were stopping the ZI from getting activated. The paper provided hope for PTSD, anxiety disorder etc. to combat maldaptive fear and quite frankly interested me into looking further into how the ZI affects our cognitive abilities and how it can be used for other disorders.

Leaf

Submitted by zalam on Fri, 09/06/2019 - 15:23

The leaf had a thin stem with three green leaves jetting out in different directions, along with a very evident sweet yet minty smell. The red stem had thin, hair-like projections all over and its color extended to a certain point after the stem divided into main veins. The edges of the leaves are straight at the bottom unlike the top. Each vein had a reddish tint like the stem, but it gradually turned greenish-yellow moving to the pointy top. On one side of the leaf, the surface had a matte effect and was paler in color. On the other side, the leaf was a darker green and had a shiny surface. Placing the leaf on its pale end, certain size and shape differences were very clear. The left leaf was slightly smaller than the right leaf - later when measured, a 0.2cm difference was found. However, they were both very similar in shape - rounded. Conversely, the leaf in the center was much bigger (5.5cm) and was wider at the top than the bottom. Furthermore, the red tint, originating from the stem, started to disappear earlier in the smaller leaves in comparison to the bigger leaf. There were brown discolorations on the leaves. Surprisingly, the two side leaves had them in the same spot as each other (left of the main vein, towards the bottom). The center leaf had it in the top right corner.

Leaf - draft

Submitted by zalam on Fri, 09/06/2019 - 15:15

The leaf had a thin stem with three green leaves jetting out in different directions, along with a very evident sweet yet minty smell. The red stem had thin, hair-like projections all over and its color extended to a certain point after it divided into three parts. The edges of the leaves are straight at the bottom unlike the top. Each vein had a reddish tint like the stem, but it gradually turned yellow moving to the pointy top. On one side of the leaf, the surface had matte effect and was paler in color. On the other side, the leaf was a darker green and had a shiny surface. Placing the leaf on its pale end, certain size and shape differences were very clear. The left leaf was slightly smaller than the right leaf - later when measured, a 0.2cm difference was found. However, they were both very similar in shape - rounded. Conversely, the leaf in the center was much bigger (5.5cm) and was wider at the top than the bottom. Furthermore, the red tint started to disappear earlier in the smaller leaves in comparison to the bigger leaf. There were brown discolorations on the leaves. Surprisingly, the two side leaves had them in the same spot as each other (left of the main vein, towards the bottom). The center leaf had it in the top right corner.

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