Review of week 5

This week we learned how to identify neurotransmitters. We learned that there are three criteria that must be met for a molecule to be considered a neurotransmitter:

  1. The molecule must be synthesized and stored in the presynaptic neuron.
  2. The molecule must be released by the k
  3. presynaptic axon terminal upon stimulation.
  4. The molecule, when experimentally applied, must produce a response in the postsynaptic cell that mimics the response produced by the release of neurotransmitter from the presynaptic neuron.

All the methods to determine whether these conditions are fulfilled were not already familiar to us. Two quite similar methods to determine whether a transmitter candidate is localized in, and synthesized by, a particular neuron was introduced; Immunocytochemistry and in Situ Hybridization. Both of them rely on a marker that is attached to a molecule that reveals whether the transmitter candidate is synthesized by, and localized in a particular neuron. With Immunocytochemistry a colorful marker is placed to an antibody that color those cells that contain the transmitter candidate. In Situ Hybridization the marker is placed to the complementary strand of mRNA that sticks, when released to the tissue, to the mRNA molecule in the cell, where there are instructions to code the transmitter candidate.

Additionally, this week gave us some perspective that how difficult it can be to find some new information from biological systems. The process to identify whether a molecule is a neurotransmitter is a complicated task and the determination whether the candidate fulfills the first criteria is easy compared to the second and third criteria.

One thing that remained unclear was the function of single cascades. In this week’s quiz it was asked what are the benefits of single cascades over simple transmitter-gated channels. We had understood that single cascades are these kind of following events and do only occur in g-coupled-protein transmitters. In transmitter-gated channels the neurotransmitter binds to the receptor and has an immediate effect and there are no chain of events such as in g-coupled-protein receptors. Therefore, the quiz question made the concept of single cascades to remain unclear.

As another achievement of this week, we can mention the relation of neurotransmitter systems with normal central nervous system development. Neurons should have an efficient communication with each other in order the nervous system to have a normal function. Release of neurotransmitters and specialized receptors on target cells are the main parts involved in neuronal communication mechanism. Here we try to focus on three classes of chemical neurotransmitters only: (1) amino acids (2) biogenic amines and (3) other (e.g., adenosine, adenosine triphosphate, and acetylcholine)

Neurotransmitter release can be regulated by neurotransmitter receptors. Also the chemical neurotransmitter and its synaptic level can be decreased by enzymatic breakdown or reuptake into the axonal terminal. The recruitment of progenitor cells into the neural plate shows the beginning of development of the nervous system. By folding the neural plate the neural tube is formed, this is where the progenitor cells are transformed into neuronal and glial cells. Axons, dendrites, and synapses are gradually acquired once immature neurons travel to their ultimate location. The fact that whether synapses should be maintained or removed is determined by exchange of information between axons and dendrites, and in each of these neuronal developmental stages the chemical neurotransmitters own the key roles. Progenitor cell proliferation, migration, and differentiations are regulated by GABA and glutamate even before synapses are formed (1.Manent and Represa 2007). Growing axons can be where these neurotransmitters are released through reverse action of neurotransmitter transporters. Also, in immature neurons, the contribution of GABA and glutamate to the maturation of dendrites and axons and their participation in the generation and refinement of synaptic contacts should be taken into consideration (2.Cline and Haas 2008). Within development and maturity, neurotransmitter systems have different properties. For example, one of the key elements in the construction of neuronal networks is oscillatory electrical activity that is generated by neurons throughout the developing central nervous system. Neuronal circuits can be formed and matured through these particular properties, also susceptibility of immature neuronal networks to genetic or environmental insults can be made through these unique properties (3.Ben-Ari 2008).

 

Regards,

Ruhoollah, Väinö and Maria

 

References

  1. Manent JB, Represa A. Neurotransmitters and brain maturation: Early paracrine actions of GABA and glutamate modulate neuronal migration. Neuroscientist. 2007;13:268–279.
  2. Cline H, Haas K. The regulation of dendritic arbor development and plasticity by glutamatergic synaptic input: A review of the synaptotrophic hypothesis. Journal of Physiology. 2008;586:1509–1517.
  3. Ben-Ari Y. Neuro-archaeology: Pre-symptomatic architecture and signature of neurological disorders. Trends in Neurosciences. 2008;31:626–636.

 

Posted by Ruhoollah Akhundzadeh

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Review of week 4

This week included much new information. We learnt about the most familiar of our senses: taste, smell and visual. The new thing we learned was the structure of the eye and the arrangement of the nerves in the eye. We were not familiar with the inside-out structure of the retina as well as the way neurons process the visual information that comes to the retina via horizontal cells and amacrine cells already before the signal goes to the brain. The polarization of bipolar cell does not depend only on the photoreceptor it is attached to but also surrounding photoreceptors via horizontal cells. An example of the surprising complexity of functions of retina is the event of depolarization and hyperpolarization of bipolar cells. If the surrounding receptors are exposed to the light and they are hyperpolarized but the center photoreceptor is not, then the bipolar cell in the middle is hyperpolarized. On the other hand, if the situation is vice versa, the hyperpolarization of the center photoreceptor causes depolarization of the bipolar cell.

In chapter 8, we came upon an interesting subject called “Memories of a very bad meal”. It stated that if we eat some food and we become nauseated and vomited, we will remember this for a long time and we will avoid eating that food again. When we read this, a question arose that do we also remember the very good meals in a similar way?

When we reviewed our memories about meals, we realized that we have some robust memory of some bad meals, but could not find any good memory of a very good meal. So, what do you think? Do you have a robust memory of a very good meal among your meal-related memories?

BR,

Maria, Väinö and Ruhoollah

Posted by Maria Haukka

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Review of week 3

This week’s exercise concentrated excessively naming different parts of the brain. It was quite difficult, especially as multiple parts were new but in addition, it was hard to name  the parts that were already familiar in English as they have been previously taught in Finnish. Building the brain out of putty, however, helped to remember different brain parts like Medulla, Cerebellum, Pons, Basal Ganglia and Hypothalamus.

There were many properties of synapses and dendrites introduced this week that were new to us. The fact that inhibitory synapses completely kills the action potential was a surprise. Also that the dendrites are passive cables rather than active, like the axon, was new information. This strengthened the picture of complexity of already complicated picture of the network of neurons in the brain. 

This week’s lecture quiz was quite difficult. Even though, you would have read the chapters the open questions were kind of difficult. Especially when you cannot remember everything from the book. Multiple choice questions would be therefore more suitable as lecture quiz questions. So overall, this week consisted of many new things that were needed to internalize quickly.

Among all the new topics of the previous week, action potential was the concept that we consider it as an important part of our nervous system. One of the big questions that we tried to answer was the relation between EEG signal and action potential. Since EEG is a signal reflecting the electrical activity of the brain, action potential can be the small components of this signal. If we simplify the definitions of EEG and action potential as well as the theories about their origins, we still have some pieces of this puzzle missing, some questions such as, how can we measure EEG signal to reflect the firing of potentials most? Should EEG be considered as a measure of the inputs to a group of neurons, or the outputs of that group? Are postsynaptic potentials the only factor contributing in generation of EEG? What are the limitations of EEG measurement? How well can we define the connection between action potential and EEG?

Kind regards,

Väinö, Maria & Ruhoollah

Posted by Väinö Mäntylä

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Review of week 2

In the second week, we got familiar with some new matters, for example we learned how neurons can be categorized. One categorization which we had never heard of it was that neurons can be classified based on their dendrites or neurotransmitters. The other one was about synapses, we did not know that there are electrical synapses in addition to chemical synapses. Symmetric synapse and asymmetric synapse which are excitatory and inhibitory, respectively, was as well new information to us.

Another interesting subject was how information travel within the human body. The mechanism for communication in our body is pretty similar to what we have in our telephone/telegraph communication system. For instance, axons fairly resemble the telephone wire or action potentials can play the role of Morse code traveling in telegraph wire.  However, there are some differences like the insulation level of pathways or the type of suspension in which wire/axon is suspended (air .vs salty fluid). It was these differences that drew our attention towards some new concepts like excitable membrane, resting membrane potential. To understand the aforementioned concepts we need to study water as the main ingredients of both intra and extracellular fluid. By assessing the water molecule, we realized that polar molecules like Na+Cl tends to dissolve in water, and that is where ions were introduced. We learned that there are two types of ions, cations with positive charge and anions with negative charge, which both are functioning as charge carriers in physiological systems.

Next, ion channels were brought up and we learned how the ion channels work. There were three types of channel including Potassium (permeable to K+), Sodium (permeable to Na+) and Calcium channels (permeable to Ca2+). Expectedly, we needed something to move the ions and enable them to go through the membrane, what we were looking for was actually some enzymes known as ion pumps. We have ion channels, let’s say a bridge and we have the means of crossing (ion pumps) and what we are missing to complete the mechanism of ionic movement are some forces to drive the ions across. Diffusion and Electricity are the two determining forces that help the ions with their migration through the membrane. we saw that diffusion comes from the imbalance of concentration and Electricity is made by zero conductance of membrane which leads to accumulation of charged ions on both sides of the membrane, and that explains membrane potential. Following the ionic movement topic, some questions were asked, for example after the action potential, how long does it take for the ion pumps to normalize the concentrations of K+ and Na+ back to normal? Or if the speed of the action potential could be increased in our neurons how it would affect us? Would it just make our reflexes better and our thinking more effective?

 

Kind regards,

Ruhoollah, Maria and Väinö

Posted by Ruhoollah Akhundzadeh

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Reflecting on week one

This blog post is about reflecting the first week’s (9.9-15.9) learnings in the course of Structure and Operation of the Brain.

The first week lecture concentrated on introductory topics. Therefore, we consider that we mainly did not learn anything new as every one of us know the basis of the brain. The lecture was a good recap of the brain and memory refresher for our group. Overall, the first lecture tuned our mind to the subject.

Although we did not learn many new things, we came up with some ideas and questions. Firstly, we wonder if there is any evidence that closes out the possibility that consciousness is somewhere else than in the brain. For example, what if the brain is just the first thing that reacts to our consciousness that exists somewhere we don’t have access to, for example, in a dimension that is out of our reach? In other words, could our body be just an appearance of us in this dimension and that is all we know because that is all that our senses can sense. Secondly, we would like to know what are the things that we do not know about the brains as it seems that we already know much. Thirdly, it is unclear to us if the sensing areas of the brain (frontal lobe etc.) are located in the same places between individuals. So, does every individual interpret a noise in the same area in the brain? In addition, do sensing happen only in the specific area known or in multiple areas in the brains. For example, it is thought that hearing happens in the temporal lobe but could a noise be sensed at the same time in multiple locations of the brain. Finally, we have heard that when a blind person reads the braille the sensing in the brain happens in vision region, which is located in the temporal lobe. Why it happens there and not in the parietal lobe where other pressure stimuli occur?

Kind regards,

Maria, Väinö and Ruhoollah

Posted by Maria Haukka

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