Week 08.10-14.10

The class on monday started with a 5 minute quiz about the 15th chapter. Then we learned about the different diffuse modulatory systems : We started with the Acetylcholinergic pathway, and the implications that a malfunction on it mean. We then went over the Catecholaminergic, Norepinephrine and Dopaminergic pathways. Some malfunctions of these pathways were also discussed. How accurately can we really evaluate these malfunctions? How soon could we expect to see some more advanced interventions  in medicine on these pathways?

We then discussed the serotonin pathway and its mediation by the hypothalamus and the pituitary gland.

To get a full image, we went over each of the hormones secreted by the pituitary gland : Oxytocin, related to birth and therefore usually linked with love and compassion; Vasopressin, our thirst regulator; Cortisol, our main stress indicator; etc…

The following matter to be discussed was the Autonomic Nervous System. This was particularly interesting when the contrasts between the sympathetic and parasympathetic systems were drawn. (arousing VS calming).




The idea of how complex and interconnected these pathways actually are are highlighted numerous times. Each pathway influences all other making some imbalances very hard to track down.


To make some sort of introduction for the following day we started the subject of how we can see and study the brain through different imaging techniques.

The first one was the PET scan.

Then a super interesting study was mentioned and discussed for a bit. It was about Adult attachment styles in social bonding and how you can evaluate them through the level of attachment avoidance.

On that same day in the afternoon we had an excursion to a company called MEGIN. We arrived and were welcomed into a very nice environment where one of their employees walked us through everything that they do on that company.

MEGIN was originally named Neuromag, it was founded in 1989 and it has been a leader in whole-head magnetoencephalography ever since then. In the office we visited they no longer manufacture their products but instead develop new ones and take care of all the logistics and business for the ones already on the market.

To better make us understand why MEGIN is so innovative and essential to Neuroscience research he gaves a good insight on how the MEG and EEG work, how they can be filtered, improved, adapted to different kinds of patients, etc…

Then we got to see the MEGIN most break-through products, from the Superconducting SQUID sensors in liquid helium in a helmet-like structure that we got to hold in our own hands, to the  new TRIUX™ neo . We got an extensive scientific explanation for how all of them worked. Some questions were raised by students about adapting the different machines to children or babies but apparently there is no need to do so. This was quite interesting. Some signal processing with specific filters is apparently sufficient.

This was the first week we had an excursion so it was quite exciting. We are very much looking forward for the next ones J

Week 01.10 – 07.10

Lecture 01.10

The focus on this week lecture was the neurotransmitter, the chapter 6 – Neurotransmitter systems – of the book “Neuroscience: Exploring the Brain (2015)”.

The first transmitter studied further was the glutamate. It is the most common excitatory neurotransmitter in the brain and if it doesn’t work properly, it may causes some serious damages that can push to the death of the neuron.

On the other hand, another important neurotransmitter is GABA which is known to be the most common inhibitory neurotransmitter in the brain. Therefore it is mainly found in inhibitory synapse that when activated and located between the excitatory synapse and the soma, will dissipate the current signal and then no change of potential will be recorded in the soma.

The G-proteins were also an important factor looked into in the lecture. It is essential to understand how they work since they are really common proteins, especially in the brain. The G-proteins induce a cascade of called second messenger. It is a significant process since it can influence the signal a lot. The main second messengers cascades advantage is the signal amplification. In consequence, more than one protein can be activated from a single G-protein activation.

I think this week lecture was really interesting as we learned more about the complexity of the neurotransmitters. In addition, I was glad the teacher showed us some little videos about the different mechanism. I personally like it because it gives me a visual approach that helps me a lot to understand and remember the different processes.


Exercises Class 02.10

This week exercise session was a bit different from the others. We were in the computer room and actually did a real experiment; we were measuring the aural and visual speed of reaction. Even though the conditions might not have been the optimal for an experiment related on quickness of mind, I still think if was interesting. It gave me an good idea of how some easy tests can already give some good information about how the brain works.

Week 24.09 – 30.09

Lecture 24.09

Today’s lecture topic was the chapter 5 – Synaptic Transmission – of the book “Neuroscience: Exploring the Brain (2015)” and we followed the book closely, going through most of the figures in this chapter and having them explained by the professors.

Synaptic transmission is a complex topic since all the operations of the nervous system (action of psychoactive drugs, the cause of mental disorders, the neural bases of learning and memory, for example) can’t be understood without knowledge of it.

In this lecture the mechanisms and details of synapses were discussed. We started with the basics – for example, by defining gap junctions, the direct openings between two cells, or discussing their structure – proceeding then to more complex issues.

We discussed the different types of synapses (electrical or chemical). Both have their roles but chemical synapses – when chemical neurotransmitters transfer information from one neuron to another at the synapse – cover the majority of synapses in the brain, which is the reason why the lecture was focused on chemical synapses from this moment on.

Something interesting and to think about is the fact that we still don’t know a lot about all the molecules involved in synaptic transmission. Here is the Box 5.3 from the book where we can learn more about it:

Bear, Connors, Paradiso: Neuroscience: Exploring the Brain, 4th edition, Lippincott, Williams & Wilkins, 2015, 125.


Exercises Class 25.09

During this week’s exercise session, we had the opportunity to do a 3D model of a brain with playdough. It was an interesting way to learn the different parts of the brain, since we were listening the teacher’s explanations and learning while sculpting the different parts of the brain at the same time.

Week 17.09 – 23.09

Lecture 17.09

We started the class with a 5 minute quizz about the chapters 2 and 3 of the book: Mark F. Bear, Barry W. Connors, Michael A. Paradiso – Neuroscience: Exploring the Brain (2015).

After that, some big questions were raised. Those were the questions that propel neuroscience to move forward and neuroscientists to still strive to learn more about how our brain works. The motivation to pursue such achievement is no small one: brain disorders have been becoming increasingly prevalent in our society and in order to cure them we must endeavour through uncharted territories, learning more about how the brain works, from a molecullar to a cognitive level. Our central nervous system has an incredibly complex structure, featuring hundreds of different kinds of transmitters and over 86 million neurons. This can be partly explained and tracked by the evolution of our species. Some questions about human brain enhancement were raised which also arose some interesting ethical questions by students in preseemo. Should we aim to enhance our brain at all? We can probably do so through magnetic stimulation. Genetic enhancement/editing is also an ever expanding field, which might show us some surprising aids to our life sooner than later. It was also pointed out that eating well and resting is a key factor in keeping the brain’s function’s at bay. After this interesting debate, we moved on to the topics on Chapter 3 of the book: The Neuronal Membrane at Rest. We went over the three main contributors to the resting membrane potential:

  1. Cytosol and Extracellular Fluids – Water is the main fluid both inside and outside of the neuron. Because of its highly polarity, it acts as a very good solvent for electrically charged atoms or molecules (ions). The molecules of water surround each ion in so called spheres of hydration, and effectively insulate the ions from one another. Ions are the major charge carriers in the conduction of electricity in biological systems, including the neuron. Water molecules attach themselves to different ions in different ways, which leads into a different transportation and membrane permeability to those ions . Some ions of particular relevance for this studies are the cations Na+ (sodium), K+ (potassium) and cation Ca2+ (calcium), and the anion Cl- (chloride).
  2. The Phospholipid Membrane – The neuronal membrane is made up of a sheet of phospholipids. They feature a stable arrangement, named phospholipid bilayer, that organizes itself in such a way that the hydrophilic heads face the outer side of the membrane and the hydrophobic tails face each other. This structure separates the neuron’s cytosol from the extracellular fluid.
  3. Proteins that span the membrane – After reviewing the basic structure of a protein, from its primary to quaternary structure, the protein’s many functions in the phospholipid bilayer were mentioned. Firstly, they provide structure, forming a cytoskeleton that provides the neuron’s its shape. Then, some proteins (enzymes) are catalizers to certain neuronal chemical reactions. The also make up the receptors that are sensitive to neurotransmitters. And last but definitely not least, they form channels and gates across the membrane which are routes for ions to cross it .

This mechanisms play an essential role in maintaining the resting potential stable. This movement of ions, however, does not happen in a random manner, but rather follows physical (diffusion) and electrical laws.

We then moved on to how the neuron membrane is at its resting potential: what are the concentrations of ions on each side of the membrane, what mechanisms help them keep it that way. The ion Potassium is more concentrated on the outside whereas Sodium, Calcium and Chloride are more concentrated on the inside. The sodium-potassium pump is mainly responsible for maintaining this large potassium concentration gradient across the membrane. At rest, the neuronal membrane is highly permeable to potassium, because of membrane potassium channels and it is negatively charged precisely due to the movement of potassium ions across the membrane.

This electrical potential difference work as one of the battery, kept stable through the work of ion pumps. We then moved on to focus on the Action Potential. We discussed the mechanisms that are responsible for the action potential and how it propagates down the axonal membrane.

We went over the different phases of an action potential, in the following order : resting potential > rising phase > overshoot > falling phase > undershoot, and its trigger, called the threshold, and how we can measure them through different experimental methods (voltage clamp). We went over each step of the depolarization (through Na+ Influx) and repolarization (through K+ exflux) of the cell membrane and were introduced to the structure and function of a voltage-gated-sodium channel (analyzed through the patch clamp technique). This channels works its way through some phases called activation, inactivation and deinactivation in order to regulate the passage of Na+ through it. Next came the propagation of the action potential through the neuron’s axon, aided by the myelin sheath that allows for a saltatory conduction of the impulse. After came the different classifications of synapses, according to mechanism and structure (electrical – gap junctions – VS chemical synapses), according to connection (axodentritic VS axosomatic VS axoaxonic VS dendrodendritic) and the neuromuscular junction complex. Finally we went through a brief overview of all the process of neurotransmitters transmissions: from synthesis and storage to release, reception, recovery and degradation. This are all complex processes mediated by different cell components in the axon, voltage-gated ion channels in its terminal and different enzymes and ion channels across the membrane. It was also discussed very briefly how the synaptic integration happens when multiple action potentials reach different dendrites of the same neuron.

Exercises Class 18.09

In the first exercise class we went over the different exercises on our first assignment. These regarded the structure of a neuron, the function of the glial cells, the different phases of the action potential, the action potential propagation velocity and finally a derivation for the equation that allows us to calculate the Equilibrium potential for a certain ion.