This weeks topics were the structures and mechanisms associated with synaptic transmission, such as neurotransmitters, receptors, synapses, transmitter synthesis and degradation etc. I was actually quite familiar with most of the structures and functions from my previous studies of physiology. For me, the most intriguing part of the chapter was the question of how to relate the observed processes of neurons to existing theories of information processing.
To come up with a theory, the first thing you need is the elementary units (i.e. building blocks) from which to start working upwards. As far as I understood, the most elementary unit considered in neural information processing is the postsynaptic reception of a single vesicle. This process is tied to our existing theories by measuring the voltage (EPSP) caused by the reception. This way, any measured voltage in the neuron can be reduced to multiples of a single EPSP. Still being new to the subject, I assume the single EPSP’s are central in the modelling of neural information processing, the same way 1’s and 0’s are in explaining computer behavior.
This led to several questions:
Can the information processing of the brain be explained or modelled by XOR operations?
What would be a sensible way to compare the processing capacities of a brain vs a computer? What are the main limitations in the underlying structures? E.g. the speed of current running in neurons vs circuits, synaptic delays vs some components of a circuit, or maybe the wiring (e.g. the brain is not wired as an optimal data processor).
Neuronal Membrane at Rest (ch. 3), Action Potential (ch. 4)
The first weeks reading requirement was chapters 2-3 and on the Monday lecture 17.09.2018, we went through chapters 3-4.
What struck me as the most interesting aspect of this weeks lecture and reading was the knowledge of the “importance of regulating the extracellular potassium (K+) concentrations within the body”. The increased extracellular potassium depolarizes neurons.
The sudden increase is prevented by the blood-brain barrier, but in the body, muscles are susceptible to this change. The sudden change causes membrane potentials of the neurons to become less negative and disrupting neuronal function. As an example, a ten-fold change in extracellular potassium causes a 48mV depolarization of the membrane and in the body would result in cardiac muscle cells no longer generating impulses that lead to contractions resulting in heart failure.
Now to understand this the relative ion permeability of the membrane, Nernst equation, Goldman equation, ionic equilibrium potential, concentration gradient, electrical potential, and the importance of water as a polar solvent in action with amino acids had to be understood within the context of the neuron. The human body seems to really be a balanced machine where even a minute defect can cause irreparable consequences for the individual. For example, this small change from the norm could be an inherent neurological disorder caused by certain mutations of the specific potassium channels resulting in forms of epilepsy.
Questions that arose this week:
- Could neuro stimulants be produced to help in more efficient potassium regulation and preventing neural fatigue and increase learning?
- How could we integrate neural chips in the future that could translate “the morse code” produced by neurons and store this information? Could we then hold more accurate information in the chip (just learned) and store it indefinitely? Could this make us smarter? Could this prevent us from having “false memories”?
- Not exactly related to current chapters: I’ve understood that some parts of the brain are less active and that the human doesn’t use all of its brain capacity. Why? Can we learn to expand our brains capacities and how?
Week 1 of the course from 10th of August to 16th of August was an introduction week when the course administrators and tutors explained the structure of the course and the requirements. Below the information on this course if you are interested in knowing more: