As partly distinct from the rest of the brain, the optic system seems to be a relatively clearly perceived entity. Far from simple in functioning, its outlines can be categorized into the eye and its structure, the cells of the retina, the optic nerve pathways and the brain areas which the optic nerves lead to. Many structures can already be explained in remarkable detail, however, the current challenge lies in explaining the way images form from the signals initiated by the retinal cells.
Most of the axons from the optic tract innervate the lateral geniculate nucleus (LGN) of the dorsal thalamus, where the information is passed onward to cortical areas of the occipital, temporal and parietal lobes. Around two dozen cortical areas have been identified to be part of visual information processing, many of which functions are still largely unclear. However, it seems different parts manage different aspects of the processing. E.g. from the two large-scale cortical streams involved, the dorsal stream appears to analyse visual motion and visual control of action, while the ventral stream is thought to be involved in building a perception of the visual world and recognition of objects.
For me, the most devouring question lies in how in the world are the initial electrical signals transformed into a subjective experience of seeing? Where in the brain does the image of the visual field reside?
Apparently, the current hypothesis of perception is that certain groups of neurons, receptive fields, are activated according to different objects of the physical world (e.g. the face of my clamorous nocturnal neighbor which occasionally resembles a punching bag). Yet, this approach opens up more questions than it answers: concepts of objects are also utilized in the act of thinking. How do thoughts utilize the concepts built by the visual system? How do initial concepts form? Which was first: the concept or the visual? Where do thoughts come from and who does the thinking? How did this text come into being, and is it understood by anyone?
Neurotransmitter Systems (ch. 6)
This post is a little late, but the reason is quite understandable as the weeks topic was one of the hardest to comprehend and digest. Putting it plainly, chemistry has never been my strongest subject so the amount of effort in googling and note taking of chapters 5 (last weeks chapter, but required for this weeks understanding) & 6 took some time. It took three times of reading the chapters through to be exact. No joke!
From neurotransmitter systems to neurotransmitter chemistry the exact mechanisms that allow for pre- & postsynaptic neurons to relay messages fast through transmitted-gated channels and slower through g-protein-coupled receptors opened my eyes to the complexity and thereby the weaknesses of our neural system. I’ve always been fascinated about how our brain can ignite memories, emotions and movement coordination with such precision. To top this, it’s amazing that there are only three types of neurotransmitters that do all of it – amino acids, amine and peptides. What creates differences is where these messages are being sent (PNS or CNS), the type of presynaptic neuron sending the neurotransmitter and the postsynaptic neuron receiving. Even the thought of the multitude of different combinations and arrangements of subunits of receptors gives rise to numerous outcomes of what happens in signaling. As said in the book:
“The immense chemical complexity of synaptic transmission makes it especially susceptible to the medical corollary of Murphys law, which states that if a physiological process can go wrong, it will go wrong.” – chapter 6, page 131
But again it was interesting to read on all the things that could go wrong! The most interesting being about cell death and how easily it can happen. And mammalian brain cells don’t regenerate so we are stuck with what we have. Glutamate the most abundant neurotransmitter is also a neuron killer when blood flow ceases. Within a few minutes permanent damage is done. With the production of ATP stopped membranes depolarize, and Ca2+ leaks into cells causing rapid depolarization of neurons. This overexciting of neurons is called excitotoxity and is equivalent to neurons digesting themselves.
What are my thoughts on all of this? Well I came to thinking about migraines. I’ve suffered from them almost my entire life and it would be interesting to find an answer to what causes them. Its said to be a chemical imbalance in the brain involving the nerves and blood vessels, but what exactly causes them is still unknown. Could it be an underlying problem with a neurotransmitter or receptor? Or a neuro transporter issue?
I don’t have any more enlightening thoughts, but hope the following weeks readings won’t be as hard to digest 😀
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. Continue reading