SNNs more closely resemble the function of biological neurons and are perfect for temporally changing inputs. I decided to teach myself rust at the same time I learned about these so I built one from scratch trying to mimic the results of this paper (or rather a follow up paper in which they change the inhibition pattern leading to behavior similar to a self organizing map; I can’t find the link to said paper right now…).

After building that net I had some ideas about how to improve symbol recognition. This lead me down a massive rabbit hole about how vision is processed in the brain and eventually spiraled out to the function and structure of the hippocampus and now back to the neocortex where I’m currently focusing now on mimicking the behavior and structure of cortical minicolumns.

The main benefit of SNNs over ANNs is also a detriment: the neurons are meant to run in parallel. This means it’s blazing fast if you have neuromorphic hardware, but it’s incredibly slow and computationally intense if you try to simulate it on a typical machine with von Neumann architecture.

I actually came across this for the first time when I was doing research into the visual pathway for the purpose of trying to structure a spiking neural net more closely to human visual processing.

The Wikipedia page mentions cephalopod eyes specifically when talking about the inverted retina of vertebrates.

The vertebrate retina is inverted in the sense that the light-sensing cells are in the back of the retina, so that light has to pass through layers of neurons and capillaries before it reaches the photosensitive sections of the rods and cones.[5] The ganglion cells, whose axons form the optic nerve, are at the front of the retina; therefore, the optic nerve must cross through the retina en route to the brain. No photoreceptors are in this region, giving rise to the blind spot.[6] In contrast, in the cephalopod retina, the photoreceptors are in front, with processing neurons and capillaries behind them. Because of this, cephalopods do not have a blind spot.

The Wikipedia page goes on to explain that our inverted retinas could be the result of evolution trying to protect color receptors by limiting their light intake, as it does appear that our glial cells do facilitate concentrating light.

However, the “positive” effects of the glial cells coming before the receptors could almost certainly be implemented in a non-inverted retina. So that’s the evolutionary duct tape I was mentioning.

It would be difficult to flip the retina back around (in fact since it originates as part of the brain we’d kind of have to grow completely different eyes), so that’s not an option for evolution.

However, slight changes to the glial cells and vasculature of the eyes is definitely more possible. So those mutations happen and evolution optimizes them as best it can.

Evolution did well to optimize a poorly structured organ but it’s still a poorly structured organ.

Honestly, it was pretty hard for me to find a source which has made me a little skeptical of my own statements.

I was able to find two case studies in which patients with liver damage that caused them to have low levels of vitamin A exhibited night blindness. Both were treated for vitamin A deficiency and saw symptoms improve.

The strongest evidence of my original claim is the fact that one of the patients had otherwise healthy eyes and vision, only having extreme trouble seeing at night. After receiving treatment for vitamin A deficiency, her night vision improved. This suggests that dark adaptation is dependent on vitamin A in the blood which is regulated by the liver.

However, I’m now somewhat skeptical and curious myself considering these two studies were almost all I could find on this topic. If I have more time I’ll try digging deeper. For now though, I’ve edited my comment with links to the studies.

I was able to find two case studies showing direct links from vitamin A levels (and liver damage) to night blindness. I’ve edited my initial comment with the links to them.

Bro myopia is the least stupid part of our eye design problems. Our retinas are built entirely backwards for no other reason besides evolution making a mistake and then duct taping over it too much to fix it later.

If your retina was the right way around (like cephalopod eyes) you would have:

• No blind spots
• Higher fidelity vision even with the same number of receptors since the nerves and blood vessels wouldn’t interfere like they do now
• much lower likelihood of retinal detachment since you could attach it for real in the first place
• possibility for better brightness/darkness resolution since blood supply could be greater without affecting light passage
• possibility for better resolution because ganglion nerves can be packed more densely without affecting light passage
• The ability to regenerate cones and rods because you could, again, ACTUALLY HAVE SUPPORT CELLS WITHOUT BLOCKING LIGHT TO THE RETINA

Our eyes are built in the stupidest way possible.

Another fun fact: retinol is regenerated by your liver. Not your eyes, not some part of your brain, not some organ near your head like your thalamus which could probably get the job done if it tried, your fucking liver. Your eyes taking a while to adjust to the dark has basically nothing to do with your eyes; it’s because of the delay in adjustment by your fucking liver to produce more retinal, dump it into your vascular system and wait for it to hopefully reach your eyes. Why are we built like this?!

Edit: A few comments asked for sources on the relation between dark adaptation and liver vitamin A. So I went looking for sources. It was honestly somewhat difficult to find information, but I was able to find two different case studies showing that night blindness in patients with damaged livers. Specifically these individuals had liver damage that affected their serum Vitamin A levels. And after raising their vitamin A levels, their symptoms improved.

This study details a patient with normal day vision and no other ocular problems besides being unable to see at night.

The patient had a medical history of stage 4 non-alcoholic liver cirrhosis, which led to a malabsorption of vitamin A, as confirmed by the very low vitamin A level in the serum analysis… …Subjective improvement in symptoms, along with better performance on visual field, were noted after initiating oral vitamin A supplementation for 6 months.

This study details a patient with night blindness caused by low levels of vitamin A presumably due to Hepatitis C.

Case description: This case describes a 64-year-old female patient with symptomatic VAD, likely secondary to liver cirrhosis in the setting of Hepatitis C. The patient presented with night blindness and blurry vision. She was successfully managed with direct replacement of Vita-min A.

These studies do show that dark adaptation is dependent on vitamin A produced by the liver, but I’ll be the first to admit it’s not exactly conclusive evidence of my initial claim that the liver must respond to dark conditions increasing retinol concentration in the blood in order for rod cells to function properly in low light conditions. That is a possible explanation for these case studies but not necessarily the only one, so take my last fun fact with a grain of salt.