For decades, Fu and his team at University of California San Diego School of Medicine studied a protein called PTB, which is well known for binding RNA and influencing which genes are turned "on" or "off" in a cell.
Just a single treatment to inhibit PTB in mice converted native astrocytes, star-shaped support cells of the brain, into neurons that produce the neurotransmitter dopamine.
The treatment works like this: The researchers developed a noninfectious virus that carries an antisense oligonucleotide sequence -- an artificial piece of DNA designed to specifically bind the RNA coding for PTB, thus degrading it, preventing it from being translated into a functional protein and stimulating neuron development.
The researchers administered the PTB antisense oligonucleotide treatment directly to the mouse's midbrain, which is responsible for regulating motor control and reward behaviors, and the part of the brain that typically loses dopamine-producing neurons in Parkinson's disease.
We found that practitioners generally had to choose between several algorithms, each with significant trade-offs such as robustness to different kinds of visual “noise” (for instance, texture), even in images much less complex than the natural images in ImageNet. For instance, this answer on StackOverflow claims “The problem [of curve detection], in general, is a very challenging one and, except for toy examples, there are no good solutions.” Additionally, many classical curve detection algorithms are too slow to run in real-time, or require often intractable amounts of memory..
Images that cause curve detectors to activate weakly, such as edges or angles, are a natural extension of the algorithm that InceptionV1 uses to implement curve detection.
Every time we use feature visualization to make curve neurons fire as strongly as possible we get images of curves, even when we explicitly incentivize the creation of different kinds of images using a diversity term.
Like the tip of the branch, this is the part where the cell can further develop and extend, either in original growth, in regeneration, or as a reaction to some factors (including a decrease in overall electric activity which causes a form of synaptic scaling – hence explaining the „devouring” of unused neural pathways of amputated body parts by nearby active structures).
There isn’t that much literature about it, unfortunately, so what I’m doing here is more of an (un)educated guess, but since guidepost cells tend to be neurons which have yet to develop an axon – but already have dendrites and can receive signals, a slightly more complex – but better targeted – system can be imagined, where guidepost cells would be a part of a wider neural network, the stimulation of which „calls forth” further cells to build connections.