In the human brain, "learning" is a very broad term. It takes many forms, from classical and operant conditioning to one-shot memorization of faces and even in some cases eidetic memory for mathematical equations or chess boards or the surfaces of musical instruments. Our brains use all of these forms, and all of the synaptic forms discussed earlier. However learning begins well before birth. Axons find their way to their targets. Synapses form, then they get pruned and some of them disappear. There are "critical periods" when connections may form quickly and with the assistance of genetically programmed neural activity, for example the retinal waves that contribute to the development of the superior colliculus, and the mapping of the auditory pathway from the inferior colliculus over the retinotopic map in the superior colliculus (the alignment of this map is essential for orienting and navigation).

Retinal Waves

Since we've already looked at the visual system and the oculomotor system, let's use these systems as examples for some specific developmental processes. We'll begin with the waves of electrical activity in the retina. These waves begin long before birth, even before rod and cone maturation and before functional vision is possible. In humans, the retina forms from the anterior neural plate. Around 3-4 weeks the optic cup differentiates into two layers, the inner layer becomes the retina and the outer layers becomes the pigment epithelium that will abut the photoreceptors. By 8 weeks the neural retina already contains photoreceptors, bipolar cells, and ganglion cells, and the retinal layers are in place. The inner and outer synaptic layers are maturing around 16 weeks. They are due to the activity of a particular kind of amacrine cell, called starburst amacrine. They begin at the periphery of the retina, around the outer boundary, and move inward as spherical waves. This activity induces direction sensitivity in the plastic synapses feeding the retinal ganglion cells. The direction of these cells ends up aligned with the "optic flow" that the organism experiences when it's moving forward in its environment.

The mechanisms associated with retinal wave activity begin with spontaneous neural activity, and include changes in neurotransmitter action. In the early retina, the neurotransmitter GABA is initially excitatory, and then becomes inhibitory once spontaneous activity has occurred. Spontaneous activity is ubiquitous in the brain, and its character can help determine the subsequent synaptic development. In the retina, early spontaneous activity involves primarily ganglion cells and amacrine cells. Before birth, there are retinal waves mediated by non-synaptic currents (probably involving gap junctions). From birth for about 10 days, waves are mediated by nicotinic acetylcholine receptors on the ganglion cells. From 10 days till 2 weeks, waves involve ionotropic glutamate receptors.

Retinal waves can be visualized with calcium imaging and multi-electrode arrays. They can be seen engaging both amacrine and ganglion cells. Waves continue during adulthood, however they acquire a different character. They become involved in things like the retinal shift effect, which is mediated by amacrine cells. The psychologist Alberta Gilinsky studied several forms of perceptual alterations caused in the retina itself, including judgements of size and distance.

Looming Reflex

Another example of specific development is the looming reflex, which also involves the superior colliculus. The looming reflex is especially prominent in rodents, that are prey for large birds flying overhead. A dark shape presented in the upper periphery of a rodent retina will cause an avoidance reaction to the opposite side. This reaction is mediated by the superior colliculus, which receives retinotopic input from peripheral magnocellular neurons in the retina that are sensitive to both motion and direction. In humans this reflex is expanded to include objects that appear to be moving rapidly towards oneself, and it usually includes a startle or flinch, some eye movements, and autonomic changes like increased heart rate or pupil dilation, as well as an orienting (avoidance) reaction. (and see Thieu et al 2024)

The looming reflex does not require visual input to develop, although it does become more specific with age. It develops before birth.

Recovering Spike Trains From Phase-Encoded Signals

The phase encoding of spatial and temporal information in the hippocampal region does not encode absolute time. It only encodes the sequence of events. How does one recover precise spike timing information upon playback? The short answer is, one doesn't. Precision in spike timing comes from somewhere else. The purpose of precise spike timing is to match environmental requirements, and so the playback is variable depending on the timing of events. However the interesting thing about the phase encoding is it's time-invariant, so sequences can be played back quickly or slowly and still retain proper ordering.

In general there are four methods for recovering spike timing from a phase encoded signal. If you know the original encoding frequency and phase, you can use it to recover spike times, but unfortunately the original frequency and phase are probably not reproducible in the stochastic and noisy brain. You can use an inverse Fourier transform, which is a mathematical procedure that would require specific brain wiring, and there is no evidence for such a thing at this time. You can cross-correlate with a known reference oscillation, and this is a usable method but it only provides estimates, not ground truth. And finally, there is spike train resampling, which would necessarily use interpolation or a delay line mechanism to recover precise timing. Somewhere between methods 3 and 4 is where the brain ends up, it's very good at sampling and correlation.

For modeling purposes, tools like FieldTrip and Elephant are available for spike train processing, analysis, and resampling.