Slow periodic activity in the longitudinal hippocampal slice can self‐propagate non‐synaptically by a mechanism consistent with ephaptic coupling
Slow oscillations are a standard feature observed in the cortex and the hippocampus during slow wave sleep. Slow oscillations are characterized by low‐frequency periodic activity (<1 Hz) and are thought to be related to memory consolidation. These waves are assumed to be a reflection of the underlying neural activity, but it is not known if they can, by themselves, be self‐sustained and propagate. Previous studies have shown that slow periodic activity can be reproduced in the in vitro preparation to mimic in vivo slow oscillations. Slow periodic activity can propagate with speeds around 0.1 m s−1 and be modulated by weak electric fields. In the present study, we show that slow periodic activity in the longitudinal hippocampal slice is a self‐regenerating wave which can propagate with and without chemical or electrical synaptic transmission at the same speeds. We also show that applying local extracellular electric fields can modulate or even block the propagation of this wave in both in silico and in vitro models. Our results support the notion that ephaptic coupling plays a significant role in the propagation of the slow hippocampal periodic activity. Moreover, these results indicate that a neural network can give rise to sustained self‐propagating waves by ephaptic coupling, suggesting a novel propagation mechanism for neural activity under normal physiological conditions.
Abstract isn't so flamboyant as the linked article
here is a recent review: http://sci-hub.tw/https://www.sciencedirect.com/science/arti...
Frequency of Brain Waves
State Frequency range State of mind
Delta 0.5Hz–4Hz Deep sleep
Theta 4Hz–8Hz Drowsiness (also first stage of sleep)
Alpha 8Hz–14Hz Relaxed but alert
Beta 14Hz–30Hz Highly alert and focused
But when a gap of 400 microns is added (4.C), the signal doesn't propagate.
I'm sure that the actual cutting causes some damage, and perfect realignment is unlikely, but I'm not sure how this is conclusive of ephaptic coupling, or how it eliminates the possibility of electrical or chemical communication by synapse, gap junction, or axonal transmission.
Instead, the transmissible gap is poorly characterized—-they cut then stick the slices back together. Depending on how clean the cut is, the gap could be quite small. Yet they argue that this unknown small distance (which presumably still contains a fluid interface) is enough to eliminate the usual explanations. That argument feels undersupported to me.
I think you’re probably right that they are, but there’s still an on-going and fairly contentious debate over the extent to which the LFP reflects vs. changes transsynaptic currents.
I wonder if this might be a basis for a biological means for "backpropagation"?
I know about chemical synapses (the "usual" synapses with gain, and which we model with weights in artificial neural networks, and which transmit information in forward mode), I also know about electrical synapses (fast, no gain, bidirectional, possibly mediator of the backpropagation signal?) but I don't know what they refer to with "axonal transmission" ? surely they don't just mean pulse propagation along the axon, can someone point me to the accepted mechanism of axonal transmission across neurons? from cell body to synapse is just transmission line along the same neuron...
also correlation is not necessarily propagation, consider for example shining a laser dot on a distant wall, and rotating the beam such that the spot moves faster than light: this is perfectly possible, but no physical signal is moving faster than light, rather the dot at some initial time and the dot at a later time are correlated, but are both the result of a laser reflecting of a rotating mirror.
in order to eliminate a mutual cause, you dont make a local cut in some neuronal tissue, you fully separate the tissue, and then measure their electrical activity (preferably optically using a nematic liquid crystal as they used in the past to inspect voltage levels on chips under microscopes) while mounted on micron precision translation stage, and starting from a distance, slowly have the samples approach and measure their correlation, and do the same experiment without a neuron culture, because the correlation may be due to stray electric fields from the environment (another common cause, like the laser for the lightspeed dots)
use 2 different wavelengths (and corresponding filters at the detectors) of light to measure the optical activity of the nematic liquid crystal sensors, in order to make sure no light is leaking through...
According to wikipedia https://en.wikipedia.org/wiki/Axonal_transport :
>Since some axons are on the order of meters long, neurons cannot rely on diffusion to carry products of the nucleus and organelles to the end of their axons.
>Vesicular cargoes move relatively fast (50–400 mm/day) whereas transport of soluble (cytosolic) and cytoskeletal proteins takes much longer (moving at less than 8 mm/day).
note that the flow of material in axonal transport is retrograde (i.e. in the opposite direction of pulse transmission), so any feedback, adjoint sensitivity or backpropagation signal - if it exists - to implement Automatic Differentiation in a physical manner, might move at such speeds. I don't know the typical axon lengths (please tell me if you know or can refer me to measured distributions of axon length), but this maximum of about 1000mm implies 125 days (8mm/day) or 2.5 days (400mm/day). If we assume the dimension of the brain as a typical axon length i.e. 10cm = 100mm then this becomes 12.5 days (400mm/day) and 0.25 days or six hours (8mm/day). For 1cm we have 30 hours (8mm/d) and 36 minutes (400mm/d). For 1cm to 10cm typical axon lengths and shorter indeed seem like the kind of time frame of learning, i.e. the weights may be modified during sleep, and the delay line of materials undergoing axonal transport in each axon contain echoes or memories of synaptic activity during the day.