Failure of Neuroscientists to explain information storage
According to Neuroscientists, synaptic plasticity is the candidate explanation for information storage. The outstretched surface of a neuron meets and communicates with neighboring cells at junctures called synapses. At a given time, a single neuron may receive input at hundreds of these. Researchers have long known that information is stored when the strength of these connections change, a process called synaptic plasticity. Synapses are supported on tiny mushroom-shaped spines, a multitude of which sprout from dendrites that branch out from neurons. Neurons use dendritic plasticity to adjust how they respond to incoming signals that target the neuron's dendritic branches. This feature changes the ability of the synapses on those branches to communicate information to the next neuron. Dendrites, the large branches that extend from the main body of a neuron, are covered with receptors that collect signals from other neurons. When bursts of neurotransmitter from a nearby neuron land on a dendrite's receptors, they trigger an electrical wave called a local dendritic spike. If the local dendritic spike is powerful enough it can propagate to the main body of the neuron, generating an action potential output or nerve impulse. The new research by Jeffrey C. Magee and his colleagues at HHMI's Janelia Farm Research Campus shows that neurons can fine tune their information processing through a mechanism that the researchers call “dendritic plasticity.” It was known that intermittent input from nearby neurons can trigger weak dendritic spikes that typically remain in the dendrites, as they are not strong enough to travel all the way to the main body of the cell. However, if these local spikes showed plasticity, adjusting themselves to become stronger after repeated input, they could eventually generate a nerve impulse, providing a means of information storage different from that produced by synaptic plasticity. The researchers also analyzed the effects of stimulating multiple dendritic branches. Magee explained that as repeated signaling increases the strength of a synaptic connection, a process called long term potentiation (LTP), this would increase the input onto a particular dendritic branch. In terms of information storage, the localized dendritic plasticity could enable neurons to store the repeated occurrence of particular patterns of neuronal activity that could represent a complicated stimulus.
But how can we explain the case of paramecium & bacteria or life forms without any neuron? How are numbers encoded this way in our brain?
LTP is similar to charging of a capacitor; storing local dendritic spikes unless the potential is strong enough to be discharged as a nerve impulse. But with that very discharge, doesn’t the cell lose the information contained in that electrical signal? Plasticity offers nothing more than a positive feedback. Is just a positive feedback enough to prove that it offers for signal storage?
I am not saying that dendritic plasticity has no role to play. It is for this very special feature of neurons that they are the signal carriers & not any other cell, not even glia.
But how can we explain the case of paramecium & bacteria or life forms without any neuron? How are numbers encoded this way in our brain?
LTP is similar to charging of a capacitor; storing local dendritic spikes unless the potential is strong enough to be discharged as a nerve impulse. But with that very discharge, doesn’t the cell lose the information contained in that electrical signal? Plasticity offers nothing more than a positive feedback. Is just a positive feedback enough to prove that it offers for signal storage?
I am not saying that dendritic plasticity has no role to play. It is for this very special feature of neurons that they are the signal carriers & not any other cell, not even glia.