Interesting. Do astrocytes actively alter this weighted effect in the neurons (similar to the backpropagation ML algorithm formula) in each individual, or, does it maintain a set weight with each individual? The differences between each of us, of which constitutes our individual attributes of memory strength and/max limitation. Also, I have avoided calcium for many years fearing they block arteries in the brain through calcification.
You're asking a simple question with a very complicated answer. I'll try to answer in less than 1000 words.
Astrocytes are known to sequester extracellular calcium. Why is this important?
Well... the answer has to do with the two main types of glutamate receptors: NMDA and AMPA.
Glutamate is the primary excitatory neurotransmitter in the brain, especially in the cerebral cortex, but also in the hippocampus and other important areas.
Some synapses have NMDA receptors, some have AMPA, and some have both. The NMDA receptor (NMDAR) is the key. These are the ones most affected by "learning rules", which the neuroscientists call "plasticity".
The NMDAR is a voltage gated cation channel. Normally it is blocked, by a big magnesium ion. When the channel is blocked, calcium can't get in.
However the other receptor type, the AMPAR, isn't subject to such blockage, so when the synapse becomes active it depolarizes the membrane, which causes the magnesium ion to dissociate from the NMDAR, which in turn lets calcium in.
The influx of calcium causes further depolarization, which may lead to a "dendritic spike" which is a mini action potential that travels locally in the dendritic tree. In theory if it's strong enough it can make it all the way down into the cell body, causing the neuron to fire with a "real" action potential, which then travels down the axon and affects other neurons.
But most of the time a dendritic spike isn't strong enough to make it all the way down the dendritic tree into the cell body. Instead, it only travels locally in the dendritic tree, meaning it only affects "nearby synapses". Why is this important?
It's important because of something called "spike timing dependent plasticity", or STDP. So now we're talking about learning rules. STDP means the synaptic weight changes based on temporal correlation - like, if the presynaptic and postsynaptic neurons are active at the same time, the synaptic weight increases. ("Neurons that fire together, wire together").
So, if there's no calcium available to enter the cell, the dendritic spike will never happen, which means STDP won't happen and no learning will take place.
By regulating the available calcium, astrocytes can determine when and where learning takes place.
To answer your question then, yes there are certainly chemical kinetics which don't vary from one individual to the next. However - the shapes of neurons and astrocytes are highly variable between individuals, they're unique like fingerprints.
As close as we come to understanding dendritic branching is the "cable model" of Wilfrid Rall, which is an approximation based on compartments (short segments of varying diameters).
www.scholarpedia.org
Dendritic spiking though, is considerably more complicated. Dendrites have synaptic "spines" which are little mushroom-shaped boutons with tiny stalks and very high input impedances. We don't yet know how these interact with NMDAR and AMPAR.
The synapses occur on the spines, they're isolated from each other by the stalks. We do know however that long term learning is associated with RNA that travels up from the cell body into the spines, where it locally makes proteins. Some of these proteins regulate the number and position of the NMDA and AMPA receptors in each synapse, as well as their turnover rates.
