I'm going to drop off all my neural questions that books have so far not given me answers for.
Two neural signaling questions, which, if I'm not mistaken, haven't seen application in neural networks as yet, and one fMRI scan question:
1) "5-HT is thought to be released from serotonergic varicosities into the extra neuronal space, in other words from swellings (varicosities) along the axon, rather than from synaptic terminal buttons (in the manner of classical neurotransmission). From here it is free to diffuse over a relatively large region of space (>20µm) and activate 5-HT receptors located on the dendrites, cell bodies and presynaptic terminals of adjacent neurons." Norepinephrine, or so I've read, also tends to find itself swimming in the extra neural space (cerebrospinal fluid I believe?) and seeking out appropriate receptors or means of metabolic degradation.
Is the extracellular diffusion of serotonin and norepinephrine (i.e. aim axon at neural cluster, spray) considered to be the functional systematic cause of sensitization, say, with animals in shock therapy sessions? I would assume serotonin's 2nd messenger signal cascade transcripts proteins from DNA to grow new synapses which add more noise into the neural network. This would smooth out over time via positive/negative feedback and prune the synapses within the grander systems of LTP/LTD, synaptic scaling and metaplasticity.
Any thoughts as to why we haven't seen this modeled in neural networks? And slaps on the wrist for my logic are also welcome.
2) Dendritic branching is what gets me the most.
..................D
.....B........../.
A...|....C.../..
..\ /......\ /....
...\......../.....
....|...../.......
[Cell Soma]
.......||.........
.......||.........
.......||.........
....../|\.........
A,B,C,D symbolize synapses.
Do signals decay as they travel afferently toward the soma?
i.e. if synapse D gets a weak signal (EPSP), if the signal is weak enough, can it decay before it reaches the Cell Soma?
Can signals that encounter branches on their afferent way down toward the soma travel efferently up the encountered branch?
i.e. if synapse A recieves an Action Potential, will it travel towards the Cell Soma AND up the branch it encounters along the way to fire synapse B?
When any signal, whether bona fide action potential or merely an EPSP/IPSP reaches the Cell Soma from one Dendrite Trunk (the trunk holding Synapses A and B ), will it travel down the axon AND up other Dendrite Trunks (the trunk holding Synapses C and D )?
If this actually happens, wouldn't that create an exponentially perpetuating signal? Well, assuming there were cautiously maintained and balanced excitation/inhibition currents, maybe not. If this isn't the case, then I guess the ratio of ~1000 dendrites per one axon helps keep the signals specialized and efficient.
Not to mention Dendrites rarely have transmitters to release. But rarely doesn't mean never: [Search Pubmed for PMID: 37984 - (sigh) that's annoying that I'm not allowed to post URL links in this forum]
3) And one last thing.
fMRI scans show us the vaso-constriction/dilation of blood vessles feeding astrocytes and the rest of the blood/brain barrier, ultimately transport nutrients (amino acids to make monoamine transmitters, electrolytes, etc.) to neurons.
Does anybody know where the signal comes from that decides to flood specific areas of the brain with blood and not others?
Is this a chicken or the egg question? Do action potentials attract blood flow around them (sucking up oxygen for ion channel pumps), or do vasoconstricting Hormones (like Vasopressin) that are already in the blood expand/contract blood vessels in areas of the brain first?
And all stressed/anxious/concentrative mental states (not to mention amphetaminically and entheogenically induced states) raise (and sometimes lower) blood pressure.
Does a raise in blood pressure primarily speed up cell metabolism and that can be considered the cause for the unusual feeling of "heightened senses" we find ourselves in when in a fight/flight situation or in a drugged state?
Or does a raise in blood pressure effectively make an fMRI scan generally more active. So that it's really the increase in Vessicle leakage into the synaptic cleft that accounts for the "heightened senses"?
