Write4U
Valued Senior Member
I agree. This behavior is apparent in the Parmecium which does not have a neural network but it does have cilia.Survival from stress involves moving away from the stress and the chemical reaction (within the organism) undergoing the stress react (under physic / chemical) processes (non sentient)
Thus, Paramecia are brainless but sentient or at least proto-sentient.There are two types of cilia: motile cilia and nonmotile, or primary, cilia, which typically serve as sensory organelles.
And learns to synthesize Adrenalin,If unable to move away will adapt
a hormone secreted by the adrenal glands, especially in conditions of stress, increasing rates of blood circulation, breathing, and carbohydrate metabolism and preparing muscles for exertion.
"performing live really gets your adrenaline going
"TRADEMARK"; the hormone epinephrine extracted from animals or prepared synthetically for medicinal purposes.
I tend to agree, but I've always wondered, why C elegans, a worm with a well mapped neural network does not respond to pain. According to Hameroff the worm has a neural network but it isn't used for "pain" transmission. The reason is that the worm has no cilia (surface receptors) to detect any introduced surface stimulation.No. Pain requires a pain network. A upway path to, a HQ to decide "it hurts" or it's "OK" and, a downward path to send instructions for the action / non action to be taken
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Thus the single celled Paramecium feels "stress" from it's cilia, the worm C. elegans cannot, in spite of its neural network. The worm was stimulated with an electric shock, but just laid there. No pain response.
https://www.livescience.com/50087-brain-pain-meter.htmlThe brain's "pain sensor" has been found, researchers say. When you step on a thumbtack or hit your funny bone, this is the part of your brain that lights up.
https://www.ncbi.nlm.nih.gov/books/NBK216/Significant photophobia is usually associated with more severe ocular surface disease or, more likely, intraocular inflammation. The pain induced by exposure to bright light represents ciliary muscle spasm and explains the use of parasympatholytic drops such as atropine in iridocyclitis; painful spasm is prevented by pharmacologically paralyzing the ciliary muscle.
It looks like cilia are a common denominator in all organisms with ability to "feel", and a neural network is required to transmit the sensation of "feel" to a central processor.
Is the microtubular "sensor/transmitter" (cilia), and the neural "transmission distribution network", terminating with the translation of the transmitted signals by "microtubules in the brain"?
Seems logically efficient to me.
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