Re: Is my PSTSN excitation hazardous?

Peripheral Somatic Tactile Sensory Neurons
PSTSN excitation

This question is interesting. There are the text-book type of answers for high animals (humans) where feedback control from the CNS will limit high pain so that one would pass out basically. This leads into cardiovascular control with a drop in blood pressure and reduced heart rate etc. But I think you are going with the point that this PSTSN excitation is broad but not so severe that it results in one passing out.

One can think that maybe the pain sensory tracts would still be firing even while passed out but higher brain centers don’t respond. Or, is it that the pain tracts are actually short circuited with other neuronal control? I just don’t know.

I could imagine so much stimulation of targeted neurons, that they could load up with Ca²⁺ ions that would be harmful to the cell, possibly inducing calcium induced apoptosis (cell death) as a result. But then again maybe the target neurons in the brain would desensitize to the continuous exposure to neurotransmitter. Thus, the receptors internalize or remain desensitized to the neurotransmitter and the target cell will not respond. Maybe a combination of both aspects would occur.

I am not aware of experimentation to address these points when considering many sensory neurons of various types all firing at once. I can envision some sort of electric shock model in mice or rats to then look for damage, but these would be extremely cruel experiments to conduct.
Basically I do not have an answer for you.

Further Reading:

Mattson MP, Chan SL (2003) Calcium Orchestrates Apoptosis Nature Cell Biology, 5(12):1041-3.
The function of calcium in apoptosis is particularly fascinating, particularly when we consider the prominence of calcium in regulating a multitude of ...
www.nature.com/ncb/journal/v5/n12/full/ncb1203-1041.html

RS Cantor (2003) Receptor Desensitization by Neurotransmitters in Membranes: are Neurotransmitters the Endogenous Anesthetics? Biochemistry, 42 (41), pp 11891–11897
nAChR in membranes lacking both phosphatidic acid and cholesterol differ from the structures of the agonist-desensitized neurotransmitter . ...
www.ionchannels.org/showabstract.php?pmid=14556619

Mellor JR, Randall AD (2001) Synaptically Released Neurotransmitter Fails to Desensitize Postsynaptic GABA_A Receptors in Cerebellar Cultures. J. Neurophysiol. 85: 1847-1857, 2001.
jn.physiology.org/cgi/content/abstract/85/5/1847
Abstract. GABA concentration jump experiments performed on membrane patches predict that postsynaptic GABA(A) receptors will become desensitized following the release of the contents of a single GABA- containing synaptic vesicle. To examine this we used a single synaptic bouton stimulation technique to directly examine whether postsynaptic GABA (A) receptors in cultured cerebellar granule cells exhibit transmitter- induced desensitization. In a large number of recordings, no evidence was found for desensitization of postsynaptic GABA(A) receptors by vesicularly released transmitter. This was the case even when as many as 40 vesicles were released from a single bouton within 1.5 s. In addition, postsynaptic depolarization and application of the benzodiazepine flunitrazepam, manipulations previously shown to enhance desensitization of GABA(A) receptors, failed to unmask transmitter-induced desensitization. In contrast, a single 2- to 3-s application of a high concentration of exogenous GABA was able to depress synaptic responsiveness for up to 70 s. Furthermore, pharmacological depletion of GABA eliminated inhibitory synaptic communication, suggesting that GABA is the transmitter and the desensitization-resistant inhibitory postsynaptic currents are not mediated by a "nondesensitizing" ligand such as beta-alanine. Overall our data indicate that a specific desensitization-resistant population of GABA (A) receptors are present at postsynaptic sites on cultured cerebellar granule cells.