Receptors of consummated or imminent necrosis


There are no pain receptors. Only perceptors, ie, suffering, receiving, addressee individuals of that hurting event that arises from the brain to catch your attention and behavioral involvement in a threat assessment. Danger! Pain!

What DO exist are the ones called NOCI-CEPTORS by Nobel Laureate Charles Sherrington: noxiousness detectors. That was back in 1906.

Nociceptors are neurons that specialize in the detection of states and agents with a violent destructive capacity: extreme temperatures, mechanical energy that’s higher than the physical strength of tissues, acids, lack of oxygen … Danger-detecting neurons are distributed over the surface and inside of the body and on their terminals they have receptors or sensors of dangerous stimuli. The receptors are proteins embedded in the membrane that, when contacting with a noxious agent, suffer a transformation that leads to the opening of a channel through which ions enter, ie, an electrical current. This electrical signal is transmitted to various processing centers and contains information on risk in a particular point. The danger may be mechanical, thermal or chemical.

Under normal conditions, nociceptors are only stimulated with what violently destroys tissues. If there are no extreme temperatures, acids, low oxygen or destructive mechanical stimuli, no signal is generated. There are no alerts of damage projected to the brain. Usually, the projection of pain doesn’t arise from the brain. The alarm doesn’t go off.

When a noxious agent has destroyed tissue, the dead cells (necrosated) release molecules that induce a change in the sensitivity of nociceptors. They make them respond to innocuous stimuli. Touching a wound generates a signal in sensitized nociceptors. Information on activated nociceptors reaches the brain and the brain projects pain on that area. While proceeding to repair the injury, the area is sensitive, with the population of nociceptors adapted to the state of vulnerability.

As the injury is being repaired, nociceptors go back to their basal state and innocuous stimuli stop generating signals. The brain is no longer informed with news of danger. The brain doesn’t project pain, it warns. The individual resumes normal activity. End of the repair process. Tissues in condition to be used. Innocuous stimuli no longer activate the nociceptors.

Nociceptors respond to local, real, actual danger at that time and place. If there is necrosis (violent cell death) or if it’s about to happen if the conditions don’t change inmediately, (I quickly move my hand away of the burning pan) the danger and consummated necrosis sensors generate a signal and, predictably, this will be enough to activate the perception of pain from the brain.

Nociceptors also respond to the prediction of danger from the various processing centers. The indication of warning, vulnerability, can be generated from above, memory and prediction systems and induce sensitization. Innocuous stimuli will generate a signal of nociceptors even when nothing dangerous is happening.

The central alert states, activated by threat assessment in the absence of consummate or imminent harm, facilitate the traffic and generation of nociceptor signals. The pain is projected from the brain in advance with no need of prior injury notifications. There is only prediction. Enough to activate perceptive messages of pain.

The central alert ends up sensitizing all the layers of processing, from the nociceptors to the conscious individual (the receptor of pain). There are warning signals everywhere. From the individual (“it hurts me”) to the sensitized nociceptor that generates a damage signal without damage.

The pain only certifies an assessment of danger. It doesn’t certify damage and the danger assessment doesn’t have to be correct.

There is erroneous inflammation (allergy) and erroneous pain (migraine, fibromyalgia…). Nociceptors in erroneous pain are sensitized.

It doesn’t hurt because there are sensitized nociceptors in the erroneous pain. It’s not the nociceptors that are wrong and have been activated for no reason. It hurts because the nociceptive system as a whole has generated a condition assessed as threatening. This includes global sensitization.

Sometimes it’s all about the facts, the burn, infection, lack of oxygen, consummated or inminent necrosis. Other times it’s about memories, fears, uncertainty, misinformation, unjustified neuronal alarmism.

The professional must assess both factors: vulnerable tissues and/or sensitizing brains and try to deactivate alarms, giving back the normal condition to the tissues and a reasonable confidence to the assessment centers.

The goal is not analgesia at any price, but the recovery of the integrity and body management from a reasonable management of danger.

Maintaining the security of the building with a chronically turned on alarm makes no sense.

Neither does disabling the siren to generate the fiction that if it doesn’t sound, there are no thieves.

The nociceptor is not a pain receptor, whoever says so…


>Generation of a necrotic signal (consummated or imminent)



Neuronal sensors of consummated or imminent necrosis convert (transduce) the threatening event into an electrical signal. Each affected point emits a tiny current which diffuses through the membrane of the neuron and the surrounding tissues. The tiny sparks are put together and when it reaches a specified voltage at the confluence of all these, some voltage sensors (voltage-sensitive channels) generate the so-called action potential, an electric current that runs along the membrane of the vigilant neuron carrying information that says that at the point the neuron controls there is necrosis (violent death of cells) and states or agents capable of causing it.

– Cells are dying! (consummated necrosis). Danger! Do something about it, fast! (imminent necrosis)

Information, electric currents and data on what is happening in a certain time and place, runs through vigilant neurons.

Cells can’t defend themselves. They can’t escape, dodge … they are fixed. They can’t cry or ask for help either. They just die violently. They get burned, frozen, torn, infarcted (due to lack of oxygen), corroded… The necrotic cell swells, its membrane breaks and molecules are spilled out, molecules that only exist inside conveniently controlled. It is as if there was a gas fugue in a home. There would be gas detectors that would say: ‘Gas, gas, gas, gas! here and now.’

Obviously if there is gas in the air, something has happened. It’s not normal and it’s dangerous. The cause of the fugue must be found.

Here come into play vigilant neurons with their thermal, mechanical and chemical sensors. Neurons sensitive to the state-agent responsible for the escape come out. If it’s the heat, neurons with thermal sensors come out; if it’s the lack of oxygen, acid-sensing neurons; if it’s a stretch or compression, neurons with mechanical sensors.  

The vigilant neuron collects two types of data: consummated necrosis (Yes or No) and presence of the agent and threatening state (temperatures, acids, mechanical energy states…)

– Danger, danger…! High temperature, compression, stretching, acids. Cells have already died … or: so far no victims… But do something about it soon!

Vigilant neurons of consummated or imminent necrosis do not flinch when danger is only theoretical, possible… Being near a fireplace, a skewer, a jar of sulfuric acid, a poisonous mushroom… it doesn’t activate any sensor of noxiousness. The facts must be consummated.

Vigilant neurons do not generate signals like “you’re next to the fireplace, you can get burned if you get too close” … The proximity to danger does not affect them. It feels cozy and warm next to the fireplace, 27ºC (80ºF) … Neurons sensitive to heat danger come out when the temperature reaches 45ºC (113ºF).

Neurons can’t generate data of what type of agent is responsible either. There are no fireplace, hot pot, rose spike or Amanita phalloides sensors. They don’t report dangerous objects, but dangerous energy: thermal, chemical, mechanical … They inform about where, when and how but, on what, they just report the kind of energy responsible for it.

Dead cells do not release pain signals. The dead don’t talk. They generate information of them being dead, but don’t ask for help. The vigilant neurons don’t have any receptors, pain sensors of necrotic cells.

There are no pain receptors. Yes, I know you already know this, but many textbooks keep describing them.



The environment contains all kinds of states, agents and events. Living beings obtain information about them through sensors, sensitive proteins capable of undergoing a change in contact with a particular physicochemical variation.

The receptors of the retina are sensitive to changes in the light reflected on objects; the ear ones, to the mechanical waves generated by interactions of objects; the smell and taste ones, to molecules with information about various elements of the environment, appetitive and/or adverse …

There are light receptors, mechanical receptors, thermal receptors, chemical receptors… and there are also necrotic damage (consummated or imminent) receptors.

The body is packed with sensors-receptors of consummated necrosis, located in the membrane of specific neurons and immune system cells, vigilant, capable of detecting violent cell death (necrosis).

Receptors of the retina (photoreceptors) detect light, photons, and the vigilant neurons of necrosis (nociceptors) detect signs of necrosis. If there is no light, there is no activation of photoreceptors. If there is no necrosis, there will be no activation of necrosis sensors (truism).

The necrotic cell loses membrane integrity and internal chemicals are released. Necrosis receptors pick them up and the reaction ‘molecules-death—necrosis sensor’ generates an electrical signal that contains information about the deadly incident, an electrical signal that is carried by the neuron to various assessment and defensive response centers.

In threat of imminent but not consummated necrosis, neurons and immune vigilant cells detect dangerous agents and states: extreme temperatures, germs, mechanical stimuli, lack of oxygen, acids… Membrane sensors react to such agents and states and report the hazard and the need to respond to the threat. Signals of necrosis danger are produced, but not signals of consummated necrosis.

In imagined, probabilistic, speculated necrosis, no nociceptors are activated for the same reason as in the dark no photoreceptors are activated or in the silence no ear receivers are activated.

In the absence of sensory activation (light, sound waves, aromatic molecules, extreme hot and cold, stretches, mechanical compressions, insufficient oxygen quantities, pH…) the brain can activate the areas responsible for visual, sound, touch, scent, taste perception, and generate a mild and fading perceptual version. We can imagine tastes, smells, sounds, images, pain, hunger…

Usually the absence of sensory signal contains the imaginative function, it reduces it to something very subtle and inconsistent.

When we sleep, sensory inputs are disconnected. The imaginative brain processes past and future sensory data, real and fantastic, constructs impossible narratives, free ones. The brain dreams, plays with the real and the unreal. The perception becomes realistic, hallucinatory. It doesn’t need any senses. They are an obstacle.

Reality can be experienced or imagined. Senses hold the imagination but don’t always succeed at doing it.

The IASP says (International Association for the Study of Pain) that pain is an unpleasant sensory and emotional experience. I disagree. Current sensory experience is not needed. Consummated or imminent necrotic damage sensors can be mute.

“… Vision is a sensory experience …”. Not always. Sometimes we see things that are not there. There is no activation of photoreceptors, but apparently what we see is real.

– Does this mean that my brain has hallucinations, delusions of mind?

– It creates hallucinatory states of imminent necrotic damage, but not mental delusion or madness. It’s just wrong. It rates some non-existent threats as true. It doesn’t wait until necrosis occurs. It tries to prevent danger. Turn on the pain…