jnmaciuch
Senior Member (Voting Rights)
A single neuron or even a small circuit potentially causing ME/CFS symptoms is improbable, because of basic mechanisms that prevent repeated firing and subsequent metabolic injury. It doesn’t take much firing to cause a build up of inhibitory adenosine that suppresses continued firing (discussed here). A failure of this fundamental mechanism would most likely result in epilepsy-like phenomena and neuronal death.
The parts of the brain that need to continuously fire likely manage this by spreading out the load over a larger group of neurons. So in order to keep up a sustained signal which is as constant as our symptoms, it would need to be a larger neural circuit. Which then begs the question that Snow Leopard brought up—even crude techniques are capable of seeing e.g. continuous activity in the medulla.
The parts of the brain that need to continuously fire likely manage this by spreading out the load over a larger group of neurons. So in order to keep up a sustained signal which is as constant as our symptoms, it would need to be a larger neural circuit. Which then begs the question that Snow Leopard brought up—even crude techniques are capable of seeing e.g. continuous activity in the medulla.
I agree, it is only an assumption that all perceptions/neural phenomena creating noticeable changes are inherently the result of “de novo” neuron firing as opposed to just modulation of existing firing patterns—which could be caused by something like cytokines acting on many regions of the brain, if the paper I posted earlier on meningeal CXCR5 mediating sickness behavior in mice is any indication."Fatigue" doesn't have to be "encoded" at all. We do know that feedback from peripheral afferents in muscles reduces the excitability of the motor cortex (this is central fatigue).