From the world of electronic device we know the terms “transducer” and “amplifier”:
A transducer is a device that converts a signal in one form of energy to another form of energy. Energy types include (but are not limited to) electrical, mechanical, electromagnetic (including light), chemical, acoustic or thermal energy. Reference: Transducer
An amplifier is an electronic device that increases the power of a signal. It does this by taking energy from a power supply and controlling the output to match the input signal shape but with a larger amplitude. In this sense, an amplifier modulates the output of the power supply. Reference: Amplifier
The electronic device is connected by wires.
There are also “transducers”, “amplifiers” and “wires” in the human body:
Various environmental stimuli exist that initiate signal transmission processes in multicellular organisms; examples include photons hitting cells in the retina of the eye, and odorants binding to odorant receptors in the nasal epithelium. The sensory transduction is the conversion of a sensory stimulus from one form to another. Transduction in the nervous system typically refers to stimulus alerting events wherein a physical stimulus is converted into an action potential, which is transmitted along axons towards the central nervous system where it is integrated. A receptor cell converts the energy in a stimulus into a change in the electrical potential across its membrane. It causes the depolarization of the membrane to allow the action potential to be transducted to the brain for integration. Reference: Signal transduction Transduction (physiology)
The human “transducers” are the sensory receptors and the human “wires” are called neurons, axons and sensory fibers/ afferent nerve fibers. Just outside the spinal cord, thousands of afferent neuronal cell bodies are aggregated in a swelling in the dorsal root known as the dorsal root ganglion. Reference: Wikipedia.
When a ME patient no longer can tolerate sunlight, soft music, the smell of toothpaste or the weight from a blanket something must be wrong with the transducers, the amplifiers and/or the wires.
To understand the disease and the symptoms we must locate and identify the problem in the transducers, the amplifiers and/or the wires in the body.
Is there a defective amplifier in the dorsal root ganglion? In the brain? Is it out of order because of an autoimmune attack? An autoimmune attack on a receptor? Is there a domino effect involved?
I am looking for answers. Am I getting closer? Is TRPA1 involved? TRPA1 amplifies pain and inflammation. What amplifies light, sound, odor and touch?
TRPA1 - A Transducer and Amplifier of Pain and Inflammation
Excessive activation of TRPA1 and TRPV1 by ROS may induce central sensitization – does it concern ME?
Is TRPV4 involved? TRPC3? P2X3? Articles from a google-brainstorm on the subject:
Neuronal IL-17 receptor upregulates TRPV4 but not TRPV1 receptors in DRG neurons and mediates mechanical but not thermal hyperalgesia
(remember Ian Lipkin’s results: IL-17 is up-regulated in spinal cord fluid in ME/CFS patients)
Transient receptor potential canonical 3 (TRPC3) is required for IgG immune complex-induced excitation of the rat dorsal root ganglion neurons
Lipid rafts control P2X3 receptor distribution and function in trigeminal sensory neurons of a transgenic migraine mouse model
P2X3 receptor: a novel ‘CASKade’ of signaling?
Identification of voltage-gated K+ channel beta 2 (Kvβ2) subunit as a novel interaction partner of the pain transducer Transient Receptor Potential Vanilloid 1 channel (TRPV1)
Mechanism of sodium channel NaV1.9 potentiation by G-protein signaling
TRPC3 and TRPC6 are essential for normal mechanotransduction in subsets of sensory neurons and cochlear hair cells
Potentiation of acid-sensing ion channel activity by the activation of 5-HT₂ receptors in rat dorsal root ganglion neurons
Methods of antagonizing signal transduction in dorsal root ganglion cells