I just wrote that it's because of :
-Large A-delta&c-fibre nociceptor activation causing a release of glutamate from Dorsal root ganglion cells to 2nd order neurones in the substantia gelatinosa of the spinal cord. This unsilences NMDA receptors and activates them causing a large ca2+ influx into 2nd order neurones. This triggers an intracellular signalling cascade e.g., MAPK pathway that activates gene transcription that promotes central sensitisation and nociceptive signalling.
-Spontaneous primary afferent discharge
There is a lowered activation threshold and receptive field size increases.
The prolonged increase in membrane excitability-caused by changes in threshold+activation kinetics of NMDAR+AMPAR strengthened excitatory synaptic inputs(changes in the trafficking of AMPAR to membrane&alterations in ion channels to increase inward currents+reduce outward currents-caused by gene expression changes&by production+trafficking of receptors,channels&downstream signalling pathways)+reduced inhibitory interneurone activity) causing a reduction in release or activity of gaba+glycine (disinhibition).
- Changes in expression& activity of caused by cytokines, growth factors (e.g., BDNF) etc. altering Nav1.3, Nav1.8, Nav1.9 expression and activity, this causes sub-threshold membrane potential oscillations and ectopic activity-as primary afferent neurones start firing spontaneously. Nav1.7-gain in function via mutation causes ectopic activity in c-fibres. Nav1.3 expressed in development but nerve injury causes adults to express it, it has fast gating kinetics which causes depolarising after potentials, contributing to pain
What are some other points I can make?
Every time I come across this card, I think it's sensory receptors!! What's the difference between sensory receptors and free nerve endings?
https://preview.redd.it/zydbk9l2mhn61.png?width=856&format=png&auto=webp&s=c92d2d8722b37f163faa56970077b98b100cdc82
Nociceptor: INTJ, ISTJ, ESTJ
Nociceptors send pain signals to the central nervous system. In other words, they make your body say "NO!" so you can get away from danger or take care of something that is wrong with your body.
Thermoreceptor: ISTP, INTP, ENTP
Thermoreceptors are dedicated to sensing temperature changes. They quickly adapt to constant stimuli.
Mechanoreceptor: ESTP, ENFP, ENTJ
Mechanoreceptors detect touch, pressure, sound, and vibration from the external environment. A specialized mechanoreceptor called a proprioceptor senses the body in relation to the environment.
Chemoreceptor: ESFJ, ENFJ, INFJ
Chemoreceptors pick up chemicals from the environment to send certain signals to the brain. Thet detect smells, tastes, and changes in the pH of the blood.
Photoreceptor: ISFP, ESFP, ISFJ
Photoreceptors are located in the human retina and allow (most of) us to see the world in full color.
Does anyone ever wonder if everyone else's senses are fundamentally different? Like... What if your red would be what you see when you see the color "green" through their eyes? What of sounds? Tastes? Thoughts?
Does anyone have a good mnemonic to remember what the functions of meisner, ruffini, pacinian, merkel's receptors...I really doubt we would need to be able to tell the difference, but I keep seeing them on my anki cards and can't remember which does which for the life of me haha. Thanks!!
Imagine if we didn't had a ability to touch and feel or if we had not developed the nose , we would have never known what it is like to smell the world around us. Imagine the world without ability to see if we didn't had eyes . Now how are we sure that we have it all. Maybe we missed out on some important sensory receptors and are not experiencing the world as it is in reality.
I have two questions regarding the fact that each sensory receptor has its specific ion channels that open in response to a specific stimulus (for example, ion channel that opens when streching for somatosensation), and is (the receptor) connected to correspondent sensory cortex.
- Did our sensory system developed perfectly so that each ion channels in the sensory receptors are connecting to the corespondent sensory cortex? If not, can you elaborate and give examples?
- Theoretically, what would happen if they weren't corresponding? And specific, if for example, we had sound receptor that was connected to the visual cortex?
In stroke patients or similar cases where feeling is lost in parts of the body but mobility is somewhat recovered, the frame work for the peropheral nerves still function but the stimulus isn't being recognised by the brain due to the injury. Would it be feasible to create an artifical somatosensory cortex that interprets the signal for the brain or perhaps "rewire" the unaffect hemisphere to take on that role?
Are slowly adapting receptors better at signaling the length or the intensity of a stimulus? Thanks in advance!
Any mnemonic for sensory receptors?
Pacinian, Ruffini...
Tks
