What is somatosensation? WHat are the 3 subdivisions of somatosensation?
the process that conveys information regarding the body surface and its interaction with the environment.
- mechanoreception (disciminative touch)
What are the receptors for the following sensations:
steady pressure = Merkel's disc
stretch = Ruffini
flutter = Meissner's corpuscles
vibration = Pacinian corpuscles
What two touch receptors adapt slowly and what two adapt rapidly?
slowly = Merkel's and Ruffini
rapidly = Meissner's and Pacinian
Of the rapidly adapting touch receptors, which one has a large receptive field and which has a small receptive field?
large - Pacinian
small - Meissners
What are the thermoreceptors? WHere are they located? Do they have small or large receptive fields? Rapid or slow adapters?
They are free nerve endings in the superficial layers of the skin
small receptive fields
What do the cold thermoreceptive proteins detect?
How about the warm theroreceptors?
Cold: 5-35 degrees, over 45 degrees and menthol
warm: warmer temperatures and capsacin
Is there a secondary messenger involved in thermoreception?
No -- the receptor proteins are coupled directly to channels so no secondary messenger is needed
How are mechanoreceptors activated?
There is a structural protein attached to the channel and when the membrane is deformed, the channel is pulled open directly
What will activate nociceptors?
stimulit hat actually open the channel:
capsaicin, heat over 45 degrees C, and protons
What will cause the threshold for the nociceptor channels to lower? What is this called?
Serotonin, Bradykinin, and prostaglandins
this is sensitization
How do NSAIDs work for pain directly at the receptor level?
They inhibit the prostaglandins, so you don't get the sensitization of the channels - making them less likely to fire
What is hyperalgesia and what is allodynia?
hyperalgesia - basically sensitization; experiencing pain from a light stimuli like a feather brush
allodynia is experiencing pain when there is no stimulus at all - it's perception of pain without sensation of nociception
What are TRP channels?
they are nonspecific cation channels similar to voltage gated channels (and nicotinic receptors) because they let in Na+ K+ and Ca2+ (although Na+ goes more than the others)
The transducer is directly connected to the channel
Implicated in many sensory processes including somatosensitizations
What is point acuity and how is it tested?
Point acuity is how well you localize a point on your skin, tested by the Two-Point Discrimination Test
It's the physical distance where you perceive two stimuli instead of one
Better on fingertips than on back
How can be divide somatosensory nerve fibres into subcategories?
conduction velocity - determined by diameter and degree of myelination
What are the 3 subgroups of somatosensory nerve fibers?
A - beta fibers (large myelinated fibers - mechanoreception)
A - gamma fibers (fast pain, mechanoreception, cold)
C fibers (mechanoreception, thermoreception, slow pain)
What nerve fibers are associated with fast pain and which are associated with slow pain?
fast = A-gamma
slow = C
What are the 3 types of pain?
1. acute nociceptive pain
2. Inflammatory pain
3. Neuropathic pain
Describe acute nociceptive pain?
It's divided into fast and slow
fast is sharp/pricking pain that is well localized
slow pain is achy/dull pain that isn't well localized
What are the two potential causes of inflammatory pain?
damage to the receptors themsevles or sensitization to receptors due to adjacent damaged cells
What is the general cause of neuropathic pain?
reorgnization of the pathways such that you don't need a stimulus to perceive pain
What are two characteristics of chronic pain syndromes and what types of pain are they more often associated with?
hyperalgesia and allodynia
associated with inflammatory and neuropathic pain
What is referred pain?
It's when activation of nociceptors in the viscera is perceived as a somatosensory stimulation - like when heart attacks hurt in the left arm
It's related to the labelled line theory
Describe the gate theory of pain
Inhibitory interneurons regulate the transmission of ascending nociceptive information at the elvel of the second order neuron, allowing modulation of the signal - either increasing or decreasing it depending on the situation
Under normal circumstances without pain, what is the status of the inhibitory interneuron?
Under normal conditions, the inhibitory interneuron - the gate - is contantly active and thus closed.
It constitutively secretes glycine onto the second order neuron such that no signals go through the nociceptive pathway
In the event of a painful stimulus, what happens to the inthibitory neuron and basic circuit?
1. The glutamate from the first order neuron acts on metabotropic glutamate receptors on the inhibitory interneuon and shuts it off, thus opening the gate
2. The same glutamate that is released from the first order neuron and acts on AMPA receptors of the second order neuron, activating it
3. Because the gate is open and no glycine is being released onto the second order neuron, the signal passes through
How does the inhibitory interneuron (the gate) get turned back on after a pinaful stimulus?
What is the significance of this clinically?
The mechanoreceptors will reactivate the inhibitory interneuron and close the gate
This is why rubbing a bumped elbow makes it feel better and why TENS electrical stimulation works - it stimulates the mechanoreceptor fibers
What effect do opioid drugs have on the basic circuit in terms of the gate theory of pain?
Opioids modify the synapse such that the inhibitory interneuron is more active
they do this by acting on opioid receptors located on the cell body of the interneuorn - the gate
keeps the gate closed