Sensory Physiology (Pierce) Flashcards
What two schemes are peripheral nerves classified as ?
Their contribution to the compound action potential
Fiber diameter, myelin thickness and conduction velocity (I, II, III and IV)
What determines a fibers contribution to the compound action potential?
Conduction velocity (often measured in diagnostic testing along with compound action potential)
What are some important properties of sensory receptors?
They are specific for a narrow range of input, perform a common functions in unique ways, convert the signal they receive into change of membrane voltage
What is a generator potential?
Stimulus received by the somatosensory receptor produces this potential. When it reaches a threshold it generates the spike potential and carried over to the CNS
Role of the thalamus in somatosensory processing
All sensory systems (except for olfaction) relay info to the nuclei of the thalamus before they go to specific places in the cortex. Usually two nuclei involved (one for body and one for face)
How are the neurons in the thalamic nuclei arranged?
Neurons performing a certain function are segregated together
What is the relationship between receptor density and stimulus strength?
The stronger the stimulus, the more receptors involved.
How do somatosensory receptors work?
Encode the intensity of the stimulus as receptor potential > digital pulse code
What is receptor adaptation?
Stimulus is unchanged (no change in position or amplitude) for several minutes - neuron response is lost (sensory adaptation)
Slowly adapting receptors vs. rapidly adapting receptors
- respond to prolonged and constant stimulation
- respond only at the beginning or end of a stimulus, only active when the stimulus intensity changes
What are receptive fields?
Made up of mechanoreceptor fibers that innervate an area of the skin (the receptive field)
Describe the significance of 2 point discrimination
It is basically the ability to distinguish that two different objects touching the skin are separate and not one.
Tactile acuity (keenness of touch) is highest in () Lowes in ()
Fingertips and lips (smallest receptive fields)
Calf, back and thigh (largest receptive fields)
How does the size of receptive fields affect 2 point discrimination?
Primary neurons converge on the same field (due to the size), so ends up being perceived as a single point. Not the case for smaller receptive fields.
What is presynaptic inhibition? What does this do?
Powerful form of inhibitory control of primary afferents. It is basically a diminished excitatory signal. End effect is that the brain’s ability to localize a signal is improved
How does presynaptic inhibition diminish the excitatory signal?
GABA > Cl- influx into axon > hyperpolarizaton > less Ca2+ enters the cell > less NT release
Affects the neighbors of the neurons receiving the stimulus. Signal is narrowed by much by the time it reaches the cortex
What is the Somatosensory Area I (SI)?
Primary somatosensory cortex. Takes care of position sense, size and shape discrimination info.
What is somatosensory area II (SII)
Secondary somatosensory cortex. Takes care of comparisons/differences between sensation and remembering sensation. Receives input from S1
What is the parieto-temporal-occipital association area (PTO)?
Takes care of high level interpretation of sensory inputs. Things like spatial perception, identification etc. Receives input from multiple sensory areas.
Describe the doctrine of specific nerve energies and how does this relate to the Law of Projections?
What you “sense” is determined by the receptors connected to the somatosensory pathway. So you can stimulate any part of the afferent pathway and you will perceive a similar sensation.
Pain vs nociception
Pain is the sensation. Nociception is the neural process of encoding the noxious stimuli
Hyperaesthesia
Hyperalgesia
Allydonia
Increased sensitivity to stimulation
Increased pain from stimulus that normally provokes pain
Pain due to stimulus that does not normally provoke pain
Fast vs slow pain
- Impulses travel through thinly myelinated A- fibers. Pain goes away quickly
- Impulses travel through non-myelinated C fibers. Pain persists longer
Nociceptors and modalities:
Also what are silent nociceptors?
- Could be thermal, mechanical, chemical or polymodal (can perceive different types of pain sensations).
- Could be related to phenotype switching
What are free nerve endings?
Terminal ends of the A-gamma or C pain fibers. They do NOT have specialized receptor cells
Peptidergic free nerve endings:
Expresses neuropeptides (Substance P, CGRP)
Respond to NGF
Includes most visceral and half of cutaneous afferents (chronic inflammation and visceral pain)
Non peptidergic free nerve endings:
(basically the opposite of peptidergic)
Does not express neuropeptides, responds to GDNF, half of cutaneous afferents and few visceral afferents (diabetic neuropathy)
TRP receptors:
Nociceptors on the ends of the nerve endings. Ligand gated and lets Ca/Na/K in. (CANaK) - aka not specialized
3 types: V1, A1, M8
Na v I.7 channel
What is it?
Mutations result in?
Another nociceptor. Permeable to sodium.
I type mutation = pain sensitive areas
Other mutations result in extreme pain disorder, when channel does not inactivate properly
Other pain receptors:
P2X - ATP activated
ASIC - H+ activated
SP&CGRP, Histamine and kinins
What modulates nociceptors and pain processing?
Interneurons and descending inhibition (input is reduced as it makes it way down to the cortex)
Describe the gate control theory of pain
No input from free nerve endings so interneuron suppresses the pain pathway and blocks it (inhibitory interneuron). No further signal to the brain = no pain.
How is gate control of pain induced (why does massaging the pain make it feel better)?
normal sensory stimulus stimulates the A-beta fiber > Central process synapses to the dorsal horn on the inhibitory interneuron, releases EAA > Activated interneuron releases glycine and inhibits the secondary sensory neuron > blockage of the nociceptive pathway.
Describe the pathway of descending inhibition
Opiates, EAA And cannaboids activate the periaqueductal gray (PAG) > Locus coeruleus/raphe > release NE and serotonin on dorsal horn > activation of inhibitory interneurons > which releases opiates > which activate mu receptors on c-fiber terminals > reduction of stimulus from the C-fiber = reduced pain sensation
Central vs peripheral sensitization
- Activity dependent synaptic plasticity in the spinal cord which increases hypersensitivity to pain post injury.
- change in structures etc. of the PNS resulting in increased pain sensation
How does central sensitization happen?
Reduced threshold of the dorsal axons to pain stimulus, alterations to ion channels, expansion of the receptive field
Persistent stimulation of various intracellular mechanisms = end result is to be hypersensitive to pain
How does peripheral sensitization happen?
Neuroimmune activation (Prostaglandin e.g. bradykinin release from nearby cells after an infection) sensitizes the peripheral nociceptors = hypersensitive to pain
How is pain processed in the cortex?
S1 and S2 receive input from nociceptors and overall localizes the pain > insular cortex > interpretation of pain
What is the insular cortex?
Located in the insula. Integrates pain related signals and important in pain interpretation.
Damage results in asymbolia - failure to interpret symbols
Emotional component of pain is thanks to the …
Amygdala
How does visceral pain get processed?
Visceral input travels via the autonomics > hypothalamus and medulla (integrates physiological changes associated with visceral pain)
General concepts about the different stimuli that activate nociceptors in different organs
Stimuli is not the same to activate nociceptors in the skin vs joints vs. muscles vs. viscera
What is referred pain?
Brain needs experience to localize pain. Early visceral pain is not localized and could travel to other areas. This is due to convergence of the afferents on the dorsal horn and antidromic signaling
(e.g why you have diffuse flank pain when you have kidney stone)
