Nociception (Exam 2) Flashcards
T/F
Transduction always refers to a painful stimulus.
False
Transdxn doesn’t necessarily mean painful; refers to converting into electrical impulse
Transduction
noxious stimuli (e.g., heat, cold, mechanical distortion)
⬇️
electrical impulse in sensory nerve endings
Whorls
spiral shape seen at end of sensory dendrite; deform/compress triggers signal to travel down dendrite to body (senses pressure)
Whorls sense what type of stimulus?
pressure
How does increasing T affect receptors?
can open and allow NA in»_space; allows stimulation
process of sensing heat
Sensing heat causes an influx of ___
Na
Tissue damage results in release of ___ ions, which can open certain receptors.
H+
Transmission
conduction of these electrical impulses to the CNS
major connections:
-dorsal horn (SC)
-thalamus with projections to the cingulate, insular, and somatosensory cortices.
Process of transmission
-Nerves enter dorsal horn (SC)
⬇️
projection pathways (somatosensory pathways)
⬇️
up SC
⬇️
brain
⬇️
branch off in certain places, esp the thalamus
Transmission
major connections:
-dorsal horn (SC)
-thalamus with projections to the cingulate, insular, and somatosensory cortices.
(T ➡️ CIS
Thalamus to Cingulate, Insular, Somatosensory)
Relay center for incoming pain signals
Thalamus
receive input; synapse to others ie neocortex
Levels of consciousness are found in
the cerebral cortex
Which cortices are a/w:
lower brain levels & emotional responses
cingulate, insular
Which cortices are a/w:
bringing things into consciousness
somatosensory
Modulation
Alters which stage of nociception?
altering pain transmission
inhibitory & excitatory mechanisms modulate pain/nociceptive impulse transmission in the PNS and CNS
T/F
mechanisms modulate pain/nociceptive impulse transmission in the PNS and CNS are inhibitory
False
inhibitory & excitatory
sensation of pain
nociception
Perception
mediated thru…
thalamus: central relay station for incoming pain signals
primary somatosensory cortex: discrimination of specific sensory experiences
T/F
Modulation can relieve pain
True
Severe sudden pain will shift focus almost 100% to it
Not sustainable
So we modulate pain immediately
Pain relieving in a sense
Perception
bringing pain into consciousness to process and make decision
primary somatosensory cortex
discrimination of specific sensory experiences
What pain is it? Biggie or no biggie? Where from?
all or nothing response
axon only has one choice: fire or dont
signal traveling down axon
axon can only signal down or not
Temporal signaling
(down an axon)
firing rate
T/F
There is no required time frame between an axon firing.
False
takes time for axon to reset and send another signal
minimum period of time between firing
Cells adjacent to an axon are sensing…
a time/signal pattern
a cell may only respond to a certain firing rate/pattern
the only way nerves can signal each other
temporal signaling
Very painful stimuli firing rate
very rapid
(type 1 neurons)
Firing rates/patterns:
Type I neuron vs. Type II neuron
Type I: more linear; can alter firing rate
Type II: have different patterns
discrimination of sensory experience is based on:
-which nerves fire
-rate/pattern of firing
Stepping on a lego vs marshmallow
The response is dependent on…
temporal signaling
(firing pattern)
The 4 components of Nociception
Transduction
Transmission
Modulation
Perception
T/F
Pain can only occur when all 4 components of nociception occur.
False
pain can occur without one or more of these steps
(ex: phantom limb pain)
phantom limb “pain”
Not always pain; sometimes just sensation
d/t higher processing neurons still responding/firing w/o stimuli
(not getting the stimuli they used to get but still firing)
T/F
phantom limb “pain” is d/t the hypersensitivity of the remaining sensory neurons.
False
d/t higher processing neurons still responding/firing w/o the original stimuli
C-fiber afferents
(unmyelinated & slowest conduction)
burning
sustained pressure
Type I fibers
(some Aβ and some Aδ)
myelinated
“polymodal fibers”
thermal, chemical & mechanical stimuli
T/F
Thermal pain is not the same as burning pain
True
Consistent firing in-between transmissions; only “pattern” is speeding up/slowing down (linear)
Type I fibers (some Aβ and some Aδ) “polymodal fibers”
T/F
Type I fibers respond to a single stimulus.
False
called “polymodal” bc they respond to multiple things
Thermal vs burning pain
burning = instantaneous pain
thermal = consistent, longer-term response
Non-linear/ “saddle transmission”
Type II fibers (some Aδ fibers; slower)
bizarre patterns
can also speed up and slow down
can signal pain from chemical and cold stimuli
Both myelinated and unmyelinated
Type II fibers
(some Aδ fibers; slower)
initial pain responses to heat
non-linear
bizarre patterns
Myelination is more critical to (motor/sensory) fxn.
motor
Myelinated Motor
“Capsation” receptor is a/w what sensation
burning
Capsation/Vanilloid Receptor/ Transient V receptor-1 (TVR1)
structure
Voltage gated
4 subunit
similar to NMDA
Capsation/Vanilloid (VR1) Receptor/ Transient V receptor-1 (TVR1)
MoA
Na & Ca in; K out
depending on state of neuron
scalding heat and pain
activated/augmented by:
PKC, PKA, Ca
PIP is located in ___ and can be broken down into ….
cell membrane
DAG & IP3
T/F
Prostaglandins and bradykinins are known to cause pain
False
do not cause
but
worsen/augment pain
substances that transmit pain when released from neurons
CGRP (Calcitonin gene-related peptide)
SP (substance P)
glutamate
T/F
Ca release aids in pain transmission
True
Ca stimulates NT release into synapse and communicates pain
What stimulates Ca release?
-Depolarization (Na influx)
-IP3
-PK3
-PKC
T/F
PKA stimulates Ca release and pain transmission
False
stimulates Ca release:
-Depolarization (Na influx)
-IP3
-PK3
-PKC
Role of bradykinin in pain
increases IP3»_space; Ca release»_space; NT release
increases DAG»_space; PKC»_space; Ca»_space; NT release
Augments pain, doesn’t cause it
Role of PGE2 in pain
(Prostaglandin E2)
increased cAMP > activates PKA > Na influx > depolarization > Ca release > NT release
Activates Na (depolarization)
PKC
PKA
Which substances act here to inhibit pain?
Endorphins
ACh
cannabinoids
Which act via G protein complexes?
Endorphins
ACh
cannabinoids
All
stimulate K channels
K out
hyperpolarize
cAMP role in nociceptive signal transduction
Increase cAMP = alter PKA = stimulate Na ion entry = depolarization & passage of signal
increase of cAMP will directly…
increase/alter PKA
end result: Na influx & depolarization
released from some sensory nerves as a means of pain transmission
Calcitonin gene-related peptide (CGRP)
Substance P (SP)
Substance P (SP)
undecapeptide
acts at Neurokinin-1 receptors (NK-1) (amygdala, hypothalamus, & periaqueductal gray)
brings pain into emotional consciousness
amygdala
“P” in SP stands for
powder
SP is found with ___ in __ __ that respond to painful stimuli
glutamate
primary afferents
Neurokinin-1 receptors (NK-1)
widely distributed in the brain
in areas a/with pain processing:
amygdala, hypothalamus, & periaqueductal gray
SP acts on this site
specific areas associated with pain processing
amygdala, hypothalamus, and periaqueductal gray
An NK-1 receptor antagonist would block…
Substance P
SP: undecapeptide that acts at Neurokinin-1 receptors (NK-1)
Aside from nociceptive pain transduction, CGRP causes ___
vasodilation
decreases BP
CGRP antagonist
MoA
attenuates the increase in BP (that causes migraine) and block pain
Gi/o receptor
“G inhibitory”
Inhibitory opioid receptor
inhibitory actions at pain receptors
Causes receptor hyperpolarization by increasing potassium conductance (K out)
T/F
Endorphin, cannabinoid, and acetylcholine receptors are examples of Transient V receptor-1 (TVR1)
False
Gi/o receptor system
hyperpolarization by increasing potassium conductance
Provides sensations of scalding heat and pain
Transient V receptor-1 (TVR1)
“Capsaicin/Vanilloid receptor”
Transient V receptor-1 (TVR1)/ Vanilloid/ Capcasin
when it is open….
K out
Na, Ca in
similar to NMDA
Increasing K conductance means…
more K flows OUT
Bradykinin is considered a..
inflammatory mediator
increasing Bradykinin results in
increased DAG & IP3
increases overall response of system
T/F
CNS neurons can be sensitized for pain transmission by many inflammatory mediators
False
peripheral
released in response to tissue damage
bradykinin
Chronic pain occurs when
inflammatory effects do not resolve
leading to hyperalgesia due to sensitization
T/F
Hyperalgesia is a result from nerve understimulation.
False
hyperalgesia is due to sensitization/overstimulation
Allodynia
perception of pain from normally non-painful stimuli
body’s response to sensitization