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Printable Handouts
Navigable Slide Index
- Introduction
- Activity generated within CNS pain circuits
- Pain pathways
- Receptors & ion channels involved in pain signaling
- Key types of pain
- Inflammation - ongoing activation of pain sensors
- Tissue damage induces cyclooxygenase 2
- Pain signaling: ligands and receptors
- Nerve growth factor
- Nerve growth factor: bone innervation
- Tanezumab: humanized monoclonal antibody
- ATP as pain mediator
- Symptoms of neuropathic pain
- Pain signaling analogy: driving a car
- Neuropathy: nerves tend not to heal
- Sodium channel changes, redistribution, activation
- Channelopathic pain syndromes
- TRPV1: two prominent members of the family
- TRPA1 mutation causes familial episodic pain
- Alpha-2 delta ligands: pregabalin and gabapentin
- Ca channels - massive changes after neuropathy
- Channels are key to neuropathic pain
- Peripheral activity causes central hyperexcitability
- Post-synaptic neuron activation
- Spinal mechanisms
- NMDA receptors and wind-up
- Central sensitization (1)
- Central sensitization (2)
- Noradrenaline and 5HT
- Descending inhibitions in humans
- Descending excitations in patients
- Pain sensitivity: pathway alterations
- When excitations increase: inhibitions decrease
- Descending controls are not simply inhibitory
- Reduced NA\increased 5HT function: effects
- Diffuse Noxious Inhibitory Controls (DNIC)
- Morphine and codeine
- Opioid mechanisms
- Pain signaling, multi-level changes & drug targets
- Similar symptoms\signs: many mechanisms
- Thank you
Topics Covered
- CNS pain circuits
- Receptors, ligands , mediators & ion channels involved in pain signaling
- Key types of pain
- Inflammation (ongoing activation of pain sensors)
- Nerve growth factor and bone innervation
- Tanezumab: humanized monoclonal antibody
- Symptoms of neuropathic pain
- Sodium channel changes, redistribution, activation
- Channelopathic pain syndromes
- Pregabalin and gabapentin
- Ca channels
- Peripheral activity causes central hyperexcitability
- Post-synaptic neuron activation
- Spinal mechanisms
- NMDA receptors
- Central sensitization
- Noradrenaline and 5HT
- Pain sensitivity: pathway alterations
- Reduced NA\increased 5HT function: effects
- Diffuse Noxious Inhibitory Controls (DNIC)
- Morphine and codeine
- Opioid mechanisms
- Pain signaling, multi-level changes & drug targets
- Similar symptoms\signs: many mechanisms
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Dickenson, A. (2014, April 2). Receptors and channels in pain [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 6, 2024, from https://doi.org/10.69645/UDKD8703.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Anthony Dickenson has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Neuroscience
Transcript
Please wait while the transcript is being prepared...
0:00
So I'm Professor Tony Dickenson
from University College London.
And this presentation is based
on receptors and channels
in pain, how the integrated function
of the nervous system, subjects
to painful messages, deals
with these external events.
0:20
Pain is an intriguing example of
understanding and trying to gauge
how external events, in this
case from the body, impact
upon function of the
central nervous system.
So peripheral events,
peripheral sensory fibers,
project into the spinal cord.
The spinal cord then sends
messages up to the higher centers.
And in the case of
pain, of course, it's
an individual, personal
experience that is built up.
But what goes up, also comes down.
And so the higher
centers of the brain
are able to alter mechanisms
within the brain stem
and change what we call
descending controls, which,
in turn, return to the spinal cord.
And so the higher centers have
the ability to modulate events
at the first synapse
within the spinal cord.
1:17
So if we look in a little bit
more detail at these pathways,
at the bottom left,
incoming peripheral nerves,
which are highly specialized,
many of them respond
to nonpainful stimuli,
such as touch and temperature.
But then we have a large
number of pain-sensing fibers.
And here there are a remarkable
number of receptors and channels
that respond to heat, to
mechanical, and to chemical
stimuli, all of which are painful.
These are altered by damage
to nerves themselves,
or, indeed, damage to tissues,
and they will input
into the spinal cord.
The spinal cord neurons
integrate these messages,
often, and unfortunately
in the context of pain,
amplify these messages and
send them on to the higher
centers of the brain.
So at the top right, we have
the cortex, the homunculus.
These columns of neurons responding
to particular parts of the body,
and neurons within these
columns are able to code
the intensity of the stimulus.
So our ability to locate
pain and describe it
are cortical mechanisms.
But at the top left, there is
the limbic brain and an equally
important input from the
spinal cord into these areas.
The limbic brain's function
is to control mood,
to generate the sleep/wake cycle,
to respond to external events.
And so it's not surprising
that ongoing painful inputs
into these parts of the
brain disrupt this function
and lead not just to pain,
but to fear, anxiety,
and sleep problems that
are common in patients.
And then, from these
limbic parts of the brain,
we have the descending controls
that return to the spinal cord.
And so cognitive,
proprioceptive, and mood changes
occurring in the higher
centers have the ability
to modulate transmission
at the spinal cord,
and they can enhance it,
or, in fact, they can inhibit it.