Sensory receptors may be simple free nerve endings or complex structures, give some examples of both?
Nociceptors & cold receptors are free nerve endings
Pacinian Corpuscles (vibration) and Meissner’s Corpuscles (Touch) are more complex structures
How is tactile acuity determined?
Larger number of smaller receptive fields (i.e. nerve ending density) allows greater acuity as you can isolate a signal to a smaller area.
What is a receptive field?
The area of which a receptor will detect a stimulus
What does an “adequate Stimulus” mean?
The specific mode of stimulus the receptor responds to
Signal transduction occurs differently for mechanoreceptors and nociceptors, how do mechanoreceptors transduce a signal?
The receptor transduces the adequate stimulus into a depolarisation called the receptor or generator potential which then evokes an AP
How is the intensity of a stimulus encoded by mechanoreceptors?
In the size of the receptor or generator potential
Then in the frequency of the APs
What are the various types of sensory primary afferent fibres?
Aalpha & Abeta:
- Large myelinated fibres
- Touch, pressure, vibration (all the innocuous mechanoreceptive modalities)
- Also carry proprioception from muscle spindles & GTOs
- Small myelinated fibres
- Carry cold and “fast” pain
- Small Unmyelinated fibres (slowest)
- Carries Warmth & “slow” pain
Describe the pathway of mechanoreceptive fibres (Aalpha & Abeta)
They all enter through the dorsal root via the DRG
- 1st order neuron projects striaght up through the ipsilateral dorsal column
- 2nd order neuron decussates in the brainstem
- Projects up to reticular formation –> Thalamus –> Cortex
Describe the pathway of thermoreceptive & nociceptive fibres (Adelta & C)
Enters through dorsal root via DRG
- 1st order neuron synapses in the dorsal horn
- 2nd order decussates in spinal cord
- Then projects up the contralateral spinothalamic (anterolateral) tract to the reticular formation –> Thalamus –> Cortex
What happens if you damage the dorsal column?
You lose ipsilateral mechanoreception (Touch, vibration, proprioception)
What happens if you damage the spinothalamic tract?
You lose contralateral thermoreception & nociception
Receptors can be divided into slow and fast adapting.
Fast adapting receptors such as pressure receptors adapt to a sustained stimulus, only telling you when the stimulus changes
Slow adapting receptors such as muscle spindles maintain the signal until the stimulus is removed
Multiple receptive fields synapsing onto one neuron, this saves on neurons but reduces acuity
What is the difference between a specific and non-specific pathway per convergence?
A specific pathway has receptors of the same modality converging on one neuron
A non-specific pathway has receptors of different modalities converging on one neuron, usually pain and touch. These can’t be distinguished
Explain the concept of lateral inhibition?
The neuron closest to the stimulus inhibits the synapses of the neighbouring neurons.
This cleans up sensory info giving you a better definition of the stimulus boundary
(So the central neuron has a higher than tonic frequency of APs and the neighbouring ones have a lower than tonic level)
What are the different types of pain?
Fast (initial) pain - Sharp & Stabbing - Uses Adelta fibres
Slow (Delayed) pain - Diffuse & Throbbing - Uses C fibres
What is a possible explanation for referred pain?
Convergence of neurons from the viscera and other tissues e.g. the skin
How are nociceptors activated?
- Low pH activates an ASIC receptor
- Heat activates a TRPV1 receptor
- Also by local chemical mediators such as prostaglandins and bradykinin (B2 Braykinin receptor) released on tissue injury
How do prostoglandins affect pain?
They stimulate nociceptors themselves but more importantly sensitize nociceptors to bradykinin
What is the Gate control theory?
The ability to “gate” pain signals, preventing them from crossing the 1st-2nd order synapse
How is pain gated by segmental control?
Mechanoreceptive fibres (Aalpha/beta) activity in the same region
- -> Activates an inhibitory internueron
- -> Releases opioid peptides (endorphins)
- -> Inhibit the nociceptive synapse
(Probably the basis for TENS & rubbing it better)
How is pain gated by Descending Control?
Peri-aqueductal grey (PAG) matter in cortex gives off a descending fibre
- > Synapses in Nucleus Raphe Magnus (NRM)
- > Travels down to the spinal level of nociceptive fibres
- > Activates the inhibitory interneuron
- > Releases opioid peptides (endorphins) that inhibit the nociceptive synapse`
What does TENS stand for and what does it do?
Transcutaneous Electrical Nerve Stimulation
Analgesic – It activates innocuous mechanoreceptors and so inhibits the nociceptive synapse. (Segmental Gate control)
How do NSAIDs work as analgesics?
Remember prostaglandins sensitize nociceptors to bradykinin
So NSAIDs prevent the formation of prostaglandins by inhibiting the cyclo-oxygenase enzyme (Arachidonic acid –> Prostaglandins)
Therefore they work best with inflammation associated pain
How do local anaesthetics work as analgesics?
The block Na+ channels preventing AP transmission
How do opiates work as analgesics?
- Directly reduce nociceptor sensitivity
- Block neurotransmitter release at the 1st-2nd order synapse in the dorsal horn (Pain Gate Control)
- Activate descending pathways in the peri-acqueductal Grey (PAG) matter (Descending Gate control) to inhibit the 1st-2nd order synapse