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Neuroscience 3 > Somatosensory system > Flashcards

Somatosensory system Flashcards

1
Q

Describe the role of pain and why its important

A

Acts as a warning system
1. short lasting pain causes us to withdraw from source thus preventing further damage
2. long lasting pain causes us to sleep, inactivity, eating/drinking to promote recovery
3. provides social signal (screaming) to alert others to avoid and to take care of the injured

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2
Q

Describe how pain stimuli are transduced into electrical signals

A

transducer receptors and polymodal receptors respond to mechanical/thermal/chemical stimuli, and open causing influx of ions into nerve terminal and depolarizes it, thus generating an AP

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3
Q

What are the neural pathways that process pain information?

A
  • ascending
  • descending
  • flexion withdrawl reflex
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4
Q

Describe the ascending pain pathway

A
  1. Location and intensity: dorsal horn-> thalamus -> somatosensory cortex
  2. Affective: dorsal horn -> parabrachial nucleus -> amygdala -> insular cortex
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5
Q

Describe the descending pain pathway

A

Frontal cortex or hypothalamus-> periaqueductal gray-> raphe nucleus -> dorsal horn
Either amplify or inhibit pain (eg stimulating the PAG causes analgesia, 5-HT releasing neuron shares synapse with primary afferent neuron synapse)

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6
Q

How can context induced and placebo induced analgesia be explained?

A

Context induced: extreme stress and emoition can act on periaqueductal gray in the descending pathway

Placebo induced: endongenous opiod analgesia was probably involved since the placebo patients felt pain relief, due to recruitment of descending pain pathways

context induced- soilders/athletes/trauma victims

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7
Q

What are the characteristics of the different primary afferent fibre types?

A

A-beta: heavily myelinated, mechanoreceptor of touch
A-delta: lightly myelinated, slower, and transmits pain and temperature
C: unmyelinated, slowest, transmits dull pain, temperature, itch

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8
Q

Explain the gate theory of pain

A

There is an inhibitory interneuron that is in series with acsending pain neuron, when active it inhibits the acsending pain neuron (dampens pain signal)
C fiber inhibits the interneuron, and activates the ascending neuron so pain is transmitted
A-alpha/A-beta activates both the interneuron and the ascending neuron-> meaning touch can dampen pain signal if it comes into brain at same time as pain signal

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9
Q

What is the peripheral nerve relay of pain?

A

Pain information is coded by the number of electrial signals (aka APs) and the time intervals between them
In built brake on pain: the longer the time interval between APs, the less painful
Activity-dependent slowing: eg C fibers, APs become more spread out as they travel along nerve so when they reach dorsal horn its less than OG stimulus

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10
Q

What are the three symptoms of chronic pain?

A
  1. Hyperalgesia (exaggerated pain)
  2. Allodynia (non-painful stimuli is painful)
  3. Spontaneous pain

these symptoms are useful in tissue injury, but are not useful in neuropathic pain

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11
Q

What is the cause of chronic pain?

A
  1. tissue injury (aka inflammatory pain) (mechanical damage or inflammatory conditions)
  2. nerve injury (aka neuropathic pain) (PNS: mechanical trauma or disease, CNS: stroke, spinal cord injury)
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12
Q

What are the differences between neuropathic and inflammatory pain?

A
  • Origin (direct damage to PNS/CNS vs mechanical damage to tissue or inflammatory conditions)
  • Usefullness (inflammatory can be useful)
  • Location (PNS/CNS vs tissue)
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13
Q

How is peripheral sensitization linked to central sensitization?

A

peripheral sensitization (increased excitability in peripheral sensory neurons) drives central neurons to become more excitable (aka central sensitization)

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14
Q

What causes peripheral sensitization?

A

Peripheral sensation= decreased threshold for activation and enhanced response to stimuli
Caused by
- inflammatory mediators (eg prostaglandin, NGF, bradykinin) from damaged tissue cause modulation and phosphorylation of ion channels and transducer receptors
- changes in gene expression can cause inc BDNF and Na channels (in inflammtory pain)
- neuroma, formed by damaged nerve has inc Na channels and decreased K channels and causes spontaneous activation (also in surrounding tissue)

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15
Q

What causes central sensitzation?

aka how does injury increase excitability of spinal cord neurons

A

Central sensitization= decreased threshold for activation and enhanced response to stimuli in central nervous system

Caused by:
- increased receptive field (causes a stimulus to activate greater number of spinal neurons)
- increased intracellular Ca2+ (leading to inc AMPA receptor and kinase-mediated phosphorylation of AMPA/NMDA)
- increased local exitatory control (via Glu release to boost AMPA/NMDA)
- decreased local inhibitory control (death of inhibitory neurons, decreased GABA/Gly, GABA reversal potential)
- altered descending control from brain (5-HT pathways more active)
- activated glial cells from spinal cord (glia release chemokines and cytokines onto neurons and influence how they process pain info)

  1. increased delivery of AMPA
  2. increased expression of AMPA
  3. increased phosphorylation of AMPA/NMDA
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16
Q

How can the somatosensory system dynamically respond to injury?

A

EARLY phase of central sensitization: increased nocioceptor activity in central nerve terminal means inc Ca2+ influx through NMDA/AMPA receptors and intracellular release of Ca2+ vesicles; which attract kinases which
1. phosphorylate AMPA/NMDA receptor (boosting activity), and
2. phosphorylate K channels which decreases K current (inc membrane excitability), and
3. promote AMPAR delivery to synapses (inc excitatory transmisson)

17
Q

What causes hyperalgesia?

A

Larger receptive field: stimulus will activate a greater number of sensory neurons/spinal cord neurons, thus a greater/prolonged pain response is generated

18
Q

What causes allodynia?

A

A-beta fibers gain access to pain circuits following injury: A-beta and C fibers become connected via interneurons in spinal cord

19
Q

What causes spontaneous pain?

A

neuromas: damages nerve forms neuroma which has increased Na channels and decreased K channels and can be so excitable that it fires on its own

20
Q

How does the somatosensory system respond to pain over a long timescale?

A

Gene expression: Central sensitization: TF (eg KREB) drive expression of genes that have long lasting modifications of neurons important in chronic pain

Inflammatory pain: gene expression causes inc BDNF/peptides/Na+ channels= inc threshold for stimuli
Neuropathic pain: gene expression alters ion channel expression (inc Na and dec K) to form a neuroma= spontaneous excitation

high levels of nocioceptor activity cause inc in inflammatory mediators; binding of inflammatory mediators can alter gene transcription
neuromas dont j occur at injury site, also in peripheral tissue (thus contributing to hyperalgesia)

21
Q

Whats the evidence for central sensitization?

A

Electrode in mouse spinal cord, and can map the area of peripheral tissue on the hindpaw in control vs chronic model
Following injury, there is
- a larger receptive field
- more spontaneously active neurons
- prolonged pain response
- novel responses to touch

shows that spinal neurons are clearly more responsive following injury

22
Q

What is the early phase of central sensitzation?

A

Kinase: AMPA relocalisation & reducing K current & phosphoyrlation

23
Q

What is the longer phase of central sensitization?

A

Gene expression:
- alters AMPA expression, and thus results in increased excitation of spinal cord neurons
- alters ion channel activity
- increased expression of inflammatory mediators

24
Q

How does central sensitization cause a decrease in inhibitory control?

A
  1. Decreased expression of GABA and glycine
  2. Death of inhibitory interneurons
  3. GABA reversal potential (inhibitory neurons become excitatory)
25
Q

Whats the role/implication of serotonin in central sensitization?

A

Controls pain processing, in the descending pathway 5-HT neruon synapses onto the same neuron that the primary afferent fibre synapses onto

5-HT also located on excitatory and a-delta fibers, so when it binds its receptors it helps boost the release of glutamate-> increased excitability also causes increased NT release

26
Q

How does chronic pain differ between sex? Give example

A

methylglyoxal: in males it increases their thermal pain (via reducing their pain brake), but in women it increases pain brake

MG is a thought to change some Na channels, and diabetes paitents who develop neuropathic pain have higher conc of MG

Neuroscience 3 (6 decks)

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