Neuro Objectives 21

1.Nociceptor: a pain receptor

Physical characteristics: exist as free nerve endings, respond to noxious stimuli without adapting (thus, nociceptors can be sensitized). Typically pseudounipolar and release neurotransmitters at both ends of the neuron. Once signal is reached at axon hillock, action potential fires bidirectionally to cause release at both ends (the axon reflex). This reflex action in the periphery is what causes redness, swelling, and tenderness (peripheral sensitization).

2.First pain: Aδ fibers (thinly myelinated with high threshold mechanoreceptors); initial, focused pain

Second pain: C fibers (unmyelinated polymodal nociceptors); secondary, throbbing, persistent pain

  • Note: Aδ fibers only respond to high intensity mechanic stimuli, and have a higher transmission velocity. Thus, the initial focused pain arrives, and is followed by the C fibers which is less localized due to the general nature of the incoming signal (a wide area can be signaled because they are polymodal receptors)

3.Dorsal horn pain neurotransmitters:

  1. Glutamate: can interact with NMDA and non-NMDA excitatory amino acid receptors
  2. Substance P: an eleven amino acid peptide

4.Describe the descending pain-control pathway and its use in modulating nociceptive input: Begins at opioid receptors in the periaqueductal gray of the midbrain and projects to the locus coerulus and the medullary reticular formation. From here, the pathway project to the dorsal horn along the dorsolateral funiculus to synapse with either the primary afferent, second order pain transmission neuron, or an interneuron. It is useful in modulating nociceptive input by giving the affective component of pain. It therefore interprets pain in its setting and can diminish/strengthen pain depending on external, environmental settings.

5.Three sites where endogenous opioids can decrease pain:

  1. Midbrain: activates opioid receptors to disinhibit descending pain modulating tracts
  2. Second order transmission cells: activates opioid receptors to block the ascending pain transmission tracts
  3. C fibers: activates opioid receptors at central terminals to block the ascending C fiber pain transmission tracts

6.Allodynia: non-noxious stimulation of pain receptors (swallowing with a sore throat)

Hyperalgesia: sensitization of nociceptors to respond more vigorously to a stimulus (painful touch when sunburned)

Central sensitization: heightened sensitivity to pain in the central nervous system (second order cells changing their response patterns after sustained afferent discharge).

Peripheral sensitization: heightened sensitivity to pain in the peripheral nervous system. (release of neurotransmitters via axon reflex can amplify signal; recruitment of additional peripheral neurons, activation of silent nociceptors during injury).

  • Note: Both central and peripheral sensitization can contribute to allodynia or hyperalgesia

7.Three different levels of plasticity:

  1. Synaptic plasticity (seconds to minutes): Increases/decreases neurotransmitter release or response to the neurotransmitter
  2. Cellular plasticity (hours to days): Changes the cell phenotype via transcriptional/translational modifications
  3. Systems plasticity (months to years): Reorganization of neural connectivity