Nociception
After the initial insult, peripheral nociceptors are activated by transduction through thin myelinated Aδ and unmyelinated C-fibers to the dorsal root group and into the posterior horn of the spinal cord. The axon bifurcates into two branches with one branch continuing to the CNS, the other innervating peripheral tissues. Action potentials are generated and the nociceptive signals initiate excitatory neurotransmitters such as glutamate and substance P, neuromodulators including brain-derived neurotrophic factor. These bind with afferent nerves which activate corresponding receptors on the postsynaptic nerve terminals (Fishman et al., p. 29).
Superficial lamina (laminae I and II) and deep laminae (lamina V and VI) receive primary afferent fibers in the dorsal horn. Projections from laminae I and V continue ventrally through the spinothalamic tract (STT) to the thalamus. The spinobulbar pathway receives input from the STT and continues to the hypothalamus, amygdala, periaqueductal gray …show more content…
Lamina II contains neurons that release γ-aminobutyric acid (GABA), glycine or enkalphins which inhibits further conduction of nociceptive stimulus (Fishman et al., p. 30). Peripheral sensitization will limit the degree of inhibition due to release of inflammatory mediators at the site of injury, or cause hyperalgesia with non-noxious stimuli (Fishman et al., p. 31). Inflammatory mediators and sensitization factors include bradykinin, leukotrienes, prostaglandin E2, nerve growth factor, serotonin (5HT), tumor necrosis factor alpha, and interleukins. Once sensitivity occurs, changes in neuronal structure (plasticity) will alter the threshold and response of the receptor. Ion channel expression and synaptic modulators will increase sensitivity to nociceptive stimulus. These changes, if continued, will lead to neurochemical and structural changes in the CNS- central sensitization (Fishman et al., p.
After the initial insult, peripheral nociceptors are activated by transduction through thin myelinated Aδ and unmyelinated C-fibers to the dorsal root group and into the posterior horn of the spinal cord. The axon bifurcates into two branches with one branch continuing to the CNS, the other innervating peripheral tissues. Action potentials are generated and the nociceptive signals initiate excitatory neurotransmitters such as glutamate and substance P, neuromodulators including brain-derived neurotrophic factor. These bind with afferent nerves which activate corresponding receptors on the postsynaptic nerve terminals (Fishman et al., p. 29).
Superficial lamina (laminae I and II) and deep laminae (lamina V and VI) receive primary afferent fibers in the dorsal horn. Projections from laminae I and V continue ventrally through the spinothalamic tract (STT) to the thalamus. The spinobulbar pathway receives input from the STT and continues to the hypothalamus, amygdala, periaqueductal gray …show more content…
Lamina II contains neurons that release γ-aminobutyric acid (GABA), glycine or enkalphins which inhibits further conduction of nociceptive stimulus (Fishman et al., p. 30). Peripheral sensitization will limit the degree of inhibition due to release of inflammatory mediators at the site of injury, or cause hyperalgesia with non-noxious stimuli (Fishman et al., p. 31). Inflammatory mediators and sensitization factors include bradykinin, leukotrienes, prostaglandin E2, nerve growth factor, serotonin (5HT), tumor necrosis factor alpha, and interleukins. Once sensitivity occurs, changes in neuronal structure (plasticity) will alter the threshold and response of the receptor. Ion channel expression and synaptic modulators will increase sensitivity to nociceptive stimulus. These changes, if continued, will lead to neurochemical and structural changes in the CNS- central sensitization (Fishman et al., p.