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A. The speed at which action potentials are conducted is a function of each fiber's cross-sectional diameter. Wave peaks in the figure are labeled alphabetically in order of latency. The first peak and its subdivisions are the summed electrical activity of myelinated A fibers. A delayed (slowly conducting) deflection represents the summed action potentials of unmyelinated C fibers. The compound action potential of the A fibers is shown on a faster time-base to depict the summation of the action potentials of several fibers.
B. First and second pain are carried by A delta and C fibers, respectively.
A. The speed at which action potentials are conducted is a function of each fiber's cross-sectional diameter. Wave peaks in the figure are labeled alphabetically in order of latency. The first peak and its subdivisions are the summed electrical activity of myelinated A fibers. A delayed (slowly conducting) deflection represents the summed action potentials of unmyelinated C fibers. The compound action potential of the A fibers is shown on a faster time-base to depict the summation of the action potentials of several fibers.
B. First and second pain are carried by A delta and C fibers, respectively.
A. There are three main classes of peripheral nociceptor as well as the silent nociceptors, which are activated by inflammation and various chemical substances.
B. Neurons in lamina I of the dorsal horn receive direct input from myelinated (Ac) nociceptive fibers and both direct and indirect input from unmyelinated (C) nociceptive fibers via interneurons in lamina II. Lamina V neurons receive low-threshold input from large-diameter myelinated Aβ mechanoreceptive fibers as well as inputs from nociceptive Aδ and C fibers. Lamina V neurons send dendrites to lamina IV, where they are contacted by the terminals of Aβ primary afferents. Axon terminals of lamina II interneurons can make contact with dendrites in lamina III that arise from cells in lamina V. Aα primary afferents contact motor neurons and interneurons in the ventral spinal cord (not shown).
B. Neurons in lamina I of the dorsal horn receive direct input from myelinated (Ac) nociceptive fibers and both direct and indirect input from unmyelinated (C) nociceptive fibers via interneurons in lamina II. Lamina V neurons receive low-threshold input from large-diameter myelinated Aβ mechanoreceptive fibers as well as inputs from nociceptive Aδ and C fibers. Lamina V neurons send dendrites to lamina IV, where they are contacted by the terminals of Aβ primary afferents. Axon terminals of lamina II interneurons can make contact with dendrites in lamina III that arise from cells in lamina V. Aα primary afferents contact motor neurons and interneurons in the ventral spinal cord (not shown).
Injury or tissue damage releases bradykinin and prostaglandins, which activate or sensitize nociceptors. Activation of nociceptors leads to the release of substance P and calcitonin gene-related peptide (CGRP). Substance P acts on mast cells (light blue) in the vicinity of sensory endings to evoke degranulation and the release of histamine, which directly excites nociceptors. Substance P also produces plasma extravasation and edema, and CGRP produces dilation of peripheral blood vessels (leading to reddening of the skin); the resultant inflammation causes additional liberation of bradykinin. These mechanisms also occur in healthy tissue, where they contribute to secondary or spreading hyperalgesia
Four major ascending pathways—the spinothalamic, spinoreticular, spinoparabrachial, and spinohypothalamic tracts—contribute sensory information to the central processes that generate pain
Sensory discriminative features of the pain experience are transmitted from the spinal cord to the ventroposterolateral thalamus via the spinothalamic tract (brown). From there, information is transmitted predominantly to the somatosensory cortex. A second pathway, (the spinoparabrachial tract (red), carries information from the spinal cord to the parabrachial nucleus of the dorsolateral pons. These neurons in turn target limbic forebrain regions, including the insular and anterior cingulate cortex, which process emotional features of the pain experience.
Sensory discriminative features of the pain experience are transmitted from the spinal cord to the ventroposterolateral thalamus via the spinothalamic tract (brown). From there, information is transmitted predominantly to the somatosensory cortex. A second pathway, (the spinoparabrachial tract (red), carries information from the spinal cord to the parabrachial nucleus of the dorsolateral pons. These neurons in turn target limbic forebrain regions, including the insular and anterior cingulate cortex, which process emotional features of the pain experience.
The gate control hypothesis was proposed in the 1960s to account for the fact that activation of low-threshold primary afferent fibers can attenuate pain. The hypothesis focused on the interaction of neurons in the dorsal horn of the spinal cord: the nociceptive (C) and nonnociceptive (Aa) sensory neurons, projection neurons, and inhibitory interneurons. In the original version of the model, as shown here, the projection neuron is excited by both classes of sensory neurons and inhibited by interneurons in the superficial dorsal horn. The two classes of sensory fibers also terminate on the inhibitory interneurons; the C fibers indirectly inhibit the interneurons, thus increasing the activity of the projection neurons (thereby "opening the gate"), whereas the Aβ fibers excite the interneurons, thus suppressing the output of the projection neurons (and "closing the gate").
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Local interneurons in the spinal cord integrate descending and afferent nociceptive pathways.
A. Nociceptor circuitry in the dorsal horn:
Nociceptive afferent fibers, local interneurons, and descending fibers interconnect in the dorsal horn of the spinal cord (see also Figure 20-3B). Nociceptive fibers terminate on second order projection neurons. Local GABAergic and enkephalin containing inhibitory interneurons exert both pre- and postsynaptic inhibitory actions at these synapses. Serotonergic and noradrenergic neurons in the brain stem activate the local interneurons and also suppress the activity of the projection neurons. Loss of these inhibitory controls contributes to ongoing pain and pain hypersensitivity.
B. Effects of opiates and opioids on nociceptor signal transmission:
Regulation of nociceptive signals at dorsal horn synapses. 1. Activation of a nociceptor leads to the release of glutamate and neuropeptides from the primary sensory neuron, producing an excitatory postsynaptic potential in the projection neuron. 2. Opiates decrease the duration of the postsynaptic potential, probably by reducing Ca2+ influx, and thus decrease the release of transmitter from the primary sensory terminals. In addition, opiates hyperpolarize the dorsal horn neurons by activating a K+ conductance and thus decrease the amplitude of the postsynaptic potential in the dorsal horn neuron.
A. Nociceptor circuitry in the dorsal horn:
Nociceptive afferent fibers, local interneurons, and descending fibers interconnect in the dorsal horn of the spinal cord (see also Figure 20-3B). Nociceptive fibers terminate on second order projection neurons. Local GABAergic and enkephalin containing inhibitory interneurons exert both pre- and postsynaptic inhibitory actions at these synapses. Serotonergic and noradrenergic neurons in the brain stem activate the local interneurons and also suppress the activity of the projection neurons. Loss of these inhibitory controls contributes to ongoing pain and pain hypersensitivity.
B. Effects of opiates and opioids on nociceptor signal transmission:
Regulation of nociceptive signals at dorsal horn synapses. 1. Activation of a nociceptor leads to the release of glutamate and neuropeptides from the primary sensory neuron, producing an excitatory postsynaptic potential in the projection neuron. 2. Opiates decrease the duration of the postsynaptic potential, probably by reducing Ca2+ influx, and thus decrease the release of transmitter from the primary sensory terminals. In addition, opiates hyperpolarize the dorsal horn neurons by activating a K+ conductance and thus decrease the amplitude of the postsynaptic potential in the dorsal horn neuron.
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