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Processing Information in the Dorsal Horn

المؤلف:  Kim E. Barrett, Susan M. Barman, Heddwen L. Brooks, Jason X.-J. Yuan

المصدر:  Ganongs Review of Medical Physiology

الجزء والصفحة:  25th E, P172-173

2026-10-14

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Transmission in nociceptive pathways can be interrupted by actions within the dorsal horn of the spinal cord at the site of sensory afferent termination. Many people have learned from practical experience that rubbing or shaking an injured area decreases the pain due to the injury. The relief may be due to the simultaneous activation of innocuous cutaneous mecha noreceptors whose afferents emit collaterals that terminate in the dorsal horn. The activity of these cutaneous mechanosensitive afferents may reduce the responsiveness of dorsal horn neurons to their input from nociceptive afferent terminals. This is called the gate-control mechanism of pain modulation and it serves as the rationale behind the use of transcutaneous electrical nerve stimulation (TENS) for pain relief. This method uses electrodes to activate Aα and Aβ fibers in the vicinity of the injury.

Opioids are a commonly used analgesic that can exert their effects at various places in the CNS, including in the spinal cord and dorsal root ganglia. Figure 1 shows some of the various modes of action of opioids to decrease nociceptive transmission. There are interneurons in the superficial regions of the dorsal horn that contain endogenous opioid peptides (enkephalin and dynorphin). These interneurons terminate in the region of the dorsal horn where nociceptive afferents terminate. Opioid receptors are located on the terminals of nociceptive fibers and on dendrites of dorsal horn neurons, allowing for both presynaptic and postsynaptic sites of actions for opioids. Activation of the postsynaptic opioid receptors hyperpolarizes the dorsal horn interneuron by causing an increase in K+ conductance. Activation of the presynaptic opioid receptors leads to a decrease in Ca2+ influx, resulting in a decrease in release of glutamate and substance P. Together these actions reduce the duration of the EPSP in the dorsal horn neuron. Activation of opioid receptors on dorsal root ganglia cell bodies also contributes to reduced transmission from nociceptive afferents.

Fig1. Actions of opioids to reduce sensory transmission in pain pathways at the level of the dorsal root ganglion (DRG) and spinal cord dorsal horn region. A) Activation of a nociceptor leads to the release of glutamate and neuropeptides from its nerve terminals that synapse on spinothalamic tract projection neurons. This leads to the depolarization (activation) of spinothalamic tract projection neurons. Enkephalin (ENK)-containing interneurons mediate their effects via opioid receptors on the terminals of nociceptive afferent fibers and on dendrites of dorsal horn neurons to exert both presynaptic and postsynaptic inhibition. B) The action of an opioid (eg, morphine) within the DRG is to decrease Ca2+ influx leading to a decrease in the duration of the invoked action potential in the nociceptive neuron and a reduction in transmitter release from the nociceptive neuron onto a neuron in the dorsal horn. Opioids also hyperpolarize the membrane of dorsal horn neuron by activation of a K+ conductance; opioids also decrease the amplitude of the excitatory postsynaptic potential (EPSP) produced by stimulation of nociceptors.

Patients who receive long-term pain management with morphine may become resistant to the drug, requiring progressively higher doses for pain relief. This acquired tolerance is different from addiction, which refers to a psycho logical craving. Psychological addiction rarely occurs when morphine is used to treat chronic pain, provided the patient does not have a history of drug abuse. Clinical Box 1 describes mechanisms involved in motivation and addiction.

CLINICAL BOX 1.