Recognition and Alleviation of Pain in Laboratory Animals (2009) / Chapter Skim
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2 Mechanisms of Pain
2 Mechanisms of Pain
Pages 33-46
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From page 33... ...
Typically, noxious stimuli, including tissue injury, activate nociceptors that are present in peripheral structures and that transmit information to the spinal cord dorsal horn or its trigeminal homologue, the nucleus caudalis. From there, the information continues to the brainstem and ultimately the cerebral cortex, where the perception of pain is generated (Figure 2-1)
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From page 34... ...
that originate throughout the neuraxis and regulate the processing of ascending nociceptive messages. The figure also illustrates several important surgical preparations used to study nociceptive processing under conditions in which different parts of the brain are disconnected from afferent nociceptive input.
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From page 35... ...
. Importantly, biochemical and molecular analysis of the nociceptor has identified many of the transducer molecules that are activated by noxious stimuli, such as TRPV1, which responds to noxious heat, reduced pH as occurs in inflammation, and the chemical capsaicin.
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From page 36... ...
Although silent nociceptors are difficult to activate within the normal range of noxious stimulus intensities, after tissue insult these nociceptors "wake up" in response to endogenous chemical mediators associated with tissue injury. Silent nociceptors are typically associated with increased spontaneous activity and responsiveness to noxious and even innocuous stimulus intensities.
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From page 37... ...
in laboratory animal research was more common years ago, but it remains useful for recording the activity of spinal cord or brainstem neurons under conditions not compromised by anesthetics or analgesics. With the animals under deep general anesthesia, the procedure involves transection of the brainstem at the level of the midbrain (typically between the inferior and superior colliculi)
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From page 38... ...
Their removal via decerebration leads to enhanced nociceptive reflexes and spinal neuron responses to nociceptive input. Accordingly, spinal cord transection often follows decerebration to enable physiological studies in unanesthetized animals, but it is not a prerequisite of the decerebrate preparation.
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From page 39... ...
, whereas secondary hyperalgesia is associated with changes in the excitability of neurons in the CNS, including the spinal cord and supraspinal sites in the brain. Accordingly, primary hyperalgesia is associated with peripheral sensitization of nociceptors and secondary hyperalgesia with central sensitization.
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From page 40... ...
The remarkable number of molecules implicated in central sensitization (whether produced by tissue or nerve injury) may lead to the development of new pharmacological approaches to managing persistent pain.
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From page 41... ...
. In addition to altered nociceptive processing, repetitive or persistent pain in the neonatal period leads to changes in brain development, widespread alterations in animal behavior, and increased vulnerability to stress and anxiety disorders or chronic pain syndromes (Anand et al.
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From page 42... ...
A recent study reported that C3H mice exposed to environmental enrichment, which can reduce stress compared with a standard environment (i.e., standard plastic cages with bedding) , reacted more quickly (i.e., exhibited a shorter freezing time)
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From page 43... ...
How data from such studies translate into the normal behavioral repertoire of animals in a laboratory environment and in other types of experimental studies remains to be determined. Nevertheless, it is important to keep in mind the possibility of stress-induced effects when assessing pain in animals because the absence of response to a noxious stimulus or of pain-indicative behavior may be due to significant stress and misleadingly suggest the absence of pain.
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From page 44... ...
2007. Ketamine re duces the cell death following inflammatory pain in newborn rat brain.
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From page 45... ...
2005. The ontogeny of neuropathic pain: Postnatal onset of mechanical allodynia in rat spared nerve injury (SNI)
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From page 46... ...
2007. The cerebral signature for pain perception and its modulation.
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