Pain: Sites of Origin, Pathways, and Neurotransmitters

Pain: Sites of Origin, Pathways, and Neurotransmitters
Source: Canadian Council on Animal Care

The precise mechanisms of pain appreciation in the central nervous system have not been fully elucidated although much is known of the pathways involved. Some of the transmitters and receptors that play an important role in pain have been identified. This has led to the development of drugs that are designed to interrupt pain pathways at specific sites, usually by occupying receptors and blocking the signals. Interruption or modification of pain transmission can occur at several sites and employ different classes of drugs. This opens up the possibility that optimal pain control may require more than one analgesic. This approach has been adopted to control pain in some human patients, and should be discussed with the veterinarians in cases of pain in laboratory animals too.

There are three primary sites at which modification of pain transmission can occur: the periphery; the spinal cord; the cerebrum. Most drugs have actions at more than one site.

At the periphery, the responsiveness of pain receptors is enhanced by the presence of prostaglandins. These prostaglandins are formed in response to tissue trauma. This means that the receptors will respond to a lesser stimulus than before they were sensitised. A number of endogenous compounds (e.g., histamine, serotonin) may be responsible for the actual pain sensation.

In the spinal cord, information on pain is received by cells in the dorsal horn and is passed on to higher centres in the brain along tracts in the spinal cord.

Pain fibres coursing into the cerebrum may end in a number of sites, particularly the reticular formation, the thalamus and the cerebral cortex. In the reticular formation, the pain stimuli may evoke arousal, changes in heart rate, blood pressure, respiration and other activities. It is in the thalamus and cerebral cortex where the appreciation or conscious awareness of pain is to be found.

The diagram above also shows pathways coming from the brain down to the spinal cord. Stimulation of these descending pathways can reduce and even abolish some forms of pain. The body also produces chemicals including endorphins that act on the same receptors as externally administered opioids, to provide pain relief. The significance of descending inhibitory pathways and chemicals in the control and modification of pain sensations is unclear, particularly in animals. Many animals (and humans) appear to tolerate pain and show very few behavioural alterations following a painful insult. This may be due in part to the central inhibitory effects and in part to other biological factors. We must accept that if pain relief is required for a human an animal should have pain relief for the same problem.

Post-traumatic Hypersensitivity

It has long been recognised that trauma to an area is often accompanied by an area of hypersensitivity surrounding the trauma. This is sometimes called secondary hyperalgesia to distinguish it from the increased sensitivity to pain within the trauma area called primary hyperalgesia. Hyperalgesia is recognised by an increase in pain produced by stimuli at the threshold for pain or by a decrease in the pain threshold in that area.

Following an injury, dorsal horn cells are bombarded by stimuli originating from pain receptors. Over a period of time, the receptive field of these cells increases. While it is likely that many chemical processes are involved in central sensitisation, N-methyl D-aspartate (NMDA) receptors are thought to be key in the process. This process of increasing central sensitisation of dorsal horn cells has been called windup.

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