Abstract

Psychophysiological sensing of pain is formed due to the activity of a number of neuronal mechanisms. Among the pain-related processes, nociception per se, peripheral sensitization, synaptic plasticity, central sensitization, forming of abnormal excitability, structural reorganization in the respective neuronal networks, modulation of recurrent suppression, and a few other phenomena/processes can be mentioned. Nociception includes the processes of transduction, transmission, spreading, and perception of the pain signals. Transduction of the pain influences is a process of transformation of excessively strong and/or (sometimes) long-lasting mechanical, thermal, or chemical stimuli in electrical spike activity generated in peripheral processes of primary nociceptive sensory neurons. This process is mediated by specific receptor-channel complexes that are expressed exclusively in the nociceptive units; it also includes synaptic transmission to secondary and higher-order neurons of the nociception system and modulation of this transmission in neuron-to-neuron synapses in the nociception ascending pathways. The abnormal excitability, structural reorganization, and modulation of recurrent suppression are especially typical of neuropathic pain. Central sensitization is a phenomenon typical of inflammation-related pain, neuropathic pain, and “functional” pain. Different mechanisms responsible for the formation of pain can be targets for analgesic agents; naturally, elucidation of the mechanisms of antinociceptive effects is critically important. Some aspects of the nociception and antinociception events can, in many cases, be examined only in model experiments on animals. In this review, we describe the classification of the types of pain, mention some particular experimental models of pain, analyze the respective physiological mechanisms acting in such models, and also discussed some advantages and limitations of different experimental approaches used in these models.

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