Role of Trace Amines and Their Receptors in Neuroinflammation Development and Posttraumatic Spinal Cord and Brain Repair

Traumatic spinal cord and brain injuries are grave neurological conditions manifesting as a partial or total disruption of motor, sensory and autonomic functions, and in the case of traumatic brain injury, able to cause headaches and migraines, memory impairment and other cognitive dysfunctions. Central nervous system injuries evoke severe neuroinflammation characterized by an acute reactivity of microglia, macrophages and astrocytes, which leads to such long-term consequences as local scarring, gliosis, and myelination defects that significantly affect brain development and function. Trace amines (TAs) can significantly contribute to the development of neuroinflammation and hypoxia in spinal cord and brain injuries. Some individual TAs are able to influence reparative processes, e.g., 3-iodothyronamine is involved in the regulation of apoptosis, octopamine modulates the state of astrocytes, agmatine affects post-injury expression of trophic factors and neurogenesis. Moreover, such TAs as tyramine, tryptamine and beta-phenylethylamine, as well as trace amine-associated receptors (TAARs), act as functional neuromodulators in the spinal cord and brain, and affect locomotor activity irrespective of the descending projections of classical monoamines. This review summarizes the data on the role of various TAs and TAARs in the development of inflammatory processes during spinal cord and brain injuries, as well as addresses the prospects for their potential therapeutic applications.