Abstract
Pain is an unpleasant sensation that alerts one to the presence of obnoxious stimuli or sensations. These stimuli are transferred by sensory neurons to the dorsal root ganglia-spinal cord and finally to the brain. Glial cells in the peripheral nervous system, astrocytes in the brain, dorsal root ganglia, and immune cells all contribute to the development, maintenance, and resolution of pain. Both innate and adaptive immune responses modulate pain perception and behavior. Neutrophils, microglial, and T cell activation, essential components of the innate and adaptive immune responses, can play both excitatory and inhibitory roles and are involved in the transition from acute to chronic pain. Immune responses may also exacerbate pain perception by modulating the function of the cortical-limbic brain regions involved in behavioral and emotional responses. The link between an emotional state and pain perception is larger than what is widely acknowledged. In positive psychological states, perception of pain along with other somatic symptoms decreases, whereas in negative psychological states, these symptoms may worsen. Sex differences in mechanisms of pain perception are not well studied. In this review, we highlight what is known, controversies, and the gaps in this field.
Highlights
Pain is a complex concept that requires the orchestration of a plethora of structures and mechanistic pathways
The degree of pain perceived largely remains a subjective or qualitative process, with “objective” or quantitative markers of pain remaining elusive. Both central and peripheral structures play a part in this complex, highly coordinated process; from the sensory neurons and dorsal root ganglia that serve as conduits, to neurotransmitters responsible for transmitting information from neuron to neuron to signal pain, and glia/support cells that help in detoxification and extinguishing processes (Figure 1 and Table 1)
Similar to satellite glial cells (SGCs) and astrocytes, Schwann cells release important mediators that interact with neurons and that are implicated in chronic pain
Summary
Pain is a complex concept that requires the orchestration of a plethora of structures and mechanistic pathways. Immune and glial cells respond to injury or noxious stimuli and modulate function of dorsal root ganglia, trigeminal ganglion, and limbic structures to alter pain perception. All these modulate function of dorsal root ganglia, trigeminal ganglion, and limbic structures to alter pain perception All these inputs are integrated and together constitute one’s cognitive state, which can affect pain perception and experience. The suppression of glial gap junction protein, connexin or glutamic acid decarboxlylase, the enzyme responsible for synthesizing GABA in SGCs of rats with infraoribital/maxillary nerve injury, reduces pain-like behavior and suggests that GABA acts at the trigeminal ganglion, not at the spinal level [11,22]. Isolated neurons do not behave or function the same as they do when surrounded by support cells that include the glia, astrocytes, and Schwann cells
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