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. 2023 Jan 13;24(2):1633. doi: 10.3390/ijms24021633

Figure 1.

Figure 1

Pain and neurogenic inflammation in endometriosis. Endometriotic cytokines in the peritoneum, prostaglandins, interleukins (ILs), calcitonin gene-related peptide (CGRP), substance P (SP), nociceptive opioid peptide (NOP), and transient receptor potential vanilloid 1 (TRPV1) stimulate sensory peripheral nerve endings. The nociceptive signal conduct in the myelinated Aδ fibers or unmyelinated C fibers to the spinal cord. Subsequently, opioid peptides, which are synthesized as chemokine receptors, promote an antinociceptive effect in the dorsal root ganglia (DRG). In the DRG, chemokine receptors and opioid receptors receive the nociceptive message and transfer it to the spinal cord. Within the spinal cord, neurotransmitters such as CGRP, SP, and glutamate are released to activate the second-order neurons. Then, CGRP will combine with the CGRP receptor complex and SP will act on the neurokine-1 receptor (NK-1). The noxious message travels up to the thalamus via ascending axons and then finally reaches the somatosensory cortex. The nociceptive input can be attenuated or facilitated through endogenous opioid release via a descending pain-modulated system, which includes two crucial structures, periaqueductal gray (PAG) and rostroventral medulla (RVM).