Table 1.
OXT Regulatory Premises | Existence of Hydroxylamine Energy Fibers | Expression of OXT Receptors | The Analgesic Mechanism of OXT | References |
---|---|---|---|---|
CeA | √ | √ | Reduces anxiety and depression to do indirect analgesia | [64, 76, 77] |
NAc | √ | √ | Regulates the opioid system | [40, 78] |
PAG | √ | √ | - | [57, 79, 80] |
DRG | × | √ | Activate the cAMP-PKA pathway to increase intracellular Ca2+ and decrease the DRG neuron current mediated by ATP The intracellular calcium signals of primary sensory neurons in rats activated by OXT have dose and PKC dependent mechanisms Increases intracellular calcium in normal KCl concentration in neurons by inhibiting membrane depolarization Activates the neuronal membrane hyperpolarization by Ca2+/nNOS/NO/K-ATP pathway |
[46, 81-83] [84] [85, 86] [81, 82, 87] |
Skin | × | √ | Activates TRPV1 channel to promote Ca2+ influx Skin Inhibits discharge of C fibers and blocks the input transmission to spinal WDR neurons |
[21, 88, 89] [35, 67] |
Spinal cord | √ | √ | Associates with extracellular signal-related protein kinase ERK1/2 Blocking Aδ and C fibers by activating the inhibitory GABAergic interneurons Promotes glutamate release, stimulate a large quantity of inhibitory GABA interneurons, block Aδ and C fiber Regulates the opioid system Inhibits the excitability of the membrane of gelatinous cells |
[90-92] [44, 93] [94-96] [43, 93] [97, 98] |