Fig. 3
From: Recent advances in basic research on the trigeminal ganglion
Schematic representation for a possible molecular mechanism involved in the trigeminal nociceptive and pathological pain. a Trigeminal nociceptive pain. Eugenol inhibits the generator potential by acting transient receptor potential ankyrin 1 (TRPA1) and P2X 3 receptor. Also eugenol suppress the action potential firing by reducing voltage-gated sodium (Nav), calcium (Cav) and potassium (Kv) channels and hyperpolarization-activated cyclic nucleotide-gated (HCN) channels of the small-diameter TG neurons. Up arrows excitation, down arrows inhibition. b Trigeminal pathological pain. Possible molecular mechanism for a activation of trigeminal neuron–neuron/neuron–satellite glial cells contributes to pathological pain (ectopic allodynia and hyperalgesia) following orofacial inflammation/trigeminal nerve injury. Interaction between neuron and satellite glial cells via substance P (SP), adenosine triphosphate (ATP), and interleukin-1β (IL-1β) signaling resulted in augementation of neuronal firing in small-diameter TG neurons following orofacial inflammation or trigeminal nerve injury, which may develop hyperalgesia. Neuron–neuron communication via SP, ATP, nerve growth factor (NGF), and nitric oxicide (NO) signaling resulted in the activation of neighboring neuronal firing in medium-/large-diameter TG neurons following orofacial inflammation or trigeminal nerve injury, which may develop ectopic allodynia pain. TRPV1 transient receptor potential vanilloid 1, IL-1RI IL-receptor type I, TrkA tyrosine kinase A, NK1R neruokinine 1 receptor, VNUT vesicular nucleotide transporter. Up arrows up-regulation, down arrows down-regulation