Fig. 4.

PRV induces Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) δ transcription in sacral spinal cord. A: Ingenuity Pathways Analyses identifies CaMKII as a candidate regulatory node in neurogenic cystitis pain. Genes that met the twofold change threshold and were mapped in the Ingenuity Pathways Knowledge are circled. Genes that were not mapped in the Ingenuity Pathways Knowledge are represented by white nodes. Nodes are displayed with various shapes that represent the functional class of the gene product. Nodes with double edges represent a group or a complex. Tac1, tachykinin 1; BDNF, brain derived neurotrophic factor; TRKB, tyrosine kinase receptor B; NMDAR, N-methyl-d-aspartate receptor; AMPAR, α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor; mGluR, metabotropic glutamate receptor; NK1R, neurokinin 1 receptor; CAMK, Ca²⁺/calmodulin-dependent protein kinase; PIP₂, phosphatidylinositol 4,5-bisphosphate; IP₃, inositol 1,4,5-trisphosphate; IP₃R, IP₃ receptor; PI3K, phosphatidylinositol 3-kinase; ER, estrogen receptor; CREB, cAMP response element binding protein. B: CaMKIIδ mRNA expression level increased in sacral spinal cord of B6 mice [wild type (WT)] at PIDs 2 and 4, compared with PID 0 (n = 4–6). *P < 0.05. CaMKIIδ mRNA expression level was not significantly increased in sacral spinal cord of mast cell-deficient C57BL6/J W^sh/W^sh mice (Sh) at PIDs 2 or 4, compared with PID 0 (n = 4–6, P > 0.05). Values are means ± SE.