Cortical spreading depression is a pathophysiological event shared in migraines, strokes, traumatic brain injuries, and epilepsy. It associated with complex hemodynamic responses, which, turn, contribute to neurological problems. In this study, we investigated the role of canonical transient receptor potential channel 3 (TRPC3) responses elicited by cortical depression. Cerebral blood flow was ...

Hypertension is associated with an elevation in agonist-induced vasoconstriction, but mechanisms involved require further investigation. Many vasoconstrictors bind to phospholipase C-coupled receptors, leading to an elevation in inositol 1,4,5-trisphosphate (IP(3)) that activates sarcoplasmic reticulum IP(3) receptors. In cerebral artery myocytes, IP(3) receptors release sarcoplasmic reticulum ...

In most non-excitable cells, calcium (Ca(2+)) release from the inositol 1,4,5-trisphosphate (InsP(3))-sensitive intracellular Ca(2+) stores is coupled to Ca(2+) influx through the plasma membrane Ca(2+) channels whose molecular composition is poorly understood. Several members of mammalian TRP-related protein family have been implicated to both receptor- and store-operated Ca(2+) influx. Here w...

Endogenously expressed canonical transient receptor potential (TRPC) homologs were investigated for their role in forming store-operated, 1-oleoyl-2-acetyl-sn-glycerol-stimulated, or carbachol (CCh)-stimulated calcium entry pathways in HEK-293 cells. Measurement of thapsigargin-stimulated Ba entry indicated that the individual suppression of TRPC1, TRPC3, or TRPC7 protein levels, by small inter...

Song T, Hao Q, Zheng YM, Liu QH, Wang YX. Inositol 1,4,5trisphosphate activates TRPC3 channels to cause extracellular Ca influx in airway smooth muscle cells. Am J Physiol Lung Cell Mol Physiol 309: L1455–L1466, 2015. First published October 9, 2015; doi:10.1152/ajplung.00148.2015.—Transient receptor potential-3 (TRPC3) channels play a predominant role in forming nonselective cation channels (N...

Recently studies found that TRPC3 and TRPC6 played an important role in cardiovascular disease. Hypertension, as a cardiovascular disease causing the highest morbidity and mortality, has close relationship with the expressions of TRPC3 and TRPC6. Unbalanced calcium homeostasis is the major factor of pathogenesis of hypertension. Changes of intracellular calcium concentration depend on calcium t...

Atrial fibrillation (AF) is a significant contributor to cardiovascular morbidity and mortality. The currently available treatments are limited and AF continues to be a major clinical challenge. Clinical studies have shown that AF is frequently associated with dysfunction in the sino-atrial node (SAN). The association between AF and SAN dysfunction is probably related to the communication betwe...

Nonvoltage-gated cation currents, which are activated following stimulation of phospholipase C (PLC), appear to be major modes for Ca2+ and Na+ entry in mammalian cells. The TRPC channels may mediate some of these conductances since their expression in vitro leads to PLC-dependent cation influx. We found that the TRPC3 protein was highly enriched in neurons of the central nervous system (CNS). ...

Memory formation requires de novo protein synthesis, and memory disorders may result from misregulated synthesis of critical proteins that remain largely unidentified. Plasma membrane ion channels and receptors are likely candidates given their role in regulating neuron excitability, a candidate memory mechanism. Here we conduct targeted molecular monitoring and quantitation of hippocampal plas...

Structural cardiac remodeling, accompanying cytoskeletal reorganization of cardiac cells, is a major clinical outcome of diastolic heart failure. A highly local Ca2+ influx across the plasma membrane has been suggested to code signals to induce Rho GTPase-mediated fibrosis, but it is obscure how the heart specifically decodes the local Ca2+ influx as a cytoskeletal reorganizing signal under the...