Mary Caulfield

Learn More
At least five muscarinic receptor genes have been cloned and expressed. Muscarinic receptors act via activation of G proteins: m1, m3 and m5 muscarinic receptors couple to stimulate phospholipase C, while m2 and m4 muscarinic receptors inhibit adenylyl cyclase. This review describes the localization, pharmacology and function of the five muscarinic receptor(More)
Bradykinin (BK) is a peptide mediator released in inflammation that potently excites sympathetic neurons. We have studied the mechanism of this excitation in dissociated rat sympathetic neurons and found that at low nanomolar (EC50 = 0.9 nM) concentrations, BK inhibited the M-type K+ current IK(M). Studies with the selective antagonist Hoe140 revealed that(More)
1. Microinjection of selective antibodies into superior cervical ganglion (SCG) neurones has identified the G-protein alpha-subunits mediating muscarinic receptor inhibition of M-type K+ current (IK(M)) and alpha-adrenoceptor inhibition of Ca2+ current (ICa). 2. Antibodies specific for G alpha q/11, but not those for G alpha o, reduced M-current inhibition(More)
Rat superior cervical ganglion (SCG) neurons express low-threshold noninactivating M-type potassium channels (IK(M)), which can be inhibited by activation of M1 muscarinic receptors. This inhibition occurs via pertussis toxin-insensitive G-proteins belonging to the Galphaq family (Caulfield et al., 1994 ). We have used DNA plasmids encoding antisense(More)
One postsynaptic action of the transmitter acetylcholine in sympathetic ganglia is to inhibit somatic N-type Ca2+ currents: this reduces Ca2+-activated K+ currents and facilitates high-frequency spiking. Previous experiments on rat superior cervical ganglion neurons have revealed two distinct pathways for this inhibitory action: a rapid, voltage-dependent(More)
Cannabinoid receptor ligands irreversibly inhibited peak voltage-activated Ca currents (44%) in NG108-15 cells; this inhibition was Pertussis toxin-sensitive. Inhibition was largely due to a reduction in the omega-conotoxin sensitive portion of high-voltage activated (HVA) current, although there was also a significant decrease in low-voltage activated(More)
One mechanism considered responsible for the hypercalcemia that frequently accompanies malignancy is secretion by the tumor of a circulating factor that alters calcium metabolism. The structure of a tumor-secreted peptide was recently determined and found to be partially homologous to parathyroid hormone (PTH). The amino-terminal 1-34 region of the factor(More)