Cody A. Boyle
University of North Dakota
11 Papers
17 Citations
Cody A. Boyle is an academic researcher from University of North Dakota. The author has contributed to research in topics: Medicine & Receptor. The author has an hindex of 4, co-authored 7 publications.
Chat about Author
Papers
Hit and run versus long-term activation of PARP-1 by its different domains fine-tunes nuclear processes
Colin Thomas,Yingbiao Ji,Chao Wu,Haily Datz,Cody A. Boyle,Brett MacLeod,Shri Patel,Michelle Ampofo,Michelle Currie,Jonathan Harbin,Kate Pechenkina,Niraj Lodhi,Sarah J. Johnson,Alexei V. Tulin +13 more
TL;DR: It is demonstrated that different functions of PARP-1 are coordinated by interactions among these domains and their targets, leading either to short-term activation of the enzyme or to prolonged and sustained activity.
Oxytocin receptors excite lateral nucleus of central amygdala by phospholipase Cβ- and protein kinase C-dependent depression of inwardly rectifying K+ channels.
Binqi Hu,Cody A. Boyle,Saobo Lei +2 more
TL;DR: Activation of oxytocin receptors facilitates neuronal excitability in rat lateral nucleus of central amygdala (CeL) and OXTR‐induced excitation is mediated by inhibition of inwardly rectifying K+ (Kir) channels.
22
Roles of K+ and cation channels in ORL-1 receptor-mediated depression of neuronal excitability and epileptic activities in the medial entorhinal cortex.
TL;DR: It is demonstrated that activation of ORL‐1 receptors remarkably inhibited the epileptiform activity in entorhinal slices induced by application of picrotoxin or by deprivation of extracellular Mg2+.
13
Activation of Oxytocin Receptors Excites Subicular Neurons by Multiple Signaling and Ionic Mechanisms.
Binqi Hu,Cody A. Boyle,Saobo Lei +2 more
TL;DR: In this article, the authors demonstrate that application of the selective OXT receptor (OXTR) agonist, [Thr4,Gly7]-oxytocin (TGOT), excited subicular neurons via activation of TRPV1 channels, and depression of K+ channels.
8
Ionic signalling mechanisms involved in neurokinin‐3 receptor‐mediated augmentation of fear‐potentiated startle response in the basolateral amygdala
TL;DR: The results provide a cellular and molecular mechanism whereby NK3R activation excites BLA neurons and enhances FPS and showed that TRPC4/5 and GIRK channels were involved in NK3 R‐elicited facilitation of FPS.
4