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Martin J. Kelly

Researcher at Oregon Health & Science University

Publications -  183
Citations -  11126

Martin J. Kelly is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Receptor & Kisspeptin. The author has an hindex of 61, co-authored 178 publications receiving 10401 citations. Previous affiliations of Martin J. Kelly include Cappagh National Orthopaedic Hospital & University College Cork.

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Rapid actions of plasma membrane estrogen receptors

TL;DR: There is now convincing in vitro evidence that E( 2) can modulate the functions of neural and vascular cells via non-genomic actions, and the actions of discrete pools of E(2) receptors are likely to contribute to the overall effects of the sex steroids.
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Rapid signaling of estrogen in hypothalamic neurons involves a novel G-protein-coupled estrogen receptor that activates protein kinase C

TL;DR: It is discovered that E2 can alter μ-opioid and GABA neurotransmission rapidly through nontranscriptional events in hypothalamic GABA, proopiomelanocortin (POMC), and dopamine neurons, and this unique Gq-coupled estrogen receptor may be involved in rapid signaling in hypothalamus neurons that are critical for normal homeostatic functions.
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Hypothalamic Proopiomelanocortin Neurons Are Glucose Responsive and Express KATP Channels

TL;DR: POMC neurons may function as an integrator of metabolic cues and synaptic input for controlling homeostasis in the mammal, and their firing rate varied with changes in glucose concentrations.
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Rapid effects of estrogen to modulate G protein-coupled receptors via activation of protein kinase A and protein kinase C pathways.

TL;DR: Beta-estradiol (E2) can activate both PKA and PKC to cause a heterologous desensitization of both mu-opioid and GABA(B) receptors, which has the potential to alter synaptic transmission in many regions of the CNS.
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Estrogen Modulation of G-protein-coupled Receptors

TL;DR: G-protein-coupled receptors are the largest class of membrane-bound receptors, and it appears that many of the rapid effects mediated by estrogen could involve changes in GPCR-effector system coupling in excitable cells within the reproductive axis.