F
Fulton T. Crews
Researcher at University of North Carolina at Chapel Hill
Publications - 281
Citations - 22207
Fulton T. Crews is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Receptor & Neurogenesis. The author has an hindex of 74, co-authored 267 publications receiving 20199 citations. Previous affiliations of Fulton T. Crews include LSU Health Sciences Center Shreveport & University at Buffalo.
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Journal ArticleDOI
Down-regulation of serotonin2, but not of beta-adrenergic receptors during chronic treatment with amitriptyline is independent of stimulation of serotonin2 and beta-adrenergic receptors
J.A. Scott,Fulton T. Crews +1 more
TL;DR: The results suggest that the 5- HT2 receptor is not down-regulated by direct stimulation by serotonin agonists and that the down-regulation of 5-HT2 receptors by amitriptyline is independent of down- regulation of beta-adrenergic receptors.
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Phorbol esters inhibit agonist-stimulated phosphoinositide hydrolysis in neuronal primary cultures.
Rueben A. Gonzales,Philip H. Greger,Stephen P. Baker,Neil I. Ganz,Carolyn Bolden,Mohan K. Raizada,Fulton T. Crews +6 more
TL;DR: The effects of phorbol esters on neurotransmitter-stimulated phosphoinositide (PI) hydrolysis in neurons in primary culture were investigated in this article, where 10-day-old neuronal cultures were incubated with [ 3 H]inositol for 2-3 days, exposed to phorbols esters, and the release of [ 3 h] inositol phosphates was measured in the presence of 10 mM lithium.
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Deficits in adult prefrontal cortex neurons and behavior following early post-natal NMDA antagonist treatment.
TL;DR: Findings indicate that early brain insults affecting glutamatergic neurotransmission lead to persistent brain pathology that could contribute to impulsivity and cognitive dysfunction.
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Adolescent Intermittent Alcohol Exposure: Deficits in Object Recognition Memory and Forebrain Cholinergic Markers
H. Scott Swartzwelder,H. Scott Swartzwelder,Shawn K. Acheson,Shawn K. Acheson,Kelsey M. Miller,Kelsey M. Miller,Hannah G. Sexton,Hannah G. Sexton,Wen Liu,Fulton T. Crews,Mary-Louise Risher,Mary-Louise Risher +11 more
TL;DR: The present results identify a specific deficit in memory function after AIE and establish a possible neural mechanism of that deficit that may be of translational significance and suggest a possible mechanism underlying the effects of AIE on memory and hippocampal function as well as possible therapeutic or preventive strategies for AIE.
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Insulin-like growth factor I receptor binding in brains of Alzheimer's and alcoholic patients.
TL;DR: Human insulin‐like growth factor I binding sites in cerebral cortex and hippocampus appear unaffected by several variables, as well as other variables such as immediate cause of death and medications administered before death.