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Jonathan Z. Long

Researcher at Stanford University

Publications -  83
Citations -  12581

Jonathan Z. Long is an academic researcher from Stanford University. The author has contributed to research in topics: JZL184 & Fatty acid amide hydrolase. The author has an hindex of 37, co-authored 69 publications receiving 10665 citations. Previous affiliations of Jonathan Z. Long include Kettering University & Harvard University.

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Journal ArticleDOI

An anatomical and temporal portrait of physiological substrates for fatty acid amide hydrolase

Jonathan Z. Long, +3 more
- 01 Feb 2011 - 
TL;DR: These studies define the anatomical and temporal features of FAAH-mediated NAE and NAT metabolism, which are complemented and probably influenced by kinetically distinguishable biosynthetic pathways that produce these lipids in vivo.
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Blockade of 2‐arachidonoylglycerol hydrolysis produces antidepressant‐like effects and enhances adult hippocampal neurogenesis and synaptic plasticity

Zhen Zhang, +9 more
- 01 Jan 2015 - 
TL;DR: The results suggest that enhanced adult neurogenesis and long‐term synaptic plasticity in the DG of the hippocampus might contribute to antidepressant‐ and anxiolytic‐like behavioral effects of JZL184.
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Characterization of tunable piperidine and piperazine carbamates as inhibitors of endocannabinoid hydrolases.

Jonathan Z. Long, +4 more
- 25 Feb 2010 - 
TL;DR: A full account of the syntheses, structure-activity relationships, and inhibitory activities of piperidine/piperazine carbamates against members of the serine hydrolase family is disclosed.
Journal ArticleDOI

Metabolomics annotates ABHD3 as a physiologic regulator of medium-chain phospholipids

Jonathan Z. Long, +7 more
- 01 Nov 2011 - 
TL;DR: A general cell-based screen for enzyme substrate discovery by untargeted metabolomics and its application to identify α/β-hydrolase domain-containing 3 (ABHD3) as a lipase that selectively cleaves medium-chain and oxidatively-truncated phospholipids is described.
Journal ArticleDOI

Dual fatty acid amide hydrolase and monoacylglycerol lipase blockade produces THC-like Morris water maze deficits in mice.

Laura E. Wise, +5 more
- 16 May 2012 - 
TL;DR: The results of this study reveal that concomitant increases in AEA and 2-AG disrupt short-term spatial memory performance in a manner similar to that of THC.