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Teniel S. Ramikie

Researcher at Harvard University

Publications -  12
Citations -  971

Teniel S. Ramikie is an academic researcher from Harvard University. The author has contributed to research in topics: Endocannabinoid system & Cannabinoid receptor. The author has an hindex of 11, co-authored 12 publications receiving 811 citations. Previous affiliations of Teniel S. Ramikie include McLean Hospital & Vanderbilt University Medical Center.

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Genetic Disruption of 2-Arachidonoylglycerol Synthesis Reveals a Key Role for Endocannabinoid Signaling in Anxiety Modulation

TL;DR: It is shown that genetic deletion of the 2-AG synthetic enzyme diacylglycerol lipase α (DAGLα) in mice reduces brain, but not circulating,2-AG levels, and that pharmacological normalization of 2- AG signaling could represent an approach for the treatment of mood and anxiety disorders.
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Reversible Gating of Endocannabinoid Plasticity in the Amygdala by Chronic Stress: A Potential Role for Monoacylglycerol Lipase Inhibition in the Prevention of Stress-Induced Behavioral Adaptation

TL;DR: It is shown that stress-induced development of anxiety-like behavior is paralleled by a transient appearance of low-frequency stimulation-induced, 2-AG-mediated long-term depression at GABAergic synapses in the basolateral amygdala, a key region involved in motivation, affective regulation, and emotional learning.
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Inhibition of parvalbumin-expressing interneurons results in complex behavioral changes

TL;DR: The results suggest that reduction of GABAergic transmission from PVALB+ interneurons primarily impacts behavioral domains related to fear and novelty seeking and that these alterations might be related to the behavioral phenotype observed in schizophrenia.
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Multiple Mechanistically Distinct Modes of Endocannabinoid Mobilization at Central Amygdala Glutamatergic Synapses

TL;DR: The subcellular localization of CB1 cannabinoid receptors and eCB synthetic machinery at glutamatergic synapses in the CeA is described and it is found that CeA neurons exhibit multiple mechanistically and temporally distinct modes of postsynaptic eCB mobilization.