J
Jacob C. Garza
Researcher at Harvard University
Publications - 21
Citations - 1281
Jacob C. Garza is an academic researcher from Harvard University. The author has contributed to research in topics: Leptin receptor & Anxiogenic. The author has an hindex of 13, co-authored 20 publications receiving 1075 citations. Previous affiliations of Jacob C. Garza include University of Texas Health Science Center at San Antonio.
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Journal ArticleDOI
Leptin Increases Adult Hippocampal Neurogenesis in Vivo and in Vitro
TL;DR: The role of leptin in adult hippocampal neurogenesis remains unknown as discussed by the authors, however, it has been shown that chronic administration of leptin to adult mice increased cell proliferation without significant effects on the differentiation and the survival of newly proliferated cells in the dentate gyrus.
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Leptin restores adult hippocampal neurogenesis in a chronic unpredictable stress model of depression and reverses glucocorticoid-induced inhibition of GSK-3β/β-catenin signaling.
TL;DR: The results suggest that adult neurogenesis is involved in the delayed long-lasting antidepressant-like behavioral effects of leptin, and leptin treatment counteracts chronic stress and glucocorticoid-induced suppression of hippocampal neuroGenesis via activating the GSK-3β/β-catenin signaling pathway.
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Acute administration of leptin produces anxiolytic-like effects: a comparison with fluoxetine
TL;DR: Results suggest that leptin has both antidepressant-like and anxiolytic-like properties, in contrast to anxiogenic-like effects induced by acute fluoxetine.
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The melanocortinergic pathway is rapidly recruited by emotional stress and contributes to stress-induced anorexia and anxiety-like behavior
TL;DR: The results indicate that the melancortinergic pathway can be rapidly recruited by acute emotional stress, and that activation of melanocortin signaling is involved in mediating stress-induced anorexia and anxiety.
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Hypothalamic neurodegeneration and adult-onset obesity in mice lacking the Ubb polyubiquitin gene.
TL;DR: It is demonstrated that maintenance of adequate supplies of cellular Ub is essential for neuronal survival and established that decreased Ub availability is sufficient to cause neuronal dysfunction and death.