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Fortunato Battaglia

Researcher at Seton Hall University

Publications -  95
Citations -  11161

Fortunato Battaglia is an academic researcher from Seton Hall University. The author has contributed to research in topics: Transcranial magnetic stimulation & Motor cortex. The author has an hindex of 34, co-authored 88 publications receiving 10294 citations. Previous affiliations of Fortunato Battaglia include Columbia University & National Institutes of Health.

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Requirement of Hippocampal Neurogenesis for the Behavioral Effects of Antidepressants

TL;DR: It is shown that disrupting antidepressant-induced neurogenesis blocks behavioral responses to antidepressants, suggesting that the behavioral effects of chronic antidepressants may be mediated by the stimulation of neuroGenesis in the hippocampus.
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Ablation of hippocampal neurogenesis impairs contextual fear conditioning and synaptic plasticity in the dentate gyrus

TL;DR: The findings show that adult-born neurons make a distinct contribution to some but not all hippocampal functions and show that new hippocampal neurons can be preferentially recruited over mature granule cells in vitro and may provide a framework for how this small cell population can influence behavior.
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Chronic Fluoxetine Stimulates Maturation and Synaptic Plasticity of Adult-Born Hippocampal Granule Cells

TL;DR: The results suggest that chronic fluoxetine accelerates the maturation of immature neurons and may be necessary for its anxiolytic/antidepressant activity and contribute to its delayed onset of therapeutic efficacy.
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Learning and Memory and Synaptic Plasticity Are Impaired in a Mouse Model of Rett Syndrome

TL;DR: Very early symptomatic Mecp2308/Y mice had increased basal synaptic transmission and deficits in the induction of long-term depression, suggesting that functional and ultrastructural synaptic dysfunction is an early event in the pathogenesis of RTT.
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Amyloid β-peptide inhibition of the PKA/CREB pathway and long-term potentiation: Reversibility by drugs that enhance cAMP signaling

TL;DR: It is demonstrated that amyloid β-peptide treatment of cultured hippocampal neurons leads to the inactivation of protein kinase A (PKA) and persistence of its regulatory subunit PKAIIα, suggesting that Αβ acts directly on the pathways involved in the formation of late LTP and agents that enhance the cAMP/PKA/CREB-signaling pathway have potential for the treatment of AD.