J
Jessica H. Chancey
Researcher at University of Alabama at Birmingham
Publications - 6
Citations - 1610
Jessica H. Chancey is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Neurogenesis & Dentate gyrus. The author has an hindex of 4, co-authored 5 publications receiving 1381 citations.
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Journal ArticleDOI
Microglia Shape Adult Hippocampal Neurogenesis through Apoptosis-Coupled Phagocytosis
Amanda Sierra,Juan M. Encinas,Juan M. Encinas,Juan J. P. Deudero,Jessica H. Chancey,Grigori Enikolopov,Linda Overstreet-Wadiche,Stella E. Tsirka,Mirjana Maletic-Savatic +8 more
TL;DR: It is shown that the majority of the newborn cells undergo death by apoptosis in the first 1 to 4 days of their life, during the transition from amplifying neuroprogenitors to neuroblasts, which suggests a new role for microglia in maintaining the homeostasis of the baseline neurogenic cascade.
Journal ArticleDOI
GABA depolarization is required for experience-dependent synapse unsilencing in adult-born neurons.
Jessica H. Chancey,Elena W Adlaf,Matthew C. Sapp,Phyllis C. Pugh,Jacques I. Wadiche,Linda Overstreet-Wadiche +5 more
TL;DR: GA depolarization acutely allows NMDAR activation required for initial synapse unsilencing, revealing that adult-generated neurons in a critical period for survival use GABA signaling to rapidly initiate functional glutamate-mediated transmission in response to experience.
Journal ArticleDOI
Hilar Mossy Cells Provide the First Glutamatergic Synapses to Adult-Born Dentate Granule Cells
TL;DR: It is shown that hilar mossy cells provide initial glutamatergic synapses as well as disynaptic GABAergic input to adult-generated dentate GCs.
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Dynamic functions of GABA signaling during granule cell maturation.
TL;DR: These dynamic functions of GABA across granule cell maturation are reviewed, focusing on the potential role of specific interneuron circuits at progressive developmental stages and questions that remain unanswered about GABA signaling ingranule cell development and excitability are highlighted.
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Synaptic Integration in CA1 Pyramidal Neurons Is Intact despite Deficits in GABAergic Transmission in the Scn1a Haploinsufficiency Mouse Model of Dravet Syndrome
TL;DR: It is shown that reduced GABA release probability and subsequent reduced short-term depression may act to overcome deficits in inhibition normalizing input/output functions in the Scn1a haploinsufficient hippocampus, and more complex circuit activity is likely required to reveal altered function in the hippocampal microcircuit.