S
Sandra M. Holley
Researcher at Semel Institute for Neuroscience and Human Behavior
Publications - 24
Citations - 1131
Sandra M. Holley is an academic researcher from Semel Institute for Neuroscience and Human Behavior. The author has contributed to research in topics: Huntington's disease & Striatum. The author has an hindex of 14, co-authored 23 publications receiving 889 citations. Previous affiliations of Sandra M. Holley include University of California, Los Angeles.
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Journal ArticleDOI
Neuronal targets for reducing mutant huntingtin expression to ameliorate disease in a mouse model of Huntington's disease
Nan Wang,Michelle Gray,Xiao-Hong Lu,Jeffrey P. Cantle,Sandra M. Holley,Erin R. Greiner,Xiaofeng Gu,Dyna I. Shirasaki,Carlos Cepeda,Yuqing Li,Hong-Wei Dong,Michael Levine,X. William Yang +12 more
TL;DR: It is shown that reduction of cortical mHTT expression in BACHD mice partially improves motor and psychiatric-like behavioral deficits but does not improve neurodegeneration, whereas reduction of mHTt expression in both neuronal populations consistently ameliorates all behavioral deficits and selective brain atrophy in this HD model.
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Basolateral Amygdala to Orbitofrontal Cortex Projections Enable Cue-Triggered Reward Expectations.
Nina T. Lichtenberg,Zachary T. Pennington,Sandra M. Holley,Venuz Y. Greenfield,Carlos Cepeda,Michael Levine,Michael Levine,Kate M. Wassum +7 more
TL;DR: It is shown that basolateral amygdala to orbitofrontal cortex projections are required for expectations of specific available rewards to influence reward seeking and decision making, and these projections facilitate adaptive behavior by enabling the orbitof prefrontal cortex to use environmental stimuli to generate expectations of potential future rewarding events.
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Multiple Sources of Striatal Inhibition Are Differentially Affected in Huntington’s Disease Mouse Models
Carlos Cepeda,Laurie Galvan,Sandra M. Holley,Shilpa P. Rao,Véronique M. André,Elian P. Botelho,Jane Y. Chen,Joseph B. Watson,Karl Deisseroth,Michael Levine +9 more
TL;DR: Findings provide strong evidence that both feedforward and to a lesser extent feedback inhibition to MSNs in HD can potentially be sources for the increased GABA synaptic activity of indirect pathway MSNs.
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Parvalbumin Interneurons Modulate Striatal Output and Enhance Performance during Associative Learning.
Kwang Lee,Sandra M. Holley,Justin L. Shobe,Natalie Chong,Carlos Cepeda,Michael S. Levine,Sotiris C. Masmanidis +6 more
TL;DR: This work unexpectedly finds that both suppressing and over-activating PV cells attenuates spontaneous MSN activity, and provides a possible mechanism by which PV interneurons modulate striatal output and selectively enhance performance early in learning.
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Forebrain deletion of the dystonia protein torsinA causes dystonic-like movements and loss of striatal cholinergic neurons
Samuel S. Pappas,Katherine Darr,Sandra M. Holley,Carlos Cepeda,Omar S. Mabrouk,Jenny Marie T. Wong,Tessa M. LeWitt,Reema Paudel,Henry Houlden,Robert T. Kennedy,Michael Levine,William T. Dauer +11 more
TL;DR: It is demonstrated that dorsal LCI have a unique requirement for torsinA function during striatal maturation, and abnormalities of these cells to dystonic-like movements in an overtly symptomatic animal model are linked.