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Georgette M. Gafford
Researcher at Emory University
Publications - 22
Citations - 1144
Georgette M. Gafford is an academic researcher from Emory University. The author has contributed to research in topics: Fear conditioning & Memory consolidation. The author has an hindex of 16, co-authored 21 publications receiving 1025 citations. Previous affiliations of Georgette M. Gafford include University of Wisconsin-Madison & Yerkes National Primate Research Center.
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Translational control via the mammalian target of rapamycin pathway is critical for the formation and stability of long-term fear memory in amygdala neurons.
TL;DR: It is reported that training rats in a simple fear conditioning procedure evokes a time-dependent increase in the phosphorylation of p70s6 kinase, a major direct downstream target of mTOR, indicating that local translational control at active synapses is required for the stability as well as the formation of long-term memory in this system.
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Time-Dependent Expression of Arc and Zif268 after Acquisition of Fear Conditioning
TL;DR: The timing of hippocampal Arc and zif268 expression coincides with the critical period for protein synthesis-dependent memory consolidation following fear conditioning, however, the expression of Arc protein appears to be driven by context exploration, whereas, zif 268 expression may be more specifically related to associative learning.
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Consolidation and reconsolidation of contextual fear memory requires mammalian target of rapamycin-dependent translation in the dorsal hippocampus
TL;DR: Results demonstrate that within the DH translational control through the mTOR pathway is important for consolidation as well as the stability of fear memory after retrieval.
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Long-term stability of fear memory depends on the synthesis of protein but not mRNA in the amygdala
TL;DR: Results showed that blocking mRNA or protein synthesis immediately after learning prevented the formation of long‐term memory, while stability of memory after retrieval required protein, but not mRNA, synthesis, which suggests that the protein needed for memory reconsolidation after retrieval may be transcribed from pre‐existing stores of mRNA.
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Cell-type specific deletion of GABA(A)α1 in corticotropin-releasing factor-containing neurons enhances anxiety and disrupts fear extinction
Georgette M. Gafford,Jidong Guo,Elizabeth I. Flandreau,Rimi Hazra,Donald G. Rainnie,Kerry J. Ressler,Kerry J. Ressler +6 more
TL;DR: Electrophysiological findings indicate that disturbance of CRF containing GABA(A)α1 neurons causes increased anxiety and impaired fear extinction, both of which are symptoms diagnostic for anxiety disorders, such as posttraumatic stress disorder.