M
Megha Sehgal
Researcher at University of California, Los Angeles
Publications - 18
Citations - 671
Megha Sehgal is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Metaplasticity & Synaptic plasticity. The author has an hindex of 7, co-authored 17 publications receiving 466 citations. Previous affiliations of Megha Sehgal include University of California, Berkeley & University of Wisconsin–Milwaukee.
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Journal ArticleDOI
Memory formation depends on both synapse-specific modifications of synaptic strength and cell-specific increases in excitability.
TL;DR: It is argued that the two mechanisms can work together to promote useful memory function, including the CREB-dependent transient change in neuronal excitability that is critical for neural assembly formation and linking of memories across time.
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Learning to learn – Intrinsic plasticity as a metaplasticity mechanism for memory formation
TL;DR: Evidence is reviewed that intrinsic plasticity is an important and evolutionarily conserved neural correlate of learning and modulation of intrinsic excitability can allow for regulation of learning ability - this can prevent or provide treatment for cognitive decline not only in patients with clinical disorders but also in the aging population.
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CCR5 is a suppressor for cortical plasticity and hippocampal learning and memory
Miou Zhou,Stuart D. Greenhill,Stuart D. Greenhill,Shan Huang,Tawnie K. Silva,Yoshitake Sano,Yoshitake Sano,Shumin Wu,Ying Cai,Yoshiko Nagaoka,Megha Sehgal,Denise J. Cai,Yong-Seok Lee,Yong-Seok Lee,Kevin Fox,Alcino J. Silva +15 more
TL;DR: It is reported that decreasing the function of CCR5 increases MAPK/CREB signaling, long-term potentiation (LTP), and hippocampus-dependent memory in mice, while neuronal Ccr5 overexpression caused memory deficits, and indicates that C CR5 has a role in the cognitive deficits caused by HIV.
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Trace fear conditioning enhances synaptic and intrinsic plasticity in rat hippocampus.
TL;DR: In trace-conditioned rats, both synaptic plasticity and intrinsic excitability were significantly correlated with behavior such that better learning corresponded with enhanced long-term potentiation, suggesting that within the hippocampus both synaptic and intrinsic mechanisms are involved in the acquisition of trace fear conditioning.
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Learning enhances intrinsic excitability in a subset of lateral amygdala neurons.
TL;DR: Fear conditioning significantly enhanced excitability of LA neurons, as evidenced by both decreased afterhyperpolarization (AHP) and increased neuronal firing, which may be clinically relevant as enhanced LA excitability following fear learning could influence future amygdala-dependent behaviors.