Repeating or spacing learning sessions are strategies for memory improvement with shared molecular and neuronal components.

Autor: Cattaneo V; IFIBIO-Houssay, Grupo de Neurociencia de Sistemas, Facultad de Medicina, Universidad de Buenos Aires - CONICET, 2155 Paraguay Street, Buenos Aires, Argentina., San Martin A; IFIBIO-Houssay, Grupo de Neurociencia de Sistemas, Facultad de Medicina, Universidad de Buenos Aires - CONICET, 2155 Paraguay Street, Buenos Aires, Argentina., Lew SE; Instituto de Ingeniería Biomédica, Facultad de Ingeniería, Universidad de Buenos Aires, Argentina., Gelb BD; Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA., Pagani MR; IFIBIO-Houssay, Grupo de Neurociencia de Sistemas, Facultad de Medicina, Universidad de Buenos Aires - CONICET, 2155 Paraguay Street, Buenos Aires, Argentina. Electronic address: pagani@fmed.uba.ar.
Jazyk: angličtina
Zdroj: Neurobiology of learning and memory [Neurobiol Learn Mem] 2020 Jul; Vol. 172, pp. 107233. Date of Electronic Publication: 2020 May 01.
DOI: 10.1016/j.nlm.2020.107233
Abstrakt: Intellectual disability is a common feature in genetic disorders with enhanced RAS-ERK1/2 signaling, including neurofibromatosis type 1 (NF1) and Noonan syndrome (NS). Additional training trials and additional spacing between trials, respectively, restores memory deficits in animal models of NF1 and NS. However, the relationship between the underlying mechanisms in these strategies remain obscure. Here, we developed an approach to examine the effect of adding training trials or spacing to a weak training protocol and used genetic and behavioral manipulations in Drosophila to explore such question. We found that repetition and spacing effects are highly related, being equally effective to improve memory in control flies and sharing mechanistic bases, including the requirement of RAS activity in mushroom body neurons and protein synthesis dependence. After spacing or repeating learning trials, memory improvement depends on the formation of long-term memory (LTM). Moreover, a disease-related gain-of-function RasV152G allele impaired LTM. Using minimal training protocols, we established that both learning strategies were also equally effective for memory rescue in the RasV152G mutant and showed non-additive interaction of the spacing and repetition effects. Memory improvement was never detected after Ras inhibition. We conclude that memory improvement by spacing or repeating training trials are two ways of using the same molecular resources, including RAS-ERK1/2-dependent signaling. This evidence supports the concept that learning problems in RAS-related disorders depend on the impaired ability to exploit the repetition and the spacing effect required for long-term memory induction.
(Copyright © 2020 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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