Prenatal treatment with rapamycin restores enhanced hippocampal mGluR-LTD and mushroom spine size in a Down’s syndrome mouse model

Urbano-Gámez, Jesús David; Casañas, Juan José; Benito, Itziar; Montesinos, Marı́a Luz

doi:10.1186/s13041-021-00795-6

Cited by 12 publications

(9 citation statements)

References 52 publications

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“…To further study rapamycin-induced reprogramming of aging, pregnant mice should be treated with a single subcutaneous injection of rapamycin and the lifespan of their offspring should be measured. Prenatal (before birth) rapamycin treatment on early postnatal development has been studied [45][46][47]. For example, prenatally rapamycin-treated neonates are small, and body weight and left ventricular mass remain reduced in adulthood [47].…”

Section: Further Suggestionsmentioning

confidence: 99%

As predicted by hyperfunction theory, rapamycin treatment during development extends lifespan

Blagosklonny

2022

Aging

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Section: Further Suggestionsmentioning

confidence: 99%

As predicted by hyperfunction theory, rapamycin treatment during development extends lifespan

Blagosklonny

2022

Aging

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“…Thus, a transient decrease in the phosphorylation of mTOR may be a novel, non-canonical mechanism by which to induce translational events that induce long-lasting synaptic changes. mTOR signaling positively regulates mGluR mediated long-term synaptic activity and mushroom-shaped dendritic spines in the hippocampus in a Down’s syndrome rodent model [ 36 ]. To the best of our knowledge, this is one of the first published instances of changes in the molecular activity of intracellular regulators for social behavior.…”

Section: Discussionmentioning

confidence: 99%

Aggression Results in the Phosphorylation of ERK1/2 in the Nucleus Accumbens and the Dephosphorylation of mTOR in the Medial Prefrontal Cortex in Female Syrian Hamsters

Borland

Dempsey

Peyla

et al. 2023

IJMS

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Like many social behaviors, aggression can be rewarding, leading to behavioral plasticity. One outcome of reward-induced aggression is the long-term increase in the speed in which future aggression-based encounters is initiated. This form of aggression impacts dendritic structure and excitatory synaptic neurotransmission in the nucleus accumbens, a brain region well known to regulate motivated behaviors. Yet, little is known about the intracellular signaling mechanisms that drive these structural/functional changes and long-term changes in aggressive behavior. This study set out to further elucidate the intracellular signaling mechanisms regulating the plasticity in neurophysiology and behavior that underlie the rewarding consequences of aggressive interactions. Female Syrian hamsters experienced zero, two or five aggressive interactions and the phosphorylation of proteins in reward-associated regions was analyzed. We report that aggressive interactions result in a transient increase in the phosphorylation of extracellular-signal related kinase 1/2 (ERK1/2) in the nucleus accumbens. We also report that aggressive interactions result in a transient decrease in the phosphorylation of mammalian target of rapamycin (mTOR) in the medial prefrontal cortex, a major input structure to the nucleus accumbens. Thus, this study identifies ERK1/2 and mTOR as potential signaling pathways for regulating the long-term rewarding consequences of aggressive interactions. Furthermore, the recruitment profile of the ERK1/2 and the mTOR pathways are distinct in different brain regions.

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“…Protein extraction, iTRAQ labeling (using AB ScieX, Ref. 4390811) and tandem mass spectrometry (MS) analysis was carried out at the Instituto de Biomedicina de Sevilla (IBiS) Proteomics Service, as described previously [26]. Two sets of samples were included in the 8-plex experiment.…”

Section: Methodsmentioning

confidence: 99%

Proteomic characterization of spinal cord synaptoneurosomes from Tg-SOD1/G93A mice supports a role for MNK1 and local translation in the early stages of amyotrophic lateral sclerosis

Casañas

Montesinos

2022

Preprint

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The isolation of synaptoneurosomes (SNs) represents a useful means to study synaptic events. However, the size and density of synapses varies in different regions of the central nervous system (CNS), and this also depends on the experimental species studied, making it difficult to define a generic protocol for SNs preparation. To characterize synaptic failure in the spinal cord (SC) in the Tg-SOD1/G93A mouse model of amyotrophic lateral sclerosis (ALS), we applied a method we originally designed to isolate cortical and hippocampal SNs to SC tissue. Interestingly, we found that the SC SNs were isolated in a different gradient fraction to the cortical/hippocampal SNs. We compared the relative levels of synaptoneurosomal proteins in control (Tg-SOD1) animals, with Tg-SOD1/G93A mice at onset and those that were symptomatic using iTRAQ proteomics. The results obtained suggest that an important regulator of local synaptic translation, MNK1 (MAP kinase interacting serine/threonine kinase 1), might well influence the early stages of ALS.

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Prenatal treatment with rapamycin restores enhanced hippocampal mGluR-LTD and mushroom spine size in a Down’s syndrome mouse model

Cited by 12 publications

References 52 publications

As predicted by hyperfunction theory, rapamycin treatment during development extends lifespan

As predicted by hyperfunction theory, rapamycin treatment during development extends lifespan

Aggression Results in the Phosphorylation of ERK1/2 in the Nucleus Accumbens and the Dephosphorylation of mTOR in the Medial Prefrontal Cortex in Female Syrian Hamsters

Proteomic characterization of spinal cord synaptoneurosomes from Tg-SOD1/G93A mice supports a role for MNK1 and local translation in the early stages of amyotrophic lateral sclerosis

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