Learning and memory consolidation: linking molecular and behavioral data

Morgado-Bernal, Ignacio

doi:10.1016/j.neuroscience.2010.12.056

Cited by 106 publications

(65 citation statements)

References 84 publications

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“…In mammals, this process takes place in the CA1 region of the hippocampus, and the underlying cellular mechanism is a form of synaptic plasticity known as long‐term potentiation or LTP (Vann & Albasser, 2011), that requires Ca +2 signaling, gene expression changes and protein synthesis (Morgado‐Bernal, 2011). The neuropathological bases of learning and memory alterations in IUGR babies are not clear, but there is consensus that within the brain the hippocampus is one of the areas most susceptible to IUGR and hypoxic damage (Fung et al., 2012; Lodygensky et al., 2008; Mallard et al., 2000), which particularly affects CA1 pyramidal neurons in the hippocampus (Kovalenko et al., 2006; Lister et al., 2005).…”

Section: Discussionmentioning

confidence: 99%

Learning and memory disabilities in IUGR babies: Functional and molecular analysis in a rat model

et al. 2017

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IntroductionIntrauterine growth restriction (IUGR) is the failure of the fetus to achieve its inherent growth potential, and it has frequently been associated with neurodevelopmental problems in childhood. Neurological disorders are mostly associated with IUGR babies with an abnormally high cephalization index (CI) and a brain sparing effect. However, a similar correlation has never been demonstrated in an animal model. The aim of this study was to determine the correlations between CI, functional deficits in learning and memory and alterations in synaptic proteins in a rat model of IUGR.MethodsUtero‐placental insufficiency was induced by meso‐ovarian vessel cauterization (CMO) in pregnant rats at embryonic day 17 (E17). Learning performance in an aquatic learning test was evaluated 25 days after birth and during 10 days. Some synaptic proteins were analyzed (PSD95, Synaptophysin) by Western blot and immunohistochemistry.ResultsPlacental insufficiency in CMO pups was associated with spatial memory deficits, which are correlated with a CI above the normal range. CMO pups presented altered levels of synaptic proteins PSD95 and synaptophysin in the hippocampus.ConclusionsThe results of this study suggest that learning disabilities may be associated with altered development of excitatory neurotransmission and synaptic plasticity. Although interspecific differences in fetal response to placental insufficiency should be taken into account, the translation of these data to humans suggest that both IUGR babies and babies with a normal birth weight but with intrauterine Doppler alterations and abnormal CI should be closely followed to detect neurodevelopmental alterations during the postnatal period.

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Section: Discussionmentioning

confidence: 99%

Learning and memory disabilities in IUGR babies: Functional and molecular analysis in a rat model

et al. 2017

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“…Initiation and maintenance of synaptic plasticity in CA1 pyramidal neurons of the hippocampus require morphological changes in dendritic spines, which constitute the main structural basis for memory formation (42). Studies in cultured neurons revealed requirements for a CaMKK/CaMKI cascade in regulation of axonal growth cone morphology and outgrowth, dendritic arborization, and spine and synapse formation (37).…”

Section: Camkk2 and Brain Functionsmentioning

confidence: 99%

Calcium/Calmodulin-dependent Protein Kinase Kinase 2: Roles in Signaling and Pathophysiology

Means

2012

Journal of Biological Chemistry

252

204

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“…Glutamate arguably constitutes the most profoundly-involved neurotransmitter in the mechanisms of consolidation and reconsolidation, both processes being consistently inhibited by antagonists or facilitated by positive modulators acting on the NMDA receptor (or its subunits) in a variety of learning-and-memory procedures in rats and mice (see reviews by Riedel et al, 2003;Morgado-Bernal, 2011). Note that reconsolidation can also be disrupted without consolidation being affected, as is the case for the positive modulator of the GABA A benzodiazepine-binding site midazolam and the beta-adrenergic antagonist propanolol, suggesting the possibility of a differential involvement of the corresponding receptor sites and neurotransmitters in these memory processes (Debiec and LeDoux, 2004;Bustos et al, 2006).…”

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confidence: 99%

Differential effects of histamine H3 receptor inverse agonist thioperamide, given alone or in combination with the N-methyl-d-aspartate receptor antagonist dizocilpine, on reconsolidation and consolidation of a contextual fear memory in mice

Charlier

Tirelli

2011

Neuroscience

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Abstract-Albeit there is no doubt that histamine and its H 3 receptors participate in several aspects of learning and memory, such as memory consolidation, nothing is known about their potential involvement in memory reconsolidation. On the basis of previous reports of pro-cognitive effects of histamine H 3 receptor inverse agonists (which augment histamine release), we investigated to what extent the most representative of them, thioperamide, is able to facilitate reconsolidation of a contextually-conditioned fear memory in C57BL/6J mice. We also examined the effects of thioperamide on the stark disruptive effect that the non-competitive N-methyl-D-aspartate (NMDA) antagonist dizocilpine (MK-801) typically exerts on both reconsolidation and consolidation. Post-training systemic injections (i.p.) of thioperamide facilitated consolidation at 10 and 20 mg/kg and reversed amnesia induced by an i.p. injection of 0.12 mg/kg dizocilpine at 5, 10 and 20 mg/kg. Importantly, none of the five thioperamide doses (2.5, 5, 10, 20 and 30 mg/kg) given right after reactivation (reexposure to the context in which training took place 48 h earlier) affected reconsolidation, whereas all similarly given doses of dizocilpine (0.03, 0.06 and 0.12 mg/kg) disrupted it more or less equally. By contrast, thioperamide was able to unambiguously reverse the deficit in reconsolidation induced by 0.12 mg/kg dizocilpine at 10 and 20, but not 5 mg/kg. This is the first demonstration of an involvement of the interactive articulation between histamine and NMDA receptors in the mechanisms of memory reconsolidation, which seems to be indifferent to an increase of brain histamine per se. The results suggest a qualitatively different participation of histaminergic signalling in the mechanisms of reconsolidation and consolidation. The precise circuits within which these interactions take place are yet to be identified.

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Learning and memory consolidation: linking molecular and behavioral data

Cited by 106 publications

References 84 publications

Learning and memory disabilities in IUGR babies: Functional and molecular analysis in a rat model

Learning and memory disabilities in IUGR babies: Functional and molecular analysis in a rat model

Calcium/Calmodulin-dependent Protein Kinase Kinase 2: Roles in Signaling and Pathophysiology

Differential effects of histamine H3 receptor inverse agonist thioperamide, given alone or in combination with the N-methyl-d-aspartate receptor antagonist dizocilpine, on reconsolidation and consolidation of a contextual fear memory in mice

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