Effects of neonatal stress on markers of synaptic plasticity in the hippocampus: Implications for spatial memory

Aisa, Bárbara; Elizalde, N.; Tordera, Rosa M.; Lasheras, B.; Rı́o, Joaquı́n Del; Ramı́rez, Marı́a J.

doi:10.1002/hipo.20586

Cited by 158 publications

(126 citation statements)

References 92 publications

(108 reference statements)

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“…However, in the current experiment we have not found differences in the levels of 5-methylcytosine immunostaining in hippocampus between MS and control animals. Our group has previously reported a significant decrease in hippocampal BDNF expression in the same rat model of 3-hour daily maternal separation [44]. A recent study has reported that methyl supplementation via methionine is able to increase BDNF DNA methylation and reduce BDNF mRNA levels in the hippocampus of epileptic rats during memory consolidation, reversing memory deficits in these animals [45].…”

Section: Discussionmentioning

confidence: 78%

Methyl donor supplementation in rats reverses the deleterious effect of maternal separation on depression-like behaviour

Paternain

Martišová

Campión

et al. 2016

Behavioural Brain Research

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Adverse early life events are associated with altered stress responsiveness and metabolic disturbances in the adult life. Dietary methyl donor supplementation could be able to reverse the negative effects of maternal separation by affecting DNA methylation in the brain. In this study, maternal separation during lactation reduced body weight gain in the female adult offspring without affecting food intake, and altered total and HDLcholesterol levels. Also, maternal separation induced a cognitive deficit as measured by NORT and an increase in the immobility time in the Porsolt forced swimming test, consistent with increased depression-like behaviour. An 18-week dietary supplementation with methyl donors (choline, betaine, folate and vitamin B12) from postnatal day 60 also reduced body weight without affecting food intake. Some of the deleterious effects induced by maternal separation, such as the abnormal levels of total and HDL-cholesterol, but especially the depression-like behaviour as measured by the Porsolt test, were reversed by methyl donor supplementation. Also, the administration of methyl donors increased total DNA methylation (measured by immunohistochemistry) and affected the expression of insulin receptor in the hippocampus of the adult offspring. However, no changes were observed in the DNA methylation status of insulin receptor and corticotropin-releasing hormone (CRH) promoter regions in the hypothalamus. In summary, methyl donor supplementation reversed some of the deleterious effects of an early life-induced model of depression in rats and altered the DNA methylation profile in the brain.

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Section: Discussionmentioning

confidence: 78%

Methyl donor supplementation in rats reverses the deleterious effect of maternal separation on depression-like behaviour

Paternain

Martišová

Campión

et al. 2016

Behavioural Brain Research

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“…Prenatal stress and maternal separation even decreases the size and complexity of the new neurons that are born in adulthood in the dentate gyrus (Leslie et al, 2011;Tamura et al, 2011). Stress during the early postnatal period produced by maternal separation reduces cell proliferation, neurogenesis, and the survival of new neurons in adult rodents in the dentate gyrus (Aisa et al, 2009;Leslie et al, 2011;Mirescu et al, 2004;Sachs et al, 2013).…”

Section: Effects Of Early-life Experiences On Adult Neurogenesis and mentioning

confidence: 99%

Adult Neurogenesis and Mental Illness

Schoenfeld

Cameron

2014

Neuropsychopharmacol

162

108

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Several lines of evidence suggest that adult neurogenesis, the production of new neurons in adulthood, may play a role in psychiatric disorders, including depression, anxiety, and schizophrenia. Medications and other treatments for mental disorders often promote the proliferation of new neurons; the time course for maturation and integration of new neurons in circuitry parallels the delayed efficacy of psychiatric therapies; adverse and beneficial experiences similarly affect development of mental illness and neurogenesis; and ablation of new neurons in adulthood alters the behavioral impact of drugs in animal models. At present, the links between adult neurogenesis and depression seem stronger than those suggesting a relationship between new neurons and anxiety or schizophrenia. Yet, even in the case of depression there is currently no direct evidence for a causative role. This article reviews the data relating adult neurogenesis to mental illness and discusses where research needs to head in the future.

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“…Protein concentration for each sample was estimated as previous [42]. NCAM levels were quantified according to a previously described protocol [25]. Flat bottom 96-well microplates were allowed to adsorb a coating solution (Na 2 CO 3 0.1 M/ NaHCO 3 , 0.1 M) for 2 h at room temperature.…”

Section: Quantification Of Total Levels Of Ncammentioning

confidence: 99%

“…NCAM can be also modified by the addition of α-2,8-polysialic acid (PSA-NCAM). At the systems level, NCAMs have been implicated as critical components in the induction of long-term potentiation (LTP) and in memory formation [20,21] NCAMs have been shown to play critical roles in ontogenetic development and are thus potential candidates in expression of age-related pathology, particularly in AD [24,25].…”

Section: Introductionmentioning

confidence: 99%

Altered NCAM Expression Associated with the Cholinergic System in Alzheimer's Disease

Aisa

Gil-Bea

Solas

et al. 2010

JAD

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Abstract. Neurotransmitter system dysfunction and synapse loss have been recognized as hallmarks of Alzheimer's disease (AD). Our hypothesis is that specific neurochemical populations of neurons might be more vulnerable to degeneration in AD due to particular deficits in synaptic plasticity. We have studied, in postmortem brain tissue, the relationship between levels of synaptic markers (NCAM and BDNF), neurochemical measurements (cholinacetyltransferase activity, serotonin, dopamine, GABA, and glutamate levels), and clinical data (cognitive status measured as MMSE score). NCAM levels in frontal and temporal cortex from AD patients were significantly lower than control patients. Interestingly, these reductions in NCAM levels were associated to an ApoE4 genotype. Levels of BDNF were also significantly reduced in both frontal and temporal regions in AD patients. The ratio between plasticity markers and neurochemical measurements was used to study which of the neurochemical populations was particularly associated to plasticity changes. In both the frontal and temporal cortex, there was a significant reduction in the ChAT/NCAM ratio in AD samples compared to controls. None of the ratios to BDNF were different between control and AD samples. Furthermore, Pearson's product moment showed a significant positive correlation between MMSE score and the ChAT/NCAM ratio in frontal cortex (n = 19; r = 0.526*; p = 0.037) as well as in temporal cortex (n = 19; r = 0.601*; p = 0.018) in AD patients. Altogether, these data suggest a potential involvement of NCAM expressing neurons in the cognitive deficits in AD.

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Effects of neonatal stress on markers of synaptic plasticity in the hippocampus: Implications for spatial memory

Cited by 158 publications

References 92 publications

Methyl donor supplementation in rats reverses the deleterious effect of maternal separation on depression-like behaviour

Methyl donor supplementation in rats reverses the deleterious effect of maternal separation on depression-like behaviour

Adult Neurogenesis and Mental Illness

Altered NCAM Expression Associated with the Cholinergic System in Alzheimer's Disease

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