Early-life stress induces cognitive disorder in middle-aged mice

Yajima, Hiroyuki; Haijima, Asahi; Khairinisa, Miski Aghnia; Shimokawa, Noriaki; Amano, Izuki; Takatsuru, Yusuke

doi:10.1016/j.neurobiolaging.2017.12.021

Cited by 22 publications

(13 citation statements)

References 33 publications

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“…On a broader perspective, our findings suggest that the use of pharmacological manipulation of glial cells 50 may be useful in the treatment of other functions known to be affected by stress. For example, it will be important to test the effects of ceftriaxone in motor 51 and cognitive functions 52,53 of stressed animals.…”

Section: Discussionmentioning

confidence: 99%

Ceftriaxone modulates the acute corticosterone effects in local field potentials in the primary somatosensory cortex of anesthetized mice

Pais-Vieira

Kunicki²,

Peres³

et al. 2019

Sci Rep

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Stress responses are associated with elevations in corticosterone levels and, as a consequence, increases in glutamate in the central nervous system which can lead to neurological impairment. Ceftriaxone promotes glutamate transport and has been used to reduce glutamate toxicity, but so far it is not known whether ceftriaxone is able to reverse the effects of corticosterone administration. Here we describe the separate and combined effects of acute ceftriaxone and acute corticosterone administration in local field potentials (LFPs) recorded from the somatosensory cortex (S1) of anesthetized mice. For this, LFPs were recorded from groups of anesthetized mice injected with saline, corticosterone, ceftriaxone, or both. Comparison of global state maps, and their displacements, as measured by ratios of different frequency bands (Ratio 1: 0.5–20 Hz/0.5–45 Hz; and Ratio 2: 0.5–4.5 Hz/0.5–9 Hz) revealed distinct and opposite effects for corticosterone and for ceftriaxone. Corticosterone specifically increased the displacement in Ratio 2, while ceftriaxone decreased it; in addition, when both corticosterone and ceftriaxone were injected, Ratio 2 displacement values were again similar to those of the control group. The present results suggest that ceftriaxone and corticosterone modulate specific frequency bands in opposite directions and reveal a potential role for ceftriaxone in counteracting the effects of corticosterone.

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Section: Discussionmentioning

confidence: 99%

Ceftriaxone modulates the acute corticosterone effects in local field potentials in the primary somatosensory cortex of anesthetized mice

Pais-Vieira

Kunicki²,

Peres³

et al. 2019

Sci Rep

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“…This vulnerability to both spatial and object memories was also unmasked with ageing [15]: 12-month-old LBN rats performed more poorly than controls in both prior studies [15] and in the current work. Indeed, early adversity may accelerate the impact of age on memory [15,63].…”

Section: Discussionmentioning

confidence: 99%

Blocking CRH receptors in adults mitigates age-related memory impairments provoked by early-life adversity

Short

Maras

Pham

et al. 2019

Neuropsychopharmacol.

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In humans, early-life adversity is associated with impairments in learning and memory that may emerge later in life. In rodent models, early-life adversity directly impacts hippocampal neuron structure and connectivity with progressive deficits in long-term potentiation and spatial memory function. Previous work has demonstrated that augmented release and actions of the stressactivated neuropeptide, CRH, contribute to the deleterious effects of early-life adversity on hippocampal dendritic arborization, synapse number and memory-function. Early-life adversity increases hippocampal CRH expression, and blocking hippocampal CRH receptor type-1 (CRHR1) immediately following early-life adversity prevented the consequent memory and LTP defects. Here, we tested if blocking CRHR1 in young adults ameliorates early-life adversityprovoked memory deficits later in life. A weeklong course of a CRHR1 antagonist in 2-monthold male rats prevented early-life adversity-induced deficits in object recognition memory that emerged by 12 months of age. Surprisingly, whereas the intervention did not mitigate early-life adversity-induced spatial memory losses at 4 and 8 months, it restored hippocampus-dependent location memory in 12-month-old rats that experienced early-life adversity. Neither early-life adversity nor CRHR1 blockade in the adult influenced anxiety-or depression-related behaviors. Altogether, these findings suggest that cognitive deficits attributable to adversity during earlylife-sensitive periods are at least partially amenable to interventions later in life.

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“…The expression levels of proteins were determined by Western blot analysis, as described previously ( 41 ). Briefly, total proteins were extracted from primary cultured hippocampal neurons in a lysis buffer containing 20 mM Tris-HCl (pH 8.0), 137 mM NaCl, 10% Glycerol, 1% Nonidet P40, and proteinase inhibitors.…”

Section: Methodsmentioning

confidence: 99%

Absence of Thyroid Hormone Induced Delayed Dendritic Arborization in Mouse Primary Hippocampal Neurons Through Insufficient Expression of Brain-Derived Neurotrophic Factor

et al. 2021

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Thyroid hormone (TH) plays important roles in the developing brain. TH deficiency in early life leads to severe developmental impairment in the hippocampus. However, the mechanisms of TH action in the developing hippocampus are still largely unknown. In this study, we generated 3,5,3’-tri-iodo-l-thyronine (T3)-free neuronal supplement, based on the composition of neuronal supplement 21 (NS21), to examine the effect of TH in the developing hippocampus using primary cultured neurons. Effects of TH on neurons were compared between cultures in this T3-free culture medium (-T3 group) and a medium in which T3 was added (+T3 group). Morphometric analysis and RT-qPCR were performed on 7, 10, and 14 days in vitro (DIV). On 10 DIV, a decreased dendrite arborization in -T3 group was observed. Such difference was not observed on 7 and 14 DIV. Brain-derived neurotrophic factor (Bdnf) mRNA levels also decreased significantly in -T3 group on 10 DIV. We then confirmed protein levels of phosphorylated neurotrophic tyrosine kinase type 2 (NTRK2, TRKB), which is a receptor for BDNF, on 10 DIV by immunocytochemistry and Western blot analysis. Phosphorylated NTRK2 levels significantly decreased in -T3 group compared to +T3 group on 10 DIV. Considering the role of BDNF on neurodevelopment, we examined its involvement by adding BDNF on 8 and 9 DIV. Addition of 10 ng/ml BDNF recovered the suppressed dendrite arborization induced by T3 deficiency on 10 DIV. We show that the lack of TH induces a developmental delay in primary hippocampal neurons, likely caused through a decreased Bdnf expression. Thus, BDNF may play a role in TH-regulated dendritogenesis.

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Early-life stress induces cognitive disorder in middle-aged mice

Cited by 22 publications

References 33 publications

Ceftriaxone modulates the acute corticosterone effects in local field potentials in the primary somatosensory cortex of anesthetized mice

Ceftriaxone modulates the acute corticosterone effects in local field potentials in the primary somatosensory cortex of anesthetized mice

Blocking CRH receptors in adults mitigates age-related memory impairments provoked by early-life adversity

Absence of Thyroid Hormone Induced Delayed Dendritic Arborization in Mouse Primary Hippocampal Neurons Through Insufficient Expression of Brain-Derived Neurotrophic Factor

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