Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models

Rice, Deborah C.; Barone, Stanley

doi:10.2307/3454543

Cited by 383 publications

(205 citation statements)

References 120 publications

(130 reference statements)

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“…Brain is one of the most sensitive body organs to environmental insults, especially in the developmental periods 11. In the present study, results of UPLC measurements demonstrate that there was a significant increase of BPA levels within the CSF after juvenile BPA exposure (Figure 1).…”

Section: Discussionsupporting

confidence: 60%

“…In the present study, BPA exposure in whole juvenile phase just has effect on the memory consolidation. It implies that the hippocampus in juvenile animals is less sensitive to BPA exposure than it in the first developmental stage, which is characterized with large amounts of mature synapses (a form of synaptic plasticity) until postnatal 21 d (end of lactation)11 and vulnerable to many chemical exposure, including nicotine, Pb, and polybrominated diphenyl ethers 21. However, BPA exposure from gestation to juvenile will have progressively worse effect on memory than perinatal exposure only.…”

Section: Discussionmentioning

confidence: 99%

“…According to previous studies, BPA exposure times are mostly gestation and lactation in rodents or primates. Although this phase is considered as critical brain developmental window with high synaptic plasticity,11 the juvenile period is also important with brain in its final development phase and the gray matter of the frontal and parietal lobes peaks at about age 12 (the end of the juvenile period) in humans 12. The current study aims to assess whether juvenile BPA exposure perturbs hippocampus‐dependent learning and memory in rats; exploring the underlying mechanism by evaluating synaptic plasticity (e.g., long‐term plasticity), dendritic morphology, and synaptic transmission.…”

Section: Introductionmentioning

confidence: 99%

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Bisphenol A Impairs Synaptic Plasticity by Both Pre‐ and Postsynaptic Mechanisms

Gong

et al. 2017

Advanced Science

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Bisphenol A (BPA), an environmental xenoestrogen, has been reported to induce learning and memory impairments in rodent animals. However, effects of BPA exposure on synaptic plasticity and the underlying physiological mechanisms remain elusive. Our behavioral and electrophysiological analyses show that BPA obviously perturbs hippocampal spatial memory of juvenile Sprague–Dawley rats after four weeks exposure, with significantly impaired long‐term potentiation (LTP) in the hippocampus. These effects involve decreased spine density of pyramidal neurons, especially the apical dendritic spine. Further presynaptic findings show an overt inhibition of pulse‐paired facilitation during electrophysiological recording, which suggest the decrease of presynaptic transmitter release and is consistent with reduced production of presynaptic glutamate after BPA exposure. Meanwhile, LTP‐related glutamate receptors, NMDA receptor 2A (NR2A) and AMPA receptor 1 (GluR1), are significantly downregulated in BPA‐exposed rats. Excitatory postsynaptic currents (EPSCs) results also show that EPSCNMDA, but not EPSCAMPA, is declined by 40% compared to the baseline in BPA‐perfused brain slices. Taken together, these findings reveal that juvenile BPA exposure has negative effects on synaptic plasticity, which result from decreases in dendritic spine density and excitatory synaptic transmission. Importantly, this study also provides new insights into the dynamics of BPA‐induced memory deterioration during the whole life of rats.

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Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Bisphenol A Impairs Synaptic Plasticity by Both Pre‐ and Postsynaptic Mechanisms

Gong

et al. 2017

Advanced Science

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“…The parietal cortex and hippocampus were studied, as in humans these regions undergo a critical phase of synaptogenesis and maturation in late gestation and the early postnatal period [26]. Additionally, under pathological conditions such as hypoxia-ischemia and seizures, these regions have been shown to undergo alterations in GABA neurotransmission [27].…”

Section: Introductionmentioning

confidence: 99%

Developmental Expression and Distribution of GABAA Receptor α1-, α3- and β2-Subunits in Pig Brain

Kalanjati

Miller²,

Ireland³

et al. 2011

Dev Neurosci

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The principal function of the γ-aminobutyric acid (GABA) system in the adult brain is inhibition; however, in the neonatal brain, GABA provides much of the excitatory drive. As the brain develops, transmembrane chloride gradients change and the inhibitory role of GABA is initiated and continues throughout juvenile and adult life. Previous studies have shown that GABA_A receptor subunit expression is developmentally regulated, and it is thought that the change in GABA function from excitation to inhibition corresponds to the changeover in expression of ‘immature’ to ‘mature’ subunit isoforms. We examined the protein expression pattern and distribution of GABA type A (GABA_A) receptor α₁-, α₃- and β₂-subunits in the parietal cortex and hippocampus of the developing piglet brain. Four perinatal ages were studied; 14 days preterm (P–14), 10 days preterm (P–10), day of birth (P0) and at postnatal day 7 (P7). Animals were obtained by either caesarean section or spontaneous birth. Protein expression levels and subunit localization were analysed by Western blotting and immunohistochemistry, respectively. In the cortex and hippocampus, GABA_A receptor α₁-subunit showed greatest expression at P7 when compared to all other age groups (p < 0.05). In contrast, α₃ expression in the cortex was elevated in preterm brain, peaking at P0, followed by a significant reduction by P7 (p < 0.05); a similar trend was observed in the hippocampus. GABA_A receptor β₂-subunit protein expression appeared relatively constant across all time points studied in both the cortex and hippocampus. Immunolabelling of the α₁-, α₃- and β₂-subunits was observed throughout all cortical layers at every age. GABA_A receptor α₃-subunit appeared to show specific localization to layers V and VI whilst labelling for the β₂-subunit was observed in layer IV. In the hippocampus of all animals, the α₁- and β₂-subunits were shown to immunolabel various cells and processes in the dentate gyrus (DG), CA1 and CA3; the α₃-subunit was barely observed except at the stratum moleculare of the DG. We report for the first time the ontogenesis of GABA_A receptor subunits α₁, α₃ and β₂ in the perinatal pig brain.

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“…There is evidence of maturation of neural connections (e.g. fronto-temporal; Rice & Barone 2000) in the second and third decades of life; GH and insulin-like growth factor 1 levels normally rise to a peak at around the period of late adolescence. Whether these are related remains unanswered, but the current study certainly suggests the possibility of an important interaction.…”

Section: Introductionmentioning

confidence: 99%

Growth hormone and memory

Wass¹,

Reddy²

2010

Journal of Endocrinology

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Growth hormone (GH) replacement unequivocally benefits growth, body composition, cardiovascular risk factors and quality of life. Less is known about the effects of GH on learning and memory. The recent paper on 'early onset -GH deficiency (GHD) results in spatial memory impairment in mid life -and is prevented by GH supplementation' by Nieves-Martinez importantly adds to this literature. Other data suggest that GH beneficially affects cognitive function in rats. In man, treatment of GHD has been associated with improvements in measures of memory and attention. There are also differences in verbal memory of patients with childhood onset GHD. Further questions remain, and the beneficial effects or otherwise of treating GHD in different age groups remain to be better defined. Certainly for reasons of maturation of neural connections and their development to young adulthood contemporaneous with rises in GH and IGF1 make these important areas for further study in man.Lastly because of what we already know in terms of cognitive effects of GHD, it is important to replace GH when studying other potential causes of adverse effects on cognition, for example, with radiotherapy.

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Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models

Cited by 383 publications

References 120 publications

Bisphenol A Impairs Synaptic Plasticity by Both Pre‐ and Postsynaptic Mechanisms

Bisphenol A Impairs Synaptic Plasticity by Both Pre‐ and Postsynaptic Mechanisms

Developmental Expression and Distribution of GABA<sub>A</sub> Receptor α<sub>1</sub>-, α<sub>3</sub>- and β<sub>2</sub>-Subunits in Pig Brain

Growth hormone and memory

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