Period In Early Postnatal Life Research Articles

Mental causation: an evolutionary perspective.

The relationship between consciousness and individual agency is examined from a bottom-up evolutionary perspective, an approach somewhat different from other ways of dealing with the issue, but one relevant to the question of animal consciousness. Two ways are identified that would decouple the two, allowing consciousness of a limited kind to exist without agency: (1) reflex pathways that incorporate conscious sensations as an intrinsic component (InCs), and (2) reflexes that are consciously conditioned and dependent on synaptic plasticity but not memory (CCRs). Whether InCs and CCRs exist as more than hypothetical constructs is not clear, and InCs are in any case limited to theories where consciousness depends directly on EM field-based effects. Consciousness with agency, as we experience it, then belongs in a third category that allows for deliberate choice of alternative actions (DCs), where the key difference between this and CCR-level pathways is that DCs require access to explicit memory systems whereas CCRs do not. CCRs are nevertheless useful from a heuristic standpoint as a conceptual model for how conscious inputs could act to refine routine behaviors while allowing evolution to optimize phenomenal experience (i.e., qualia) in the absence of individual agency, a somewhat counterintuitive result. However, so long as CCRs are not a required precondition for the evolution of memory-dependent DC-level processes, the later could have evolved first. If so, the adaptive benefit of consciousness when it first evolved may be linked as much to the role it plays in encoding memories as to any other function. The possibility that CCRs are more than a theoretical construct, and have played a role in the evolution of consciousness, argues against theories of consciousness focussed exclusively on higher-order functions as the appropriate way to deal with consciousness as it first evolved, as it develops in the early postnatal period of life, or with the conscious experiences of animals other than ourselves. An evolutionary perspective also resolves the problem of free will, that it is best treated as a property of a species rather than the individuals belonging to that species whereas, in contrast, agency is an attribute of individuals.

FEATURES OF ENDOCRINE CELLS OF THE DUODENUM 12 IN THE EARLY POSTNATAL PERIOD OF LIFE AND ITS DEVELOPMENT

This article analyzes and discusses the characteristics of 12 endocrine cells of the duodenum and its development in the early postnatal period of life.

Diseases associated with prematurity in correlation with N-terminal pro-brain natriuretic peptide levels during the early postnatal life

The aim of this observational study was to investigate the influence of different typical preterm diseases on NT-proBNP serum levels in the early postnatal period of life of a preterm infant. NT-proBNP levels of 118 preterm infants born ≤ 31 weeks GA were determined at the first week of life, after 4 ± 1 weeks of life, and at a corrected gestational age of 36 + 2 weeks. Relevant complications with a possible influence on NT-proBNP values in the first week of life such as early neonatal infection, hemodynamically significant PDA (hsPDA), early pulmonary hypertension (early PH), and intraventricular hemorrhage (IVH) were evaluated; at 4 ± 1 weeks of life, bronchopulmonary dysplasia (BPD), BPD-related pulmonary hypertension (BPD-associated PH), late infection, IVH, and intestinal complications were evaluated. At a corrected gestational age of 36 ± 2 weeks, we examined the effect of retinopathy of prematurity (ROP), BPD, BPD-associated PH, and late infection on NT-proBNP levels. In the first days of life, only the isolated occurrence of hsPDA resulted in significantly increased NT-proBNP levels. In multiple linear regression analysis, early infection remained independently associated with NT-proBNP levels. At 4 ± 1 weeks of age, the isolated presence of BPD and BPD-related PH resulted in increased levels, and the effect remained significant in the multiple regression analysis. At a corrected gestational age of 36 ± 2 weeks, infants with relevant complications at this final evaluation time tended to have lower NT-proBNP values than our exploratory reference values. Conlusion: NT-proBNP in the first week of life seems to be mainly influenced by an hsPDA and infection or inflammation. BPD and BPD-related PH are the most important factors influencing NT-proBNP serum levels in the first month of life. When preterm infants reach a corrected GA of 36 ± 2 weeks, chronological age rather than complications of prematurity must be considered when interpreting NT-proBNP levels.What is Known:• Several complications associated with prematurity, such as hemodynamically significant PDA, pulmonary hypertension, bronchopulmonary dysplasia, and retinopathy of prematurity, have been shown to influence NT-proBNP levels in preterm infants in their early postnatal life.What is New:• Hemodynamically relevant PDA is a major factor in the increase of NT-proBNP levels in the first week of life.• Bronchopulmonary dysplasia and pulmonary hypertension associated with bronchopulmonary dysplasia are important factors in the increase in NT-proBNP levels in preterm infants at approximately 1 month of age.

SLC30A10 manganese transporter in the brain protects against deficits in motor function and dopaminergic neurotransmission under physiological conditions.

Loss-of-function mutations in SLC30A10 induce hereditary manganese (Mn)-induced neuromotor disease in humans. We previously identified SLC30A10 to be a critical Mn efflux transporter that controls physiological brain Mn levels by mediating hepatic and intestinal Mn excretion in adolescence/adulthood. Our studies also revealed that in adulthood, SLC30A10 in the brain regulates brain Mn levels when Mn excretion capacity is overwhelmed (e.g. after Mn exposure). But, the functional role of brain SLC30A10 under physiological conditions is unknown. We hypothesized that, under physiological conditions, brain SLC30A10 may modulate brain Mn levels and Mn neurotoxicity in early postnatal life because body Mn excretion capacity is reduced in this developmental stage. We discovered that Mn levels of pan-neuronal/glial Slc30a10 knockout mice were elevated in specific brain regions (thalamus) during specific stages of early postnatal development (postnatal day 21), but not in adulthood. Furthermore, adolescent or adult pan-neuronal/glial Slc30a10 knockouts exhibited neuromotor deficits. The neuromotor dysfunction of adult pan-neuronal/glial Slc30a10 knockouts was associated with a profound reduction in evoked striatal dopamine release without dopaminergic neurodegeneration or changes in striatal tissue dopamine levels. Put together, our results identify a critical physiological function of brain SLC30A10-SLC30A10 in the brain regulates Mn levels in specific brain regions and periods of early postnatal life, which protects against lasting deficits in neuromotor function and dopaminergic neurotransmission. These findings further suggest that a deficit in dopamine release may be a likely cause of early-life Mn-induced motor disease.

Early life sleep disruption has long lasting, sex specific effects on later development of sleep in prairie voles

In mammals, sleep duration is highest in the early postnatal period of life and is critical for shaping neural circuits that control the development of complex behaviors. The prairie vole is a wild, highly social rodent that serves as a unique model for the study of complex, species-typical social behaviors. Previous work in our laboratory has found that early life sleep disruption (ELSD) in prairie voles during a sensitive window of postnatal development leads to long lasting changes in social and cognitive behaviors as well as structural changes in excitatory and inhibitory neural circuits in the brain. However, it is currently unknown how later sleep is impacted by ELSD, both shortly after ELSD and over the long term. Therefore, the aim of this study was to describe the effects of ELSD on later life sleep, compared to sleep in normally developing prairie voles. First, we conducted tethered electroencephalogram/electromyogram (EEG/EMG) recordings in juvenile prairie voles undergoing ELSD, compared to Control conditions. Second, we conducted 24 h of home cage tethered EEG/EMG recordings in either adolescent or adult male and female prairie voles that had previously undergone ELSD or Control conditions as juveniles. We found that, as adults, male ELSD prairie voles showed persistently lower REM sleep duration and female ELSD prairie voles showed persistently higher NREM sleep duration compared to Controls, but no other sleep parameters differed. We concluded that 1) persistent effects of ELSD on sleep into adulthood may contribute to the social and cognitive deficits observed in adult voles, and 2) sleep disruption early in life can influence later sleep patterns in adulthood.

Effects of early postnatal life nutritional interventions on immune-microbiome interactions in the gastrointestinal tract and implications for brain development and function.

The gastrointestinal (GI) microbiota has co-evolved with the host in an intricate relationship for mutual benefit, however, inappropriate development of this relationship can have detrimental effects. The developing GI microbiota plays a vital role during the first 1,000 days of postnatal life, during which occurs parallel development and maturation of the GI tract, immune system, and brain. Several factors such as mode of delivery, gestational age at birth, exposure to antibiotics, host genetics, and nutrition affect the establishment and resultant composition of the GI microbiota, and therefore play a role in shaping host development. Nutrition during the first 1,000 days is considered to have the most potential in shaping microbiota structure and function, influencing its interactions with the immune system in the GI tract and consequent impact on brain development. The importance of the microbiota-GI-brain (MGB) axis is also increasingly recognized for its importance in these developmental changes. This narrative review focuses on the importance of the GI microbiota and the impact of nutrition on MGB axis during the immune system and brain developmental period in early postnatal life of infants.

Morphological changes in neuroimmunoendorinee cells off the small intestine in the early postnatal period of life

Morphological changes in neuroimmunoendorinee cells off the small intestine in the early postnatal period of life

Morphological characteristics of the small intestine during absorption in the early postnatal period of life.

Morphological characteristics of the small intestine during absorption in the early postnatal period of life.

In Silico Predictions on the Productive Life Span and Theory of Its Developmental Origin in Dairy Cows.

Simple SummaryDairy cows are susceptible to a range of welfare factors, which lead to worsening health problems and shorten their productive life span. The health and welfare status of dairy cows could be improved if unwanted abnormalities and risk factors are detected in a timely manner, i.e., before diseases start to occur. Therefore, in addition to veterinary monitoring, quantitative parameters are necessary to predict the risks of early culling of cows. In the study of the age dynamics of culling rate in dairy cow populations, it was found that the average productive life span can be predicted by registration of the reciprocal relative disposal rate (culling for sum of reasons + death). This indicator represents the viability index, which has a maximal value at the first lactation and decreases in subsequent lactations with an inverse exponential trend. According to available scientific information, the structural prerequisites for this index are laid down during prenatal development and in the early periods of postnatal life; therefore, it is necessary to create a system of continuous monitoring of the physiological status of mothers and young animals.Animal welfare includes health but also concerns the need for natural factors that contribute to the increase in viability. Therefore, quantitative parameters are necessary to predict the risks of early culling of cows. In the study of the age dynamics of the disposal rate (culling for sum of reasons + death) in dairy cow populations, it was found that the average productive life span can be predicted by the value of the reciprocal culling/death rate (reciprocal value of Gompertz function) at the first lactation. This means that this potential of viability is formed during the developmental periods preceding the onset of lactation activity. Therefore, taking into account current data in the field of developmental biology, it can be assumed that the structural prerequisites for viability potential are laid down during prenatal development and in the early periods of postnatal life. To prevent unfavorable deviations in these processes due to negative welfare effects, it is advisable to monitor the physiological status of mothers and young animals using biosensors and Big Data systems.

The Influence of Cesarean Section on the Composition and Development of Gut Microbiota During the First 3 Months of Life.

The intestinal microbiota has emerged as a critical regulator of growth and development in the early postnatal period of life. Cesarean section (CS) delivery is one of the strongest disrupting factors of the normal colonization process and has been reported as a risk factor for disorders in later life. In this study, we dynamically and longitudinally evaluated the impact of CS on the initial colonization pattern and development of gut microbiota by 16 healthy Chinese infants with fecal samples collected at 9 time points (day 5, day 8, day 11, week 2, week 4, week 6, week 7, month 2, and month 3) during the first 3 months of life. The V3–V4 regions of 16S rRNA gene were analyzed by Illumina sequencing. In comparison with vaginally delivered (VD) infants, infants born by CS showed decreased relative abundance of Bacteroides and Parabacteroides and enrichment of Clostridium_sensu_stricto_1, Enterococcus, Klebsiella, Clostridioides, and Veillonella. Most interestingly, Firmicutes/Bacteroidetes ratio was found to be significantly higher in the CS group than in the VD group from day 5 until month 3. Besides, the results of microbial functions showed that the VD group harbored significantly higher levels of functional genes in vitamin B6 metabolism at day 5, day 8, week 2, week 4, week 6, week 7, month 2, and month 3 and taurine and hypotaurine metabolism at day 5, while the phosphotransferase system and starch and sucrose metabolism involved functional genes were plentiful in the CS group at day 11, week 2, week 4, week 6, week 7, and month 2 and at week 2, week 7, and month 2, respectively. Our results establish a new evidence that CS affected the composition and development of gut microbiota in the first 3 months and provide a novel insight into strategies for CS-related disorders in later life.

Pharmacological and optical activation of TrkB in Parvalbumin interneurons regulate intrinsic states to orchestrate cortical plasticity

Elevated states of brain plasticity typical for critical periods of early postnatal life can be reinstated in the adult brain through interventions, such as antidepressant treatment and environmental enrichment, and induced plasticity may be critical for the antidepressant action. Parvalbumin-positive (PV) interneurons regulate the closure of developmental critical periods and can alternate between high and low plasticity states in response to experience in adulthood. We now show that PV plasticity states and cortical networks are regulated through the activation of TrkB neurotrophin receptors. Visual cortical plasticity induced by fluoxetine, a widely prescribed selective serotonin reuptake inhibitor (SSRI) antidepressant, was lost in mice with reduced expression of TrkB in PV interneurons. Conversely, optogenetic gain-of-function studies revealed that activation of an optically activatable TrkB (optoTrkB) specifically in PV interneurons switches adult cortical networks into a state of elevated plasticity within minutes by decreasing the intrinsic excitability of PV interneurons, recapitulating the effects of fluoxetine. TrkB activation shifted cortical networks towards a low PV configuration, promoting oscillatory synchrony, increased excitatory-inhibitory balance, and ocular dominance plasticity. OptoTrkB activation promotes the phosphorylation of Kv3.1 channels and reduces the expression of Kv3.2 mRNA providing a mechanism for the lower excitability. In addition, decreased expression and puncta of Synaptotagmin2 (Syt2), a presynaptic marker of PV interneurons involved in Ca2+-dependent neurotransmitter release, suggests lower inputs onto pyramidal neurons suppressing feed-forward inhibition. Together, the results provide mechanistic insights into how TrkB activation in PV interneurons orchestrates the activity of cortical networks and mediating antidepressant responses in the adult brain.

The need to study human milk as a biological system

ABSTRACTCritical advancement is needed in the study of human milk as a biological system that intersects and interacts with myriad internal (maternal biology) and external (diet, environment, infections) factors and its plethora of influences on the developing infant. Human-milk composition and its resulting biological function is more than the sum of its parts. Our failure to fully understand this biology in a large part contributes to why the duration of exclusive breastfeeding remains an unsettled science (if not policy). Our current understanding of human-milk composition and its individual components and their functions fails to fully recognize the importance of the chronobiology and systems biology of human milk in the context of milk synthesis, optimal timing and duration of feeding, and period of lactation. The overly simplistic, but common, approach to analyzing single, mostly nutritive components of human milk is insufficient to understand the contribution of either individual components or the matrix within which they exist to both maternal and child health. There is a need for a shift in the conceptual approach to studying human milk to improve strategies and interventions to support better lactation, breastfeeding, and the full range of infant feeding practices, particularly for women and infants living in undernourished and infectious environments. Recent technological advances have led to a rising movement towards advancing the science of human-milk biology. Herein, we describe the rationale and critical need for unveiling the multifunctionality of the various nutritional, nonnutritional, immune, and biological signaling pathways of the components in human milk that drive system development and maturation, growth, and development in the very early postnatal period of life. We provide a vision and conceptual framework for a research strategy and agenda to change the field of human-milk biology with implications for global policy, innovation, and interventions.

MEF2C and HDAC5 regulate Egr1 and Arc genes to increase dendritic spine density and complexity in early enriched environment.

We investigated the effects of environmental enrichment during critical period of early postnatal life and how it interplays with the epigenome to affect experience-dependent visual cortical plasticity. Mice raised in an EE from birth to during CP have increased spine density and dendritic complexity in the visual cortex. EE upregulates synaptic plasticity genes, Arc and Egr1, and a transcription factor MEF2C. We also observed an increase in MEF2C binding to the promoters of Arc and Egr1. In addition, pups raised in EE show a reduction in HDAC5 and its binding to promoters of Mef2c, Arc and Egr1 genes. With an overexpression of Mef2c, neurite outgrowth increased in complexity. Our results suggest a possible underlying molecular mechanism of EE, acting through MEF2C and HDAC5, which drive Arc and Egr1. This could lead to the observed increased dendritic spine density and complexity induced by early EE.

Implications of accumulative stress burdens during critical periods of early postnatal life for mortality risk among Guale interred in a colonial era cemetery in Spanish Florida (ca. AD 1605-1680).

Research situated within the Developmental Origins of Health and Disease demonstrates that stressors are correlated with future mortality risk, especially if experienced frequently and during early periods of postnatal life. This study examines if the developmental timing and frequency of early life stressors influenced mortality risk for Indigenous Guale in Spanish Florida during the 17th century. The present study examines internal enamel microgrowth disruptions (accentuated lines-AL) from Guale individuals (n = 52) interred at Mission Santa Catalina de Guale on St. Catherines Island, Georgia (AD 1605-1680). Teeth were thin-sectioned and microscopically analyzed to document AL variables as predictors of age-at-death. Individuals with AL died earlier than those without AL. This difference, however, was not significant. Individuals who exhibit AL formed during their first year of life died on average three times earlier than those who did not. The frequency of AL and age-at-first-AL are significantly correlated with age-at-death, and Cox hazard analyses indicates that individuals with early forming and frequent AL had increased risks of early death. This study emphasizes how the lived experiences of Guale children shaped demographic patterns during the 17th century. The survival of early life stressors resulted in life history trade-offs and increased risks for early death. Mortality risks were exacerbated for individuals who experienced frequent stressors during the earliest periods of life. This underscores a role for bioarchaeology in understanding of how accumulative stress burdens during the earliest years of postnatal life may influence mortality risk.

Fetal Gene Therapy Using a Single Injection of Recombinant AAV9 Rescued SMA Phenotype in Mice.

Symptoms of spinal muscular atrophy (SMA) disease typically begin in the late prenatal or the early postnatal period of life. The intrauterine (IU) correction of gene expression, fetal gene therapy, could offer effective gene therapy approach for early onset diseases. Hence, the overall goal of this study was to investigate the efficacy of human survival motor neuron (hSMN) gene expression after IU delivery in SMA mouse embryos. First, we found that IU-intracerebroventricular (i.c.v.) injection of adeno-associated virus serotype-9 (AAV9)-EGFP led to extensive expression of EGFP protein in different parts of the CNS with a great number of transduced neural stem cells. Then, to implement the fetal gene therapy, mouse fetuses received a single i.c.v. injection of a single-stranded (ss) or self-complementary (sc) AAV9-SMN vector that led to a lifespan of 93 (median of 63) or 171 (median 105) days for SMA mice. The muscle pathology and number of the motor neurons also improved in both study groups, with slightly better results coming from scAAV treatment. Consequently, fetal gene therapy may provide an alternative therapeutic approach for treating inherited diseases such as SMA that lead to prenatal death or lifelong irreversible damage.

Chondroitin Sulfate Is Required for Onset and Offset of Critical Period Plasticity in Visual Cortex

Ocular dominance plasticity is easily observed during the critical period in early postnatal life. Chondroitin sulfate (CS) is the most abundant component in extracellular structures called perineuronal nets (PNNs), which surround parvalbumin-expressing interneurons (PV-cells). CS accumulates in PNNs at the critical period, but its function in earlier life is unclear. Here, we show that initiation of ocular dominance plasticity was impaired with reduced CS, using mice lacking a key CS-synthesizing enzyme, CSGalNAcT1. Two-photon in vivo imaging showed a weaker visual response of PV-cells with reduced CS compared to wild-type mice. Plasticity onset was restored by a homeoprotein Otx2, which binds the major CS-proteoglycan aggrecan and promotes its further expression. Continuous CS accumulation together with Otx2 contributed bidirectionally to both onset and offset of plasticity, and was substituted by diazepam, which enhances GABA function. Therefore, CS and Otx2 may act as common inducers of both onset and offset of the critical period by promoting PV-cell function throughout the lifetime.

Adult neurogenesis – accent on subgranular and subventricular zone in mammals

Tillrecently was assumed that neural cells stop dividing in early postnatal period of life, but last two decades large ammount ofresearches on that field proved contrary. There are evidences confirming existance of adult neurogenesis in most mammalian species, including humans.This process occurs spontaneouslyin physiological termsin two germinal brain regionscontaining neural stem cells; in subgranular zone of hippocampal dentate gyrus and subventricular zone of lateral ventricule.Neural stem cells in this germinal regions posses higher proliferative and differential capacity toward new future neurons, astrocytes and oligidendrocytes than neural stem cells from other regions in nervous system. Proliferative and regenerative power of this two niches has important role in brain adjustment to exterior stimuli during life which is called neuroplasticity. Germinal niches in brain are specific microenvironment in which close interaction of specific proneurogenic factors and resident neural stem cells and blood vessels form strictly controled conditions providing neuroblast and glioblast proliferation, differentiation, migration andmaturation and also survival and integration of newly created neuron or glial cell in existing brain sinaptic cirtuits. In case of harming this and other germinal brain centers different psichoneurologic disorders occur. Better understanding of germinal microenvironment function in human brainopens a new possibilities in neuroscience for creating a therapy based on adult neurogenesis manipulation through creating neurons “de novo”.

The Clinical Case Of Symptomatic Epilepsy In Newborn With Neonatal Hypoglycemic Encephalopathy

Symptomatic epilepsy is common disorder in neonatal period. One of the reasons of symptomatic epilepsy can be neonatal hypoglycemia. Hypoglycemia is the commonest metabolic disorder in neonatal period. Neonatal hypoglycemia can cause neonatal hypoglycemic encephalopathy (NHE) with damage of occipital cortex, symptomatic epilepsy in early postnatal period of life and severe neurological impairment in childhood. Early diagnosis of the NHE is possibly by using brain’s MRI and EEG in neonatal period. Presented clinical case of symptomatic epilepsy in newborn with NHE and results of his clinical examination and findings on brain’s MRI, EEG. There has been performance twice EEG recoding in the acute clinical phase of the hypoglycemic encephalopathy with video monitoring. We used multichannel EEG record in the neonatal modification. Once there has been fulfillment MRI (1,5T scanner) in early period of the case disease (after the convulsion discontinuation). We routinely used T1 weighted imaging, T2 weighted imaging, DWI and Flair. We show the correlation functional brain discharge and structural brain damages by MRI in the case of the neonatal hypoglycemic encephalopathy. The EEG recorded epileptiform activity (sharp theta-waves, spices) in central-occipital and temporal regions. We detected the changes MR-signal from central-occipital and temporal brains regions and thinning of occipital cortex with normal cortex architecture

Prenatal programming: adverse cardiac programming by gestational testosterone excess.

Adverse events during the prenatal and early postnatal period of life are associated with development of cardiovascular disease in adulthood. Prenatal exposure to excess testosterone (T) in sheep induces adverse reproductive and metabolic programming leading to polycystic ovarian syndrome, insulin resistance and hypertension in the female offspring. We hypothesized that prenatal T excess disrupts insulin signaling in the cardiac left ventricle leading to adverse cardiac programming. Left ventricular tissues were obtained from 2-year-old female sheep treated prenatally with T or oil (control) from days 30–90 of gestation. Molecular markers of insulin signaling and cardiac hypertrophy were analyzed. Prenatal T excess increased the gene expression of molecular markers involved in insulin signaling and those associated with cardiac hypertrophy and stress including insulin receptor substrate-1 (IRS-1), phosphatidyl inositol-3 kinase (PI3K), Mammalian target of rapamycin complex 1 (mTORC1), nuclear factor of activated T cells –c3 (NFATc3), and brain natriuretic peptide (BNP) compared to controls. Furthermore, prenatal T excess increased the phosphorylation of PI3K, AKT and mTOR. Myocardial disarray (multifocal) and increase in cardiomyocyte diameter was evident on histological investigation in T-treated females. These findings support adverse left ventricular remodeling by prenatal T excess.

The distinct role of NR2B subunit in the enhancement of visual plasticity in adulthood

BackgroundExperience-dependent plasticity is confined to the critical period of early postnatal life, and declines dramatically thereafter. This attenuation promotes the stabilization of cortical circuits, but also limits functional recovery of several brain diseases. The cognitive functions and synaptic plasticity in the hippocampus and prefrontal cortex are elevated following chronic magnesium treatment. Here, we explored the effect of magnesium treatment on visual plasticity and the potential clinical significance.ResultsVisual plasticity in adult mice was dramatically enhanced following magnesium treatment, which was concurrent with an increase in the expression of NR2 subunits of N-methyl-D-aspartate receptors. Blockade of NR2B activity in both the induction and expression periods of plasticity prevented this reinstatement. However, the plasticity restored via a decrease in cortical inhibition was independent on the activation of NR2B, indicating a different underlying mechanism. The functional excitatory synapses on layer 2/3 pyramidal neurons were increased following magnesium supplementation. Moreover, the synaptic and neuronal responses were reminiscent of that within the critical period, and this rejuvenation of adult visual cortex facilitated the recovery of visual functions in amblyopia.ConclusionsCollectively, our data reveal two distinct mechanisms underlying the restoration of visual plasticity in adulthood, and the rejuvenation of adult visual cortex following magnesium treatment provides a new avenue to develop clinical therapies for adult amblyopia, as well as to explore plasticity-based treatment of other brain diseases, such as stroke and aphasia.Electronic supplementary materialThe online version of this article (doi:10.1186/s13041-015-0141-y) contains supplementary material, which is available to authorized users.