Multiple Early Life Stressors as Risk Factors for Neurodevelopmental Abnormalities in the F1 Wistar Rats.

Cumulative exposure to multiple early life stressors is expected to affect behavioral development, causing increased susceptibility to neuropsychiatric disorders. The present study was designed to mimic such conditions in a rat model to study behavioral impairments during adolescence and adulthood. Female Wistar rats (n = 32; 140-150 gm) were switched to a low protein (LP; 8% protein) or control (20% protein) diet 15 days prior to conception, and then the diet regime was maintained throughout the experimental period.

Astrogliosis and associated CSPG upregulation adversely affect dendritogenesis, spinogenesis and synaptic activity in the cerebellum of a double-hit rat model of protein malnutrition (PMN) and lipopolysaccharide (LPS) induced bacterial infection.

The extracellular matrix (ECM) plays a vital role in growth, guidance and survival of neurons in the central nervous system (CNS). The chondroitin sulphate proteoglycans (CSPGs) are a type of ECM proteins that are crucial for CNS homeostasis. The major goal of this study was to uncover the effects of astroglial activation and associated intensified expression of CSPGs on dendritogenesis, spinogenesis as well as on synaptic activity in cerebellum following protein malnutrition (PMN) and lipopolysaccharide (LPS) induced bacterial infection.

Perineuronal nets: Cruise from a honeycomb to the safety nets.

The extracellular matrix (ECM) is a significant component of the brain, constituting up to 20 % of the brain volume and perform multifarious functions during development, maturation and regeneration of the central nervous system (CNS). ECM molecules assemble systematically to form a relatively rigid and unique lattice-like structure, known as perineuronal nets (PNNs). The PNNs usually envelop the cell body and initial axon segment and are characterized by a mesh-like structure extending along dendrites of neurons.

Microglia activation and inflammation in hippocampus attenuates memory and mood functions during experimentally induced diabetes in rat.

Incidence of cognitive and emotional alterations are reportedly two times more in diabetic patients than in non-diabetic population with hitherto unexplained causation and mechanism. Purview of the hippocampus functional diversity sanctions the accessibility and the necessity to investigate the regional neuro-immunological aspects of neurodegeneration and related functional alterations following diabetes. We examined the possible involvement of microglia activation, macrophage response, oxidative stress and inflammatory stature in both ventral and dorsal hippocampus of rats rendered diabetic by a single injection of streptozotocin (STZ; 45 mg/ kg body weight; intraperitoneal).

Perinatal exposure to synergistic multiple stressors leads to cellular and behavioral deficits mimicking Schizophrenia-like pathology.

Protein malnourishment and immune stress are potent perinatal stressors, encountered by children born under poor socioeconomic conditions. Thus, it is necessary to investigate how such stressors synergistically contribute towards developing neurological disorders in affected individuals. Pups from Wistar females, maintained on normal (high-protein, HP:20%) and low-protein (LP:8%) diets were used.

Early life exposure to poly I:C impairs striatal DA-D2 receptor binding, myelination and associated behavioural abilities in rats.

Early-life viral infections critically influence the brain development and have been variously reported to cause neuropsychiatric diseases such as Schizophrenia, Parkinson's diseases, demyelinating diseases, etc. To investigate the alterations in the dopaminergic system, myelination and associated behavioral impairments following neonatal viral infection, the viral immune activation model was created by an intraperitoneal injection of Poly I:C (5 mg/kg bw/ip) to neonatal rat pups on PND-7. The DA-D2 receptor binding was assessed in corpus striatum by using H-Spiperone at 3, 6 and 12 weeks of age.

Maternal Spirulina supplementation during pregnancy and lactation partially prevents oxidative stress, glial activation and neuronal damage in protein malnourished F1 progeny.

Protein malnutrition (PMN) is a global health issue but most prevalent in Africa and Asia. It exerts detrimental effect on structural and physiological aspects of hippocampal circuitry. Despite accumulating evidence for PMN induced changes in nervous system, relatively very little is known about how maternal nutritional supplementation during malnutrition affects glial cells and neurons.

Neuronal changes and cognitive deficits in a multi-hit rat model following cumulative impact of early life stressors.

Perinatal protein malnourishment (LP) is a leading cause for mental and physical retardation in children from poor socioeconomic conditions. Such malnourished children are vulnerable to additional stressors that may synergistically act to cause neurological disorders in adulthood. In this study, the above mentioned condition was mimicked via a multi-hit rat model in which pups born to LP mothers were co-injected with polyinosinic:polycytidylic acid (Poly I:C; viral mimetic) at postnatal day (PND) 3 and lipopolysaccharide (LPS; bacterial mimetic) at PND 9.

Amelioration of neurobehavioral and cognitive abilities of F1 progeny following dietary supplementation with Spirulina to protein malnourished mothers.

Early life adversities (stress, infection and mal/undernutrition) can affect neurocognitive, hippocampal and immunological functioning of the brain throughout life. Substantial evidence suggests that maternal protein malnutrition contributes to the progression of neurocognitive abnormalities and psychopathologies in adolescence and adulthood in offspring. Maternal malnutrition is prevalent in low and middle resource populations.

Cumulative multiple early life hits- a potent threat leading to neurological disorders.

Early life Stress is a worldwide concern linked with development of later life neurological disorders. Early developmental age is sensitive to many prominent environmental insults like malnourishment, immune inflammation, abuse, maternal separation, alcohol and drugs. Hence, an individual during an early age encounters more than one simultaneous stressor that leads to impairment of cognitive and behavioral abilities, a symptom common to most of the neurological disorders.

Maternal Protein Malnutrition: Current and Future Perspectives of Spirulina Supplementation in Neuroprotection.

Malnutrition has been widely recognized as a grave burden restricting the progress of underdeveloped and developing countries. Maternal, neonatal and postnatal nutritional immunity provides an effective approach to decrease the risk of malnutrition associated stress in adulthood. Particularly, maternal nutritional status is a critical contributor for determining the long-term health aspects of an offspring.

Postnatal exposure to poly (I:C) impairs learning and memory through changes in synaptic plasticity gene expression in developing rat brain.

Viral infection during early stage of life influences brain development and results in several neurodevelopmental disorders such as schizophrenia, autism and behavioral abnormalities. However, the mechanism through which infection causes long-term behavioral defects is not well known. To elucidate this, we have used synthetic polyinosinic-polycytidylic acid [poly (I:C)] which acts as a dsRNA molecule and interacts with toll-like receptor-3 (TLR-3) of microglia cells to evoke the immune system, thus mimicking the viral infection.

Developmental Changes in Oligodendrocyte Genesis, Myelination, and Associated Behavioral Dysfunction in a Rat Model of Intra-generational Protein Malnutrition.

Impairments in oligodendrocyte development and resultant myelination deficits appear as a common denominator to all neurological diseases. An optimal in utero environment is obligatory for normal fetal brain development and later life brain functioning. Late embryonic and early postnatal brains from F1 rat born to protein malnourished mothers were studied through a combination of immunocytochemical and quantitative PCR assay for analyzing the relative expression of platelet-derived growth factor receptor-α (PDGFRα), myelin-associated glycoprotein (MAG), proteolipid protein (PLP), and myelin oligodendrocyte glycoprotein (MOG) to determine oligodendrocyte genesis, differentiation, maturation, and myelination.

Neonatal Lipopolysaccharide Infection Causes Demyelination and Behavioral Deficits in Adult and Senile Rat Brain.

Background: Neonatal bacterial infections have been reported to cause white matter loss, although studies concerning the influence of infection on the expression of myelin and aging are still in their emerging state.

Purpose: The present study aimed to investigate the effects of perinatal lipopolysaccharide (LPS) exposure on the myelination at different age points using histochemical and immunocytochemical techniques and the relative motor coordination.

Methods: A rat bacterial infection model was established by exposing the neonatal rats with LPS (0.

Intra-generational protein malnutrition impairs temporal astrogenesis in rat brain.

The lack of information on astrogenesis following stressor effect, notwithstanding the imperative roles of astroglia in normal physiology and pathophysiology, incited us to assess temporal astrogenesis and astrocyte density in an intra-generational protein malnutrition (PMN) rat model. Standard immunohistochemical procedures for glial lineage markers and their intensity measurements, and qRT-PCR studies, were performed to reveal the spatio-temporal origin and density of astrocytes. Reduced AB+ glia restricted precursor population in ventricles and caused poor dissemination to cortex at embryonic days (E)11-14, and low BLBP+ secondary radial glia in the subventricular zone (SVZ) of E16 low protein (LP) brains reflect compromised progenitor pooling.

Slow Physical Growth, Delayed Reflex Ontogeny, and Permanent Behavioral as Well as Cognitive Impairments in Rats Following Intra-generational Protein Malnutrition.

Environmental stressors including protein malnutrition (PMN) during pre-, neo- and post-natal age have been documented to affect cognitive development and cause increased susceptibility to neuropsychiatric disorders. Most studies have addressed either of the three windows and that does not emulate the clinical conditions of intra-uterine growth restriction (IUGR). Such data fail to provide a complete picture of the behavioral alterations in the F1 generation.

Curcumin attenuates inflammatory response and cognitive deficits in experimental model of chronic epilepsy.

Evidence suggests that glial cells play a critical role in inflammation in chronic epilepsy, contributing to perpetuation of seizures and cognitive dysfunctions. The present study was designed to evaluate the beneficial effect of curcumin, a polyphenol with pleiotropic properties, on cognitive deficits and inflammation in chronic epilepsy. Kindled model of epilepsy was induced by administering sub-convulsive dose of pentylenetetrazole (PTZ) at 40 mg/kg, i.

Lipopolysaccharide-Induced Apoptosis of Astrocytes: Therapeutic Intervention by Minocycline.

Astrocytes are most abundant glial cell type in the brain and play a main defensive role in central nervous system against glutamate-induced toxicity by virtue of numerous transporters residing in their membranes and an astrocyte-specific enzyme glutamine synthetase (GS). In view of that, a dysregulation in the astrocytic activity following an insult may result in glutamate-mediated toxicity accompanied with astrocyte and microglial activation. The present study suggests that the lipopolysaccharide (LPS)-induced inflammation results in significant astrocytic apoptosis compared to other cell types in hippocampus and minocycline could not efficiently restrict the glutamate-mediated toxicity and apoptosis of astrocytes.

Differential temporal expression of S100β in developing rat brain.

Radial glial cells (RGs) originally considered to provide scaffold to the radially migrating neurons constitute a heterogeneous population of the regionally variable precursor cells that generate both neurons as well as glia depending upon the location and the timing of development. Hence specific immunohistochemical markers are required to specify their spatiotemporal location and fate in the neurogenic and gliogenic zones. We hypothesize S100β as a potential and unified marker for both primary and secondary progenitors.

Experimentally induced diabetes causes glial activation, glutamate toxicity and cellular damage leading to changes in motor function.

Behavioral impairments are the most empirical consequence of diabetes mellitus documented in both humans and animal models, but the underlying causes are still poorly understood. As the cerebellum plays a major role in coordination and execution of the motor functions, we investigated the possible involvement of glial activation, cellular degeneration and glutamate transportation in the cerebellum of rats, rendered diabetic by a single injection of streptozotocin (STZ; 45 mg/kg body weight; intraperitoneally). Motor function alterations were studied using Rotarod test (motor coordination) and grip strength (muscle activity) at 2nd, 4th, 6th, 8th, 10th, and 12th week post-diabetic confirmation.

Glial alterations in tuberculous and cryptococcal meningitis and their relation to HIV co-infection--a study on human brains.

Introduction: Tuberculosis and cryptococcal infection of the central nervous system are common AIDS-associated opportunistic infections in tropical underdeveloped and developing countries. To date, research on these infections has focused on clinical, imaging, laboratory diagnosis, and animal models to elucidate the pathogenesis. There is paucity of information on astroglial and microglial alterations in the human nervous system following these infections.

Astrocytic and microglial response in experimentally induced diabetic rat brain.

Diabetes Mellitus is associated with increased risk of cognitive and behavioural disorders with hitherto undeciphered role of glia. Glia as majority population in brain serve several vital functions, thus require pertinent revelation to further explicate the mechanisms affecting the brain function following diabetes. In this study we have evaluated glial changes in terms of phenotypic switching, proliferation and expression of activation cell surface markers and associated cellular degeneration in hippocampus following STZ-induced diabetes and caused cognitive impairments.

Quick Golgi method: modified for high clarity and better neuronal anatomy.

The Golgi methods have long been used to study the neuronal soma, axons, dendritic arborization and spines. The major concerns of the Golgi method have been its unpredictable nature (inconsistency of impregnation of the stain), time consumed, tissue hardening and clear background, resulting in several modifications to improve the cellular visualization. In the present work we describe a modification of the rapid-Golgi method that takes the benefit of perfusion fixation (with rapid-Golgi solution) then post-fixation in the same fixative for 36 h followed by 36 h impregnation in aqueous AgNO3 followed by vibratomy.

Differential microglial and astrocytic response to bacterial and viral infection in the developing hippocampus of neonatal rats.

Polyinosinic:polycytidylic acid (Poly I:C; 5 mg/kg body weight, ip) and lipopolysaccharide (LPS; 0.3 mg/kg body weight, ip) induced microglial and astrocytic activation in Sprague Dawley rats. Higher microglial and astrocytic activities were noticed in Poly I:C infused rats throughout the hippocampus till postnatal day 21 with a comparatively weaker response in LPS group.