Algorithm of diagnostics of cognitive functions development violation in children born extremally premature

A qualitative improvement in the management of pregnancy and delivery, optimization of General care and provision of intensive care for children born prematurely, particularly with low and extremely low body weight, significantly reduced the risk of damage to the nervous system of perinatal hypoxic-ischemic genesis. At the same time, there is a significant number of children born at low gestational age, with a significant violation of intellectual, cognitive development and behavior change. One of the assumptions about cause of improper maturation of the brain is the role of unbalanced chromosomal and genomic micro anomalies. There is provided the data on the survey of 22 children with approximately the same clinic of developmental disorders, 19 of which revealed various structural micro-damages of genesis, but their interpretation is difficult today. The algorithm of selection of children for the extended genetic examination is given.

Download Full-text

Plasticity: Cells, Circuits, Brains, and Behavior

The Computational Brain ◽

10.7551/mitpress/9780262533393.003.0005 ◽

2016 ◽

Author(s):

Patricia S. Churchland ◽

Terrence J. Sejnowski

Keyword(s):

Nervous System ◽

Synaptic Plasticity ◽

Classical Conditioning ◽

Neuronal Plasticity ◽

Neural Mechanism ◽

Synaptic Strength ◽

Physical Mechanisms ◽

And Behavior ◽

The Brain

This chapter examines the physical mechanisms in nervous systems in order to elucidate the structural bases and functional principles of synaptic plasticity. Neuroscientific research on plasticity can be divided into four main streams: the neural mechanism for relatively simple kinds of plasticity, such as classical conditioning or habituation; anatomical and physiological studies of temporal lobe structures, including the hippocampus and the amygdala; study of the development of the visual system; and the relation between the animal's genes and the development of its nervous system. The chapter first considers the role of the mammalian hippocampus in learning and memory before discussing Donald Hebb's views on synaptic plasticity. It then explores the mechanisms underlying neuronal plasticity and those that decrease synaptic strength, the relevance of time with respect to plasticity, and the occurrence of plasticity during the development of the nervous system. It also describes modules, modularity, and networks in the brain.

Download Full-text

The Role of Neuropeptide Y in the Nucleus Accumbens

International Journal of Molecular Sciences ◽

10.3390/ijms22147287 ◽

2021 ◽

Vol 22 (14) ◽

pp. 7287

Author(s):

Masaki Tanaka ◽

Shunji Yamada ◽

Yoshihisa Watanabe

Keyword(s):

Nervous System ◽

Nucleus Accumbens ◽

Neuropeptide Y ◽

Emotional Behavior ◽

Characteristic Functions ◽

Receptor Subtypes ◽

Neuroendocrine Mechanisms ◽

Fear And Anxiety ◽

The Brain

Neuropeptide Y (NPY), an abundant peptide in the central nervous system, is expressed in neurons of various regions throughout the brain. The physiological and behavioral effects of NPY are mainly mediated through Y1, Y2, and Y5 receptor subtypes, which are expressed in regions regulating food intake, fear and anxiety, learning and memory, depression, and posttraumatic stress. In particular, the nucleus accumbens (NAc) has one of the highest NPY concentrations in the brain. In this review, we summarize the role of NPY in the NAc. NPY is expressed principally in medium-sized aspiny neurons, and numerous NPY immunoreactive fibers are observed in the NAc. Alterations in NPY expression under certain conditions through intra-NAc injections of NPY or receptor agonists/antagonists revealed NPY to be involved in the characteristic functions of the NAc, such as alcohol intake and drug addiction. In addition, control of mesolimbic dopaminergic release via NPY receptors may take part in these functions. NPY in the NAc also participates in fat intake and emotional behavior. Accumbal NPY neurons and fibers may exert physiological and pathophysiological actions partly through neuroendocrine mechanisms and the autonomic nervous system.

Download Full-text

Roles of Drosophila Hox Genes in the Assembly of Neuromuscular Networks and Behavior

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.786993 ◽

2022 ◽

Vol 9 ◽

Author(s):

Rohit Joshi ◽

Rashmi Sipani ◽

Asif Bakshi

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Motor Neuron ◽

Hox Genes ◽

Neural Circuitry ◽

Neuron Morphology ◽

Developing Region ◽

And Behavior ◽

Anterior Posterior

Hox genes have been known for specifying the anterior-posterior axis (AP) in bilaterian body plans. Studies in vertebrates have shown their importance in developing region-specific neural circuitry and diversifying motor neuron pools. In Drosophila, they are instrumental for segment-specific neurogenesis and myogenesis early in development. Their robust expression in differentiated neurons implied their role in assembling region-specific neuromuscular networks. In the last decade, studies in Drosophila have unequivocally established that Hox genes go beyond their conventional functions of generating cellular diversity along the AP axis of the developing central nervous system. These roles range from establishing and maintaining the neuromuscular networks to controlling their function by regulating the motor neuron morphology and neurophysiology, thereby directly impacting the behavior. Here we summarize the limited knowledge on the role of Drosophila Hox genes in the assembly of region-specific neuromuscular networks and their effect on associated behavior.

Download Full-text

Activation of central 5-HT2A receptor in brain inhibited the seizure-induced respiratory arrest in the DBA/1 mouse SUDEP model

10.1101/2020.12.04.410969 ◽

2020 ◽

Author(s):

Yue Shen ◽

HaiXiang Ma ◽

XiTing Lian ◽

LeYuan Gu ◽

Qian Yu ◽

...

Keyword(s):

Central Nervous System ◽

Drug Resistance ◽

Nervous System ◽

Underlying Mechanism ◽

Respiratory Arrest ◽

Acoustic Stimulation ◽

Unexpected Death ◽

Anti Epileptic Drug ◽

The Brain

AbstractSudden unexpected death in epilepsy (SUDEP) is the fatal cause leading to the death of epilepsy patients with anti-epileptic drug resistance. However, the underlying mechanism of SUDEP remains to be elusive. Our previous study demonstrated that enhancement of serotonin (5-HT) synthesis by intraperitoneal (IP) injection of 5-hydroxytryptophan in brain significantly reduced the incidence of seizure-induced respiratory arrest (S-IRA) in DBA/1 mice SUDEP models. Given that 5-HT2A receptor (5-HT2AR) acts an important role in mediating respiration system in brain, we hypothesized that 5-HT2AR is of great significance to modulate S-IRA and SUDEP. To test this hypothesis, we examined whether the decreased incidence S-IRA evoked by either acoustic stimulation or PTZ by blocking 5-HT2AR by administration with ketanserin (KET), a selective antagonist of 5HT2AR, in DBA/1 mice SUDEP models to test the role of 5-HT2AR modulating S-IRA. Our results suggested that the decreased incidence of S-IRA by 5-Hydroxytryptophan (5-HTP), a precursor for central nervous system (CNS) serotonin (5-HT) synthesis, was significantly reversed by IP and intracerebroventricularly (ICV) injection of ketanserin in our models. Thus, our data suggested that 5-HT2AR in the brain may be a potential and specific target to prevent SUDEP.

Download Full-text

The role of Bisphenol A in shaping the brain, epigenome and behavior

Hormones and Behavior ◽

10.1016/j.yhbeh.2010.10.001 ◽

2011 ◽

Vol 59 (3) ◽

pp. 296-305 ◽

Cited By ~ 192

Author(s):

Jennifer T. Wolstenholme ◽

Emilie F. Rissman ◽

Jessica J. Connelly

Keyword(s):

Bisphenol A ◽

And Behavior ◽

The Brain

Download Full-text

Сellular and Molecular Mechanisms of Proinflammatory Monocytes Participation in the Pathogenesis of Mental Disorders. Part 3

Psychiatry ◽

10.30629/2618-6667-2021-19-4-125-134 ◽

2021 ◽

Vol 19 (4) ◽

pp. 125-134

Author(s):

E. F. Vasilyeva ◽

O. S. Brusov

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Mental Disorders ◽

Molecular Mechanisms ◽

Microglial Cells ◽

Inflammatory Reactions ◽

Mental Diseases ◽

The Central Nervous System ◽

The Brain

Background: at present, the important role of the monocyte-macrophage link of immunity in the pathogenesis of mental diseases has been determined. In the first and second parts of our review, the cellular and molecular mechanisms of activation of monocytes/macrophages, which secreting proinflammatory CD16 receptors, cytokines, chemokines and receptors to them, in the development of systemic immune inflammation in the pathogenesis of somatic diseases and mental disorders, including schizophrenia, bipolar affective disorder (BAD) and depression were analyzed. The association of high levels of proinflammatory activity of monocytes/macrophages in patients with mental disorders with somatic comorbidity, including immune system diseases, is shown. It is known that proinflammatory monocytes of peripheral blood, as a result of violation of the integrity of the hematoencephalic barrier can migrate to the central nervous system and activate the resident brain cells — microglia, causing its activation. Activation of microglia can lead to the development of neuroinammation and neurodegenerative processes in the brain and, as a result, to cognitive disorders. The aim of review: to analyze the results of the main scientific studies concerning the role of cellular and molecular mechanisms of peripheral blood monocytes interaction with microglial cells and platelets in the development of neuroinflammation in the pathogenesis of mental disorders, including Alzheimer’s disease (AD). Material and methods: keywords “mental disorders, AD, proinflammatory monocytes, microglia, neuroinflammation, cytokines, chemokines, cell adhesion molecules, platelets, microvesicles” were used to search for articles of domestic and foreign authors published over the past 30 years in the databases PubMed, eLibrary, Science Direct and EMBASE. Conclusion: this review analyzes the results of studies which show that monocytes/macrophages and microglia have similar gene expression profiles in schizophrenia, BAD, depression, and AD and also perform similar functions: phagocytosis and inflammatory responses. Monocytes recruited to the central nervous system stimulate the increased production of proinflammatory cytokines IL-1, IL-6, tumor necrosis factor alpha (TNF-α), chemokines, for example, MCP-1 (Monocyte chemotactic protein-1) by microglial cells. This promotes the recruitment of microglial cells to the sites of neuronal damage, and also enhances the formation of the brain protein beta-amyloid (Aβ). The results of modern studies are presented, indicating that platelets are involved in systemic inflammatory reactions, where they interact with monocytes to form monocyte-platelet aggregates (MTA), which induce the activation of monocytes with a pro inflammatory phenotype. In the last decade, it has been established that activated platelets and other cells of the immune system, including monocytes, detached microvesicles (MV) from the membrane. It has been shown that MV are involved as messengers in the transport of biologically active lipids, cytokines, complement, and other molecules that can cause exacerbation of systemic inflammatory reactions. The presented review allows us to expand our knowledge about the cellular and molecular aspects of the interaction of monocytes/macrophages with microglial cells and platelets in the development of neuroinflammation and cognitive decline in the pathogenesis of mental diseases and in AD, and also helps in the search for specific biomarkers of the clinical severity of mental disorder in patients and the prospects for their response to treatment.

Download Full-text

COVID-19 Beyond the Lungs

10.4018/978-1-7998-8225-1.ch007 ◽

2022 ◽

pp. 109-126

Author(s):

Omar El Hiba ◽

Hicham Chatoui ◽

Nadia Zouhairi ◽

Lahoucine Bahi ◽

Lhoussaine Ammouta ◽

...

Keyword(s):

Experimental Data ◽

Nervous System ◽

Clinical Symptoms ◽

Case Reports ◽

The World ◽

Acute Pneumonia ◽

The Brain ◽

Cardinal Feature ◽

Shed Light

Since December 2019, the world has been shaken by the spread of a highly pathogen virus, causing severe acute respiratory syndrome (SARS-Cov2), which emerged in Wuhan, China. SARS-Cov2 is known to cause acute pneumonia: the cardinal feature of coronavirus disease 2019 (COVID-19). Clinical features of the disease include respiratory distress, loss of spontaneous breathing, and sometimes neurologic signs such as headache and nausea and anosmia, leading to suppose a possible involvement of the nervous system as a potential target of SARS-CoV2. The chapter will shed light on the recent clinical and experimental data sustaining the involvement of the nervous system in the pathophysiology of COVID-19, based on several case reports and experimental data reporting the possible transmission of SARS-CoV2 throughout the peripheral nerves to the brain cardiorespiratory centers. Thus, understanding the role of the nervous system in the course of clinical symptoms of COVID-19 is important in determining the appropriate therapeutic approach to combat the disease.

Download Full-text

Neuropsychiatry of neurometabolic, neuroendocrine, and mitochondrial disorders

Oxford Textbook of Neuropsychiatry ◽

10.1093/med/9780198757139.003.0026 ◽

2020 ◽

pp. 309-322

Author(s):

Mark Walterfang ◽

Ramon Mocellin ◽

Dennis Velakoulis

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Psychiatric Illness ◽

Mitochondrial Disorders ◽

Endocrine Function ◽

Endocrine Disorders ◽

Endocrine Tumours ◽

Neurometabolic Disorders ◽

The Brain

This chapter examines the role of neurometabolic, neuroendocrine, and mitochondrial disorders in causing neuropsychiatric syndromes. It examines how disorders of cellular metabolic processes, particularly those that affect the brain, can result in major psychiatric syndromes and the over-representation of some neurometabolic disorders in psychiatric illness. It also discusses a range of endocrine disorders, particularly disorders of increased or reduced endocrine function and endocrine tumours, in producing psychiatric syndromes. The chapter also reviews the role of mitochondrial disorders in disrupting central nervous system processes and metabolism, and how some mitochondrial disorders result in psychiatric illness.

Download Full-text

A sart1 Zebrafish Mutant Results in Developmental Defects in the Central Nervous System

Cells ◽

10.3390/cells9112340 ◽

2020 ◽

Vol 9 (11) ◽

pp. 2340

Author(s):

Hannah E. Henson ◽

Michael R. Taylor

Keyword(s):

Central Nervous System ◽

Cell Death ◽

Nervous System ◽

Developmental Defects ◽

Whole Exome ◽

The Central Nervous System ◽

And Function ◽

Upregulated Genes ◽

The Brain

The spliceosome consists of accessory proteins and small nuclear ribonucleoproteins (snRNPs) that remove introns from RNA. As splicing defects are associated with degenerative conditions, a better understanding of spliceosome formation and function is essential. We provide insight into the role of a spliceosome protein U4/U6.U5 tri-snRNP-associated protein 1, or Squamous cell carcinoma antigen recognized by T-cells (Sart1). Sart1 recruits the U4.U6/U5 tri-snRNP complex to nuclear RNA. The complex then associates with U1 and U2 snRNPs to form the spliceosome. A forward genetic screen identifying defects in choroid plexus development and whole-exome sequencing (WES) identified a point mutation in exon 12 of sart1 in Danio rerio (zebrafish). This mutation caused an up-regulation of sart1. Using RNA-Seq analysis, we identified additional upregulated genes, including those involved in apoptosis. We also observed increased activated caspase 3 in the brain and eye and down-regulation of vision-related genes. Although splicing occurs in numerous cells types, sart1 expression in zebrafish was restricted to the brain. By identifying sart1 expression in the brain and cell death within the central nervous system (CNS), we provide additional insights into the role of sart1 in specific tissues. We also characterized sart1’s involvement in cell death and vision-related pathways.

Download Full-text

Neural Control of Immunity in Hypertension: Council on Hypertension Mid Career Award for Research Excellence, 2019

Hypertension ◽

10.1161/hypertensionaha.120.14637 ◽

2020 ◽

Vol 76 (3) ◽

pp. 622-628

Author(s):

Daniela Carnevale

Keyword(s):

Immune Response ◽

Nervous System ◽

Neural Control ◽

Neural Signals ◽

The Past ◽

Target Organs ◽

Long Time ◽

The Common ◽

The Brain

The nervous system and the immune system share the common ability to exert gatekeeper roles at the interfaces between internal and external environment. Although interaction between these 2 evolutionarily highly conserved systems has been recognized for long time, the investigation into the pathophysiological mechanisms underlying their crosstalk has been tackled only in recent decades. Recent work of the past years elucidated how the autonomic nervous system controls the splenic immunity recruited by hypertensive challenges. This review will focus on the neural mechanisms regulating the immune response and the role of this neuroimmune crosstalk in hypertension. In this context, the review highlights the components of the brain-spleen axis with a focus on the neuroimmune interface established in the spleen, where neural signals shape the immune response recruited to target organs of high blood pressure.

Download Full-text