scholarly journals Dopamine-induced pruning in Monocyte-Derived-Neuronal-like cells (MDNCs) from patients with Schizophrenia

2021 ◽  
Author(s):  
Alfredo Bellon ◽  
Vincent Feuillet ◽  
Alonso Cortez-Resendiz ◽  
Faycal Mouaffak ◽  
Lan Kong ◽  
...  
Keyword(s):  
Brain Development ◽  
Early Development ◽  
Neuronal Development ◽  
Brain Volume ◽  
Late Adolescence ◽  
Consistent Finding ◽  
Developing Neurons ◽  
Number Of Individuals ◽  
Increased Susceptibility

The long lapse between the presumptive origin of schizophrenia (SCZ) during early development and its diagnosis in late adolescence has hindered the study of crucial neurodevelopmental processes directly in living patients. Dopamine, a neurotransmitter consistently associated with the pathophysiology of SCZ, participates in several aspects of brain development including pruning of neuronal extensions. Excessive pruning is considered the cause of the most consistent finding in SCZ, namely decreased brain volume. It is therefore possible that patients with SCZ carry an increased susceptibility to dopamine's pruning effects and that this susceptibility would be more obvious in the early stages of neuronal development when dopamine pruning effects appear to be more prominent. Obtaining developing neurons from living patients is not feasible. Instead, we used Monocyte-Derived-Neuronal-like Cells (MDNCs) as these cells can be generated in only 20 days and deliver reproducible results. In this study, we expanded the number of individuals in whom we tested the reproducibility of MDNCs and deepened the neurostructural comparison between human developing neurons and these neuronal-like cells. Moreover, we studied MDNCs from 12 controls and 13 patients with SCZ. Patients' cells differentiate more efficiently, extend longer secondary neurites and grow more primary neurites. In addition, MDNCs from a subset of patients expresses less D1R and prune more primary neurites when exposed to dopamine. Haloperidol did not influence our results but the role of other antipsychotics was not examined.

Ethanol neurobehavioural teratogenesis and the role of L-glutamate in the fetal hippocampus

1995 ◽  
Vol 73 (9) ◽  
pp. 1209-1223 ◽  
Author(s):  
James D. Reynolds ◽  
James F. Brien
Keyword(s):  
Fetal Alcohol Syndrome ◽  
Neuronal Development ◽  
Excitatory Amino Acid ◽  
Fetal Brain ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Fetal Alcohol ◽  
Current State ◽  
Developing Neurons

The purpose of this article is to review the current state of knowledge of ethanol neurobehavioural teratogenesis and its postulated mechanisms. The review comprises an examination of ethanol teratogenesis in the human, including the fetal alcohol syndrome, and in experimental animals. Several current proposed mechanisms of ethanol neurobehavioural teratogenesis are critically assessed, including the role of acetaldehyde as the proximate metabolite of ethanol; fetal hypoxia; placental dysfunction; fetal prostaglandin metabolism; and action of ethanol on developing neurons in the fetal brain, including the hippocampus, one of ethanol's main target sites. The effect of ethanol on the release of L-glutamate, an excitatory amino acid neurotransmitter, in the fetal hippocampus is described, and the role of L-glutamate in ethanol teratogenesis involving the hippocampus is discussed. A novel mechanism for abnormal neuronal development in the fetal hippocampus produced by prenatal ethanol exposure is presented, and future experiments to test this hypothesis are proposed.Key words: ethanol neurobehavioural teratogenesis, fetal alcohol syndrome, hippocampus, L-glutamate.

scholarly journals Gut–neuroimmune interactions: the unexpected role of the immune system in brain development

2019 ◽  
Vol 41 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Simon Spichak ◽  
Timothy G. Dinan ◽  
John F. Cryan
Keyword(s):  
Immune System ◽  
Brain Development ◽  
Neuronal Development ◽  
Inflammatory Responses ◽  
Later Life ◽  
Innate Immune ◽  
Brain Health ◽  
Cytokines And Chemokines ◽  
The Brain

How does the immune system impact brain development? The exciting and somewhat unexpected relationship between the immune system and the brain has become one of the most fascinating topics in neuroscience. Even though the immune system was initially implicated in resolving viral and bacterial threats, it is now becoming more evident that it also plays a role in processes in the brain, both under healthy and pathological conditions. This novel role of the immune system in brain health has been implicated in various psychopathologies where neurodevelopment, stress and mood are central. In particular, its role in healthy brain development is becoming more evident, and understanding neuroimmune communication is becoming crucial in treating neurodevelopmental and mood disorders in later life. In the brain, glia function as part of the innate immune system and are programmed to respond to pathogens and physical injury. They also play an important role in neuronal development and pruning. These cells communicate with and respond to chemical signals, such as cytokines and chemokines, which can then initiate or downregulate inflammatory responses. Finally, the trillions of microbes residing in the gut can also stimulate cytokine and chemokine responses in the periphery and play an important role in both immunity and brain development.

Magnesium and Hearing

2003 ◽  
Vol 14 (04) ◽  
pp. 202-212 ◽  
Author(s):  
Michael J. Cevette ◽  
Jürgen Vormann ◽  
Kay Franz
Keyword(s):  
Hair Cells ◽  
Auditory Nerve ◽  
Mg Deficiency ◽  
Noise Damage ◽  
Susceptibility To Noise ◽  
Major Progress ◽  
A Current ◽  
Putative Mechanism ◽  
Increased Susceptibility

The last several decades have revealed clinical and experimental data regarding the importance of magnesium (Mg) in hearing. Increased susceptibility to noise damage, ototoxicity, and auditory hyperexcitibility are linked to states of Mg deficiency. Evidence for these processes has come slowly and direct effects have remained elusive because plasma Mg levels do not always correlate with its deficiency. Despite the major progress in the understanding of cochlear mechanical and auditory nerve function, the neurochemical and pharmacologic role of Mg is not clear. The putative mechanism suggests that Mg deficiency may contribute to a metabolic cellular cascade of events. Mg deficiency leads to an increased permeability of the calcium channel in the hair cells with a consequent over influx of calcium, an increased release of glutamate via exocytosis, and over stimulation of NMDA receptors on the auditory nerve. This paper provides a current overview of relevant Mg metabolism and deficiency and its influence on hearing.

PO-0904: Irradiated brain volume is not related to the risk of radionecrosis: reconsidering the role of V12Gy

2020 ◽  
Vol 152 ◽  
pp. S483-S484
Author(s):  
D. Versnel ◽  
S.H. Nagtegaal ◽  
A. Claes ◽  
E. Seravalli ◽  
J.J. Verhoeff
Keyword(s):  
Brain Volume

scholarly journals Neuroplacentology in congenital heart disease: placental connections to neurodevelopmental outcomes

2021 ◽  
Author(s):  
Rachel L. Leon ◽  
Imran N. Mir ◽  
Christina L. Herrera ◽  
Kavita Sharma ◽  
Catherine Y. Spong ◽  
...  
Keyword(s):  
Brain Development ◽  
Congenital Heart ◽  
Fetal Brain ◽  
In Utero ◽  
Structure And Function ◽  
Brain Growth ◽  
Neurodevelopmental Outcomes ◽  
Fetal Brain Development ◽  
And Function

Abstract Children with congenital heart disease (CHD) are living longer due to effective medical and surgical management. However, the majority have neurodevelopmental delays or disorders. The role of the placenta in fetal brain development is unclear and is the focus of an emerging field known as neuroplacentology. In this review, we summarize neurodevelopmental outcomes in CHD and their brain imaging correlates both in utero and postnatally. We review differences in the structure and function of the placenta in pregnancies complicated by fetal CHD and introduce the concept of a placental inefficiency phenotype that occurs in severe forms of fetal CHD, characterized by a myriad of pathologies. We propose that in CHD placental dysfunction contributes to decreased fetal cerebral oxygen delivery resulting in poor brain growth, brain abnormalities, and impaired neurodevelopment. We conclude the review with key areas for future research in neuroplacentology in the fetal CHD population, including (1) differences in structure and function of the CHD placenta, (2) modifiable and nonmodifiable factors that impact the hemodynamic balance between placental and cerebral circulations, (3) interventions to improve placental function and protect brain development in utero, and (4) the role of genetic and epigenetic influences on the placenta–heart–brain connection. Impact Neuroplacentology seeks to understand placental connections to fetal brain development. In fetuses with CHD, brain growth abnormalities begin in utero. Placental microstructure as well as perfusion and function are abnormal in fetal CHD.

scholarly journals The Interaction between the Sheet/Tool Surface Texture and the Friction/Galling Behaviour on Aluminium Deep Drawing Operations

Metals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 979
Author(s):  
Alaitz Zabala ◽  
Lander Galdos ◽  
Chris Childs ◽  
Iñigo Llavori ◽  
Andrea Aginagalde ◽  
...  
Keyword(s):  
Lightweight Design ◽  
Severity Index ◽  
Tribological Behaviour ◽  
Die Surface ◽  
Tool Surface ◽  
Strip Drawing ◽  
Aluminium Sheets ◽  
Increased Susceptibility

The increasing demands for lightweight design in the transport industry have led to an extensive use of lightweight materials such as aluminium alloys. The forming of aluminium sheets however presents significant challenges due to the low formability and the increased susceptibility to galling. The use of tailored workpieces and controlled die roughness surfaces are common strategies to improve the tribological behaviour, whilst galling is still not well understood. This work is aimed at analysing the interplay between the sheet and tool surface roughness on the friction and galling performance. Different degrees of Electro Discharge Texturing (EDT) textures were generated in AA1050 material strips, and tooling presenting different polishing degrees were prepared. Strip drawing tests were carried out to model the tribological condition and results were corroborated through cup drawing tests. A new galling severity index (GSI) is presented for a quick and quantitative determination of both galling occurrence and severity. The present study underlines the key role of die topography and the potential of die surface functionalization for galling prevention.

scholarly journals Illuminating the Role of Vitamin A in Skin Innate Immunity and the Skin Microbiome: A Narrative Review

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 302
Author(s):  
Fritzlaine C. Roche ◽  
Tamia A. Harris-Tryon
Keyword(s):  
Vitamin A ◽  
Innate Immune ◽  
Narrative Review ◽  
Skin Microbiome ◽  
Skin Infections ◽  
Inflammatory Skin Disease ◽  
Skin Immunity ◽  
Impaired Immune Response ◽  
Increased Susceptibility

Vitamin A is a fat-soluble vitamin that plays an important role in skin immunity. Deficiencies in Vitamin A have been linked to impaired immune response and increased susceptibility to skin infections and inflammatory skin disease. This narrative review summarizes recent primary evidence that elucidates the role of vitamin A and its derivatives on innate immune regulators through mechanisms that promote skin immunity and sustain the skin microbiome.

scholarly journals Tcf4 Is Involved in Subset Specification of Mesodiencephalic Dopaminergic Neurons

Biomedicines ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 317
Author(s):  
Simone Mesman ◽  
Iris Wever ◽  
Marten P. Smidt
Keyword(s):  
Neuronal Differentiation ◽  
Dopaminergic Neurons ◽  
Neuronal Development ◽  
Neuronal Population ◽  
Minor Role ◽  
Initial Increase ◽  
E Box ◽  
A Minor ◽  
Bhlh Factor

During development, mesodiencephalic dopaminergic (mdDA) neurons form into different molecular subsets. Knowledge of which factors contribute to the specification of these subsets is currently insufficient. In this study, we examined the role of Tcf4, a member of the E-box protein family, in mdDA neuronal development and subset specification. We show that Tcf4 is expressed throughout development, but is no longer detected in adult midbrain. Deletion of Tcf4 results in an initial increase in TH-expressing neurons at E11.5, but this normalizes at later embryonic stages. However, the caudal subset marker Nxph3 and rostral subset marker Ahd2 are affected at E14.5, indicating that Tcf4 is involved in correct differentiation of mdDA neuronal subsets. At P0, expression of these markers partially recovers, whereas expression of Th transcript and TH protein appears to be affected in lateral parts of the mdDA neuronal population. The initial increase in TH-expressing cells and delay in subset specification could be due to the increase in expression of the bHLH factor Ascl1, known for its role in mdDA neuronal differentiation, upon loss of Tcf4. Taken together, our data identified a minor role for Tcf4 in mdDA neuronal development and subset specification.

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