Deciphering the Morphology of Motor Evoked Potentials

Deciphering the Morphology of Motor Evoked Potentials, Motor Evoked Potentials (MEPs) are used to monitor disability progression in multiple sclerosis (MS). Their morphology plays an important role in this process. Currently, however, there is no clear definition of what constitutes a normal or abnormal morphology. To address this, five experts independently labeled the morphology (normal or abnormal) of the same set of 1,000 MEPs.,

Motor Evoked Potentials (MEPs) are used to monitor disability progression in multiple sclerosis (MS). Their morphology plays an important role in this process. Currently, however, there is no clear definition of what constitutes a normal or abnormal morphology. To address this, five experts independently labeled the morphology (normal or abnormal) of the same set of 1,000 MEPs. The intra- and inter-rater agreement between the experts indicates they agree on the concept of morphology, but differ in their choice of threshold between normal and abnormal morphology. We subsequently performed an automated extraction of 5,943 time series features from the MEPs to identify a valid proxy for morphology, based on the provided labels. To do this, we compared the cross-validation performances of one-dimensional logistic regression models fitted to each of the features individually. We find that the approximate entropy (ApEn) feature can accurately reproduce the majority-vote labels. The performance of this feature is evaluated on an independent test set by comparing to the majority vote of the neurologists, obtaining an AUC score of 0.92. The model slightly outperforms the average neurologist at reproducing the neurologists consensus-vote labels. We can conclude that MEP morphology can be consistently defined by pooling the interpretations from multiple neurologists and that ApEn is a valid continuous score for this. Having an objective and reproducible MEP morphological abnormality score will allow researchers to include this feature in their models, without manual annotation becoming a bottleneck. This is crucial for large-scale, multi-center datasets. An exploratory analysis on a large single-center dataset shows that ApEn is potentially clinically useful. Introducing an automated, objective, and reproducible definition of morphology could help overcome some of the barriers that are currently obstructing broad adoption of evoked potentials in daily care and patient follow-up, such as standardization of measurements between different centers, and formulating guidelines for clinical use.

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Experimental Pipeline (Expipe): A Lightweight Data Management Platform to Simplify the Steps From Experiment...

Experimental Pipeline (Expipe): A Lightweight Data Management Platform to Simplify the Steps From Experiment..., As experimental neuroscience is moving toward more integrative approaches, with a variety of acquisition techniques covering multiple spatiotemporal scales, data management is becoming increasingly challenging for neuroscience laboratories. Often, datasets are too large to practically be stored on a laptop or a workstation.,

As experimental neuroscience is moving toward more integrative approaches, with a variety of acquisition techniques covering multiple spatiotemporal scales, data management is becoming increasingly challenging for neuroscience laboratories. Often, datasets are too large to practically be stored on a laptop or a workstation. The ability to query metadata collections without retrieving complete datasets is therefore critical to efficiently perform new analyses and explore the data. At the same time, new experimental paradigms lead to constantly changing specifications for the metadata to be stored. Despite this, there is currently a serious lack of agile software tools for data management in neuroscience laboratories. To meet this need, we have developed Expipe, a lightweight data management framework that simplifies the steps from experiment to data analysis. Expipe provides the functionality to store and organize experimental data and metadata for easy retrieval in exploration and analysis throughout the experimental pipeline. It is flexible in terms of defining the metadata to store and aims to solve the storage and retrieval challenges of data/metadata due to ever changing experimental pipelines. Due to its simplicity and lightweight design, we envision Expipe as an easy-to-use data management solution for experimental laboratories, that can improve provenance, reproducibility, and sharing of scientific projects.

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Advances in Astrocyte Computational Models: From Metabolic Reconstructions to Multi-omic Approaches

Advances in Astrocyte Computational Models: From Metabolic Reconstructions to Multi-omic Approaches, The growing importance of astrocytes in the field of neuroscience has led to a greater number of computational models devoted to the study of astrocytic functions and their metabolic interactions with neurons.,

The growing importance of astrocytes in the field of neuroscience has led to a greater number of computational models devoted to the study of astrocytic functions and their metabolic interactions with neurons. The modeling of these interactions demands a combined understanding of brain physiology and the development of computational frameworks based on genomic-scale reconstructions, system biology, and dynamic models. These computational approaches have helped to highlight the neuroprotective mechanisms triggered by astrocytes and other glial cells, both under normal conditions and during neurodegenerative processes. In the present review, we evaluate some of the most relevant models of astrocyte metabolism, including genome-scale reconstructions and astrocyte-neuron interactions developed in the last few years. Additionally, we discuss novel strategies from the multi-omics perspective and computational models of other glial cell types that will increase our knowledge in brain metabolism and its association with neurodegenerative diseases.

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A Quantitative EEG Toolbox for the MNI Neuroinformatics Ecosystem: Normative SPM of EEG Source Spectra

A Quantitative EEG Toolbox for the MNI Neuroinformatics Ecosystem: Normative SPM of EEG Source Spectra, The Tomographic Quantitative Electroencephalography (qEEGt) toolbox is integrated with the Montreal Neurological Institute (MNI) Neuroinformatics Ecosystem as a docker into the Canadian Brain Imaging Research Platform (CBRAIN). qEEGt produces age-corrected normative Statistical Parametric Maps of EEG log source spectra testing compliance to a normative database.,

The Tomographic Quantitative Electroencephalography (qEEGt) toolbox is integrated with the Montreal Neurological Institute (MNI) Neuroinformatics Ecosystem as a docker into the Canadian Brain Imaging Research Platform (CBRAIN). qEEGt produces age-corrected normative Statistical Parametric Maps of EEG log source spectra testing compliance to a normative database. This toolbox was developed at the Cuban Neuroscience Center as part of the first wave of the Cuban Human Brain Mapping Project (CHBMP) and has been validated and used in different health systems for several decades. Incorporation into the MNI ecosystem now provides CBRAIN registered users access to its full functionality and is accompanied by a public release of the source code on GitHub and Zenodo repositories. Among other features are the calculation of EEG scalp spectra, and the estimation of their source spectra using the Variable Resolution Electrical Tomography (VARETA) source imaging. Crucially, this is completed by the evaluation of z spectra by means of the built-in age regression equations obtained from the CHBMP database (ages 5–87) to provide normative Statistical Parametric Mapping of EEG log source spectra. Different scalp and source visualization tools are also provided for evaluation of individual subjects prior to further post-processing. Openly releasing this software in the CBRAIN platform will facilitate the use of standardized qEEGt methods in different research and clinical settings. An updated precis of the methods is provided in Appendix I as a reference for the toolbox. qEEGt/CBRAIN is the first installment of instruments developed by the neuroinformatic platform of the Cuba-Canada-China (CCC) project.

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Sparse Logistic Regression With L1/2 Penalty for Emotion Recognition in Electroencephalography Classification

Sparse Logistic Regression With L1/2 Penalty for Emotion Recognition in Electroencephalography Classification, Emotion recognition based on electroencephalography (EEG) signals is a current focus in brain-computer interface research. However, the classification of EEG is difficult owing to large amounts of data and high levels of noise. Therefore, it is important to determine how to effectively extract features that include important information.,

Emotion recognition based on electroencephalography (EEG) signals is a current focus in brain-computer interface research. However, the classification of EEG is difficult owing to large amounts of data and high levels of noise. Therefore, it is important to determine how to effectively extract features that include important information. Regularization, one of the effective methods for EEG signal processing, can effectively extract important features from the signal and has potential applications in EEG emotion recognition. Currently, the most popular regularization technique is Lasso (L1) and Ridge Regression (L2). In recent years, researchers have proposed many other regularization terms. In theory, Lq-type regularization has a lower q value, which means that it can be used to find solutions with better sparsity. L1/2 regularization is of Lq type (0 < q < 1) and has been shown to have many attractive properties. In this work, we studied the L1/2 penalty in sparse logistic regression for three-classification EEG emotion recognition, and used a coordinate descent algorithm and a univariate semi-threshold operator to implement L1/2 penalty logistic regression. The experimental results on simulation and real data demonstrate that our proposed method is better than other existing regularization methods. Sparse logistic regression with L1/2 penalty achieves higher classification accuracy than the conventional L1, Ridge Regression, and Elastic Net regularization methods, using fewer but more informative EEG signals. This is very important for high-dimensional small-sample EEG data and can help researchers to reduce computational complexity and improve computational accuracy. Therefore, we propose that sparse logistic regression with the L1/2 penalty is an effective technique for emotion recognition in practical classification problems.

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Location of the Cell Adhesion Molecule “Coxsackievirus and Adenovirus Receptor” in the Adult Mouse Brain

Location of the Cell Adhesion Molecule “Coxsackievirus and Adenovirus Receptor” in the Adult Mouse Brain, The coxsackievirus and adenovirus receptor (CAR) is a single-pass transmembrane cell adhesion molecule (CAM). CAR is expressed in numerous mammalian tissues including the brain, heart, lung, and testes. In epithelial cells, CAR functions are typical of the quintessential roles of numerous CAMs. However, in the brain the multiple roles of CAR are poorly understood.,

The coxsackievirus and adenovirus receptor (CAR) is a single-pass transmembrane cell adhesion molecule (CAM). CAR is expressed in numerous mammalian tissues including the brain, heart, lung, and testes. In epithelial cells, CAR functions are typical of the quintessential roles of numerous CAMs. However, in the brain the multiple roles of CAR are poorly understood. To better understand the physiological role of CAR in the adult brain, characterizing its location is a primordial step to advance our knowledge of its functions. In addition, CAR is responsible for the attachment, internalization, and retrograde transport of canine adenovirus type 2 (CAV-2) vectors, which have found a niche in the mapping of neuronal circuits and gene transfer to treat and model neurodegenerative diseases. In this study, we used immunohistochemistry and immunofluorescence to document the global location of CAR in the healthy, young adult mouse brain. Globally, we found that CAR is expressed by maturing and mature neurons in the brain parenchyma and located on the soma and on projections. While CAR occasionally colocalizes with glial fibrillary acidic protein, this overlap was restricted to areas that are associated with adult neurogenesis.

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Interactions Between the Serotonergic and Other Neurotransmitter Systems in the Basal Ganglia: Role in...

Interactions Between the Serotonergic and Other Neurotransmitter Systems in the Basal Ganglia: Role in..., Parkinson’s disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra. However, other non-dopaminergic neuronal systems such as the serotonergic system are also involved. Serotonergic dysfunction is associated with non-motor symptoms and complications, including anxiety, depression, dementia, and sleep disturbances.,

Parkinson’s disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra. However, other non-dopaminergic neuronal systems such as the serotonergic system are also involved. Serotonergic dysfunction is associated with non-motor symptoms and complications, including anxiety, depression, dementia, and sleep disturbances. This pathology reduces patient quality of life. Interaction between the serotonergic and other neurotransmitters systems such as dopamine, noradrenaline, glutamate, and GABA controls the activity of striatal neurons and are particularly interesting for understanding the pathophysiology of PD. Moreover, serotonergic dysfunction also causes motor symptoms. Interestingly, serotonergic neurons play an important role in the effects of L-DOPA in advanced PD stages. Serotonergic terminals can convert L-DOPA to dopamine, which mediates dopamine release as a “false” transmitter. The lack of any autoregulatory feedback control in serotonergic neurons to regulate L-DOPA-derived dopamine release contributes to the appearance of L-DOPA-induced dyskinesia (LID). This mechanism may also be involved in the development of graft-induced dyskinesias (GID), possibly due to the inclusion of serotonin neurons in the grafted tissue. Consistent with this, the administration of serotonergic agonists suppressed LID. In this review article, we summarize the interactions between the serotonergic and other systems. We also discuss the role of the serotonergic system in LID and if therapeutic approaches specifically targeting this system may constitute an effective strategy in PD.

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Gestational Exposure to Sodium Valproate Disrupts Fasciculation of the Mesotelencephalic Dopaminergic Tract,...

Gestational Exposure to Sodium Valproate Disrupts Fasciculation of the Mesotelencephalic Dopaminergic Tract,..., Gestational exposure to valproic acid (VPA) is known to cause behavioral deficits of sociability, matching similar alterations in human autism spectrum disorder (ASD). Available data are scarce on the neuromorphological changes in VPA-exposed animals. Here, we focused on alterations of the dopaminergic system, which is implicated in motivation and reward, with relevance to social cohesion.,

Gestational exposure to valproic acid (VPA) is known to cause behavioral deficits of sociability, matching similar alterations in human autism spectrum disorder (ASD). Available data are scarce on the neuromorphological changes in VPA-exposed animals. Here, we focused on alterations of the dopaminergic system, which is implicated in motivation and reward, with relevance to social cohesion. Whole brains from 7-day-old mice born to mothers given a single injection of VPA (400 mg/kg b.wt.) on E13.5 were immunostained against tyrosine hydroxylase (TH). They were scanned using the iDISCO method with a laser light-sheet microscope, and the reconstructed images were analyzed in 3D for quantitative morphometry. A marked reduction of mesotelencephalic (MT) axonal fascicles together with a widening of the MT tract were observed in VPA treated mice, while other major brain tracts appeared anatomically intact. We also found a reduction in the abundance of dopaminergic ventral tegmental (VTA) neurons, accompanied by diminished tissue level of DA in ventrobasal telencephalic regions (including the nucleus accumbens (NAc), olfactory tubercle, BST, substantia innominata). Such a reduction of DA was not observed in the non-limbic caudate-putamen. Conversely, the abundance of TH+ cells in the substantia nigra (SN) was increased, presumably due to a compensatory mechanism or to an altered distribution of TH+ neurons occupying the SN and the VTA. The findings suggest that defasciculation of the MT tract and neuronal loss in VTA, followed by diminished dopaminergic input to the ventrobasal telencephalon at a critical time point of embryonic development (E13-E14) may hinder the patterning of certain brain centers underlying decision making and sociability.

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Differential Susceptibility and Vulnerability of Brain Cells in C57BL/6 Mouse to Mitochondrial Dysfunction...

Differential Susceptibility and Vulnerability of Brain Cells in C57BL/6 Mouse to Mitochondrial Dysfunction..., Cuprizone (CPZ) is a chemical chelator toxic to mitochondria of cells. While inducing oligodendrocyte (OL) loss and demyelination, CPZ caused no fatal damage to the other brain cells (neurons, astrocytes, and microglia) in previous studies, suggesting differential susceptibility and vulnerability of brain cells to the CPZ intoxication.,

Cuprizone (CPZ) is a chemical chelator toxic to mitochondria of cells. While inducing oligodendrocyte (OL) loss and demyelination, CPZ caused no fatal damage to the other brain cells (neurons, astrocytes, and microglia) in previous studies, suggesting differential susceptibility and vulnerability of brain cells to the CPZ intoxication. To demonstrate this interpretation, C57BL/6 mice were fed rodent chow without or with CPZ (0.2%, w/w) for 7 days. One day later, mitochondrial function of brain cells was assessed by proton magnetic resonance spectroscopy (1H-MRS) and biochemical analysis. Another batch of mice were processed to localize the CPZ-induced damage to mitochondrial DNA, label brain cells, and identify apoptotic cells. Compared to controls, CPZ-exposed mice showed significantly lower levels of N-acetyl-L-aspartate, phosphocreatine, and ATP detected by 1H-MRS, indicating mitochondrial dysfunction in brain cells. Susceptibility analysis showed an order of OLs, microglia, and astrocytes from high to low, in terms of the proportion of 8-OHdG labeled cells in each type of these cells in corpus callosum. Vulnerability analysis showed the highest proportion of caspase-3 positive cells in labeled OLs in cerebral cortex and hippocampus, where neurons showed no caspase-3 labeling, but the highest proportion of 8-OHdG labeling, indicating a lowest vulnerability but highest susceptibility to CPZ-induced mitochondrial dysfunction. Immature OLs, microglia, and astrocytes showed adaptive changes in proliferation and activation in response to CPZ-exposure. These data for the first time demonstrated the CPZ-induced mitochondria dysfunction in brain cells of living mouse and specified the differential susceptibility and vulnerability of brain cells to the CPZ intoxication.

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Neurexin and Neuroligins Maintain the Balance of Ghost and Satellite Boutons at the Drosophila Neuromuscular...

Neurexin and Neuroligins Maintain the Balance of Ghost and Satellite Boutons at the Drosophila Neuromuscular..., Neurexins and neuroligins are common synaptic adhesion molecules that are associated with autism and interact with each other in the synaptic cleft. The Drosophila neuromuscular junction (NMJ) bouton is a well-known model system in neuroscience, and ghost and satellite boutons, respectively, indicate the poor development and overgrowth of the NMJ boutons.,

Neurexins and neuroligins are common synaptic adhesion molecules that are associated with autism and interact with each other in the synaptic cleft. The Drosophila neuromuscular junction (NMJ) bouton is a well-known model system in neuroscience, and ghost and satellite boutons, respectively, indicate the poor development and overgrowth of the NMJ boutons. However, the Drosophila neurexin (DNrx) and Drosophila neuroligins (DNlgs) are mainly observed in type Ib boutons, indicating the ultrastructural and developmental phenotypes of the Drosophila NMJ. Here, we identified the ultrastructural and developmental features of ghost and satellite boutons by utilizing dneurexin (dnrx) and dneuroligins (dnlgs) fly mutants and other associated fly strains. Ghost boutons contain synaptic vesicles with multiple diameters but very rarely contain T-bar structures and swollen or thin subsynaptic reticulum (SSR) membranes. The muscle cell membrane is invaginated at different sites, stretches to the ghost bouton from different directions, forms several layers that enwrap the ghost bouton, and then branches into the complex SSR. Satellite boutons share a common SSR membrane and present either a typical profile in which a main bouton is encircled by small boutons or two atypical profiles in which the small boutons are grouped together or distributed in beads without a main bouton. Electron and confocal microscopy data showed that dnrx, dnlg1, dnlg2, dnlg3, and dnlg4 mutations led to ghost boutons; the overexpression of dnrx, dnlg1, dnlg2, dnlg3, and dnlg4 led to satellite boutons; and the dnlg2;dnlg3 double mutation also led to satellite boutons. These results suggested that DNrx and DNlgs jointly maintain the development and function of NMJ boutons by regulating the balance of ghost and satellite boutons in Drosophila.

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Epilepsy and Neuroscience: Evolution and Interaction

Epilepsy and Neuroscience: Evolution and Interaction, Neuroscience is a relatively new and fashionable word that emerged in the 1950s in several countries, including the UK, to describe a multidisciplinary clinical and laboratory approach to the study of the brain, mind, and neuropsychiatric disorders. However collaborative study of neurological and psychiatric disorders can be traced to the 17th century with roots in antiquity.,

Neuroscience is a relatively new and fashionable word that emerged in the 1950s in several countries, including the UK, to describe a multidisciplinary clinical and laboratory approach to the study of the brain, mind, and neuropsychiatric disorders. However collaborative study of neurological and psychiatric disorders can be traced to the 17th century with roots in antiquity. I describe the evolution of our understanding of epilepsy beginning with the first detailed clinical descriptions, associated with supernatural theories, in Babylonian medicine in the second millennium BC. Interest in natural causation arose in the Greco-Roman period when it was first suggested that “the sacred disease” was a disorder of the brain. However, this theory did not take root until the 17th and 18th centuries AD when epilepsy began to be separated from other “convulsive” diseases, including hysteria. In the 19th century developments in neuropathology and our understanding of cortical localization led to the much-debated separation of idiopathic from symptomatic epilepsy which continues to influence international classifications of seizures and epilepsies. Also in the 19th century, the concept of seizures as electrical discharges in the brain evolved, reinforced in the 20th century by the discovery of the electroencephalogram. For many reasons, people with epilepsy have experienced a high incidence of cognitive and psychosocial disorders. Epilepsy, which is a global problem, has, therefore, remained a bridge between neurology and psychiatry. Furthermore, the study of epilepsy continues to shed light on brain function and other neuropsychiatric disorders.

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Neuromechanisms of SARS-CoV-2: A Review

Neuromechanisms of SARS-CoV-2: A Review, Recent studies have suggested the neuroinvasive potential of severe acute respiratory coronavirus 2 (SARS-CoV-2). Notably, neuroinvasiveness might be involved in the pathophysiology of coronavirus disease 2019 (COVID-19). Some studies have demonstrated that synapse-connected routes may enable coronaviruses to access the central nervous system (CNS).,

Recent studies have suggested the neuroinvasive potential of severe acute respiratory coronavirus 2 (SARS-CoV-2). Notably, neuroinvasiveness might be involved in the pathophysiology of coronavirus disease 2019 (COVID-19). Some studies have demonstrated that synapse-connected routes may enable coronaviruses to access the central nervous system (CNS). However, evidence related to the presence of SARS-CoV-2 in the CNS, its direct impact on the CNS, and the contribution to symptoms suffered, remain sparse. Here, we review the current literature that indicates that SARS-CoV-2 can invade the nervous system. We also describe the neural circuits that are potentially affected by the virus and their possible role in the progress of COVID-19. In addition, we propose several strategies to understand, diagnose, and treat the neurological symptoms of COVID-19.

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Evidence for Reciprocal Structural Network Interactions Between Bilateral Crus Lobes and Broca’s Complex

Evidence for Reciprocal Structural Network Interactions Between Bilateral Crus Lobes and Broca’s Complex, While the proximal dentatothalamocortical tracts are considered pivotal in the occurrence of cerebellar mutism syndrome (CMS) after medulloblastoma resection, how the cerebellum participates in motor–speech networks through direct structural connectivity is still unclear.,

While the proximal dentatothalamocortical tracts are considered pivotal in the occurrence of cerebellar mutism syndrome (CMS) after medulloblastoma resection, how the cerebellum participates in motor–speech networks through direct structural connectivity is still unclear. Via tractography, we provide evidence of cerebellar streamlines projecting into the left inferior frontal gyrus majorly connecting Broca’s complex and the bilateral Crus lobes. The streamlines, named Crus–Broca tracts, originated from the bilateral Crus lobes, synapsed onto the dentate nucleus, ascended into the superior cerebellar peduncle (where these streamlines were closely superior to the superior border of the supratonsillar cleft and the superolateral roof of the fourth ventricle), surprisingly bypassed the left red nucleus and the left thalamus, and ended at the subregions of Broca’s complex. The streamlines, named Broca–Crus tracts, originated from the subregions of Broca’s complex and ended predominantly at the right Crus lobes. If verified, the existence of these connections would support the notion of the bilateral cerebellums’ participation in motor–speech planning, and the anatomical relationship of Broca–Crus tracts with the supratonsillar cleft would merit consideration for further studies aimed at further elucidating CMS mechanisms.

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Transient Hypothyroidism During Lactation Alters the Development of the Corpus Callosum in Rats. An in vivo...

Transient Hypothyroidism During Lactation Alters the Development of the Corpus Callosum in Rats. An in vivo..., Magnetic resonance imaging (MRI) data of children with late diagnosed congenital hypothyroidism and cognitive alterations such as abnormal verbal memory processing suggest altered telencephalic commissural connections. The corpus callosum (CC) is the major inter-hemispheric commissure that contra-laterally connects neocortical areas.,

Magnetic resonance imaging (MRI) data of children with late diagnosed congenital hypothyroidism and cognitive alterations such as abnormal verbal memory processing suggest altered telencephalic commissural connections. The corpus callosum (CC) is the major inter-hemispheric commissure that contra-laterally connects neocortical areas. However, in late diagnosed neonates with congenital hypothyroidism, the possible effect of early transient and chronic postnatal hypothyroidism still remains unknown. We have studied the development of the anterior, middle and posterior CC, using in vivo MRI and electron microscopy in hypothyroid and control male rats. Four groups of methimazole (MMI) treated rats were studied. One group, as a model for early transient hypothyroidism, was MMI-treated from postnatal day (P) 0 to P21; some of these rats were also treated with L-thyroxine (T4) from P15 to 21. Another group modeling chronic hypothyroid, were treated with MMI from P0 to 150 and from embryonic day 10 to P170. The results obtained from these groups were compared with same age control rats. The normalized T2 signal obtained using MRI was higher in MMI-treated rats and correlated with a low number and percentage of myelinated axons. The number and density of myelinated axons decreased in transient and chronic hypothyroid rats at P150. The g-ratio (inner to outer diameter ratio) and the estimated conduction velocity of myelinated axons were similar between MMI-treated and controls, but the conduction delay decreased in the posterior CC of MMI-treated rats compared to controls. These data show that early postnatal transient and chronic hypothyroidism alters CC maturation in a way that may affect the callosal transfer of information. These alterations cannot be reversed after delayed T4-treatment. Our data support the findings of neurocognitive delay in late T4-treated children with congenital hypothyroidism.

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Distribution of Molecules Related to Neurotransmission in the Nervous System of the Mussel Crenomytilus...

Distribution of Molecules Related to Neurotransmission in the Nervous System of the Mussel Crenomytilus..., In bivalves neurotransmitters are involved in a variety of behaviors, but their diversity and distribution in the nervous system of these organisms remains somewhat unclear.,

In bivalves neurotransmitters are involved in a variety of behaviors, but their diversity and distribution in the nervous system of these organisms remains somewhat unclear. Here, we first examined immunohistochemically the distributions of neurons containing different neurotransmitters, neuropeptides, and related enzymes, as well as the proliferative status of neurons in the ganglia of the mussel Crenomytilus grayanus. H-Phe-Met-Arg-Phe-NH2 (FMRFamide), choline acetyltransferase (ChAT), γ-aminobutyric acid (GABA) and tyrosine hydroxylase (TH) were found to be expressed by neurons in all the ganglia, whereas serotonin (5-HT) neurons were found only in the cerebropleural and pedal, but not visceral ganglia. Moreover, incubation of living mussels in the presence of a 5-HT precursor (5-HTP) confirmed the absence of 5-HT-containing neurons from the visceral ganglia, indicating that the “serotonin center” of the visceral nervous system is located in the cerebral ganglia. Furthermore, immunostaining of molecules related to neurotransmission together with α-acetylated tubulin demonstrated that this cytoskeletal protein may be a potential pan-neuronal marker in bivalves. Adult mussel neurons do not proliferate, but a population of proliferating PCNA-LIP cells which do not express any of the neurotransmitters examined, perhaps glia cells, was detected in the ganglia. These novel findings suggest that the nervous system of bivalves contains a broad variety of signal molecules most likely involved in the regulation of different physiological and behavioral processes. In addition, proliferating cells may maintain and renew glial cells and neurons throughout the lives of bivalves.

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