The Brain of an Outstanding Scientist-Inventor: Structural Organization of Area 10 of the Frontal Cortex

2021 ◽  
Author(s):  
I. N. Bogolepova ◽  
L. I. Malofeeva ◽  
P. A. Agapov
Keyword(s):  
Frontal Cortex ◽  
Structural Organization ◽  
Outstanding Scientist ◽  
The Brain

Neural Mechanisms of Negative Symptoms

1989 ◽  
Vol 155 (S7) ◽  
pp. 93-98 ◽  
Author(s):  
Nancy C. Andreasen
Keyword(s):  
Frontal Cortex ◽  
Negative Symptoms ◽  
Neural Mechanism ◽  
Brain Regions ◽  
Brain Dysfunction ◽  
Neural Mechanisms ◽  
Dementia Praecox ◽  
Intellectual Abilities ◽  
The Brain ◽  
Psychic Mechanisms

When Kraepelin originally defined and described dementia praecox, he assumed that it was due to some type of neural mechanism. He hypothesised that abnormalities could occur in a variety of brain regions, including the prefrontal, auditory, and language regions of the cortex. Many members of his department, including Alzheimer and Nissl, were actively involved in the search for the neuropathological lesions that would characterise schizophrenia. Although Kraepelin did not use the term ‘negative symptoms', he describes them comprehensively and states explicitly that he believes the symptoms of schizophrenia can be explained in terms of brain dysfunction:“If it should be confirmed that the disease attacks by preference the frontal areas of the brain, the central convolutions and central lobes, this distribution would in a certain measure agree with our present views about the site of the psychic mechanisms which are principally injured by the disease. On various grounds, it is easy to believe that the frontal cortex, which is specially well developed in man, stands in closer relation to his higher intellectual abilities, and these are the faculties which in our patients invariably suffer profound loss in contrast to memory and acquired ability.” Kraepelin (1919, p. 219)

the Comparred Effect of Zyprasidone and Haloperidol at Hippocampal and Frontal Cortex at Rats

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
D. Marinescu ◽  
L. Mogoanta ◽  
T. Udristoiu
Keyword(s):  
Adverse Event ◽  
Frontal Cortex ◽  
Negative Symptoms ◽  
Structural Changes ◽  
Saline Solution ◽  
Neuroprotective Effect ◽  
Neuronal Loss ◽  
D2 Receptors ◽  
Cerebral Structure ◽  
The Brain

Background:The alteration of hippocampal and prefrontal structures is linked with schizophrenia cognitive impairment and negative symptoms. the antipsychotics can induced apoptotic mechanisms correlated with the psychopharmacological mechanism of excesive blocking of the D2 receptors. Distress determined increase of the glucocorticoid aggression wich drive to the decrease of neuroprotective capacity at the brain level.Methods:We formed 5 study lots (5 adults rats) and a control lot. the substancies were administrated intraperitoneal, daily, saline solution equivalent to: ziprasidone (1.25mg/kg/day) and haloperidole (0.20mg/kg/day), dexametasone (0.20mg/kg/day):N1 - Haloperidole; N2 - Dexametasone; N3 - Ziprasidone; N4 - Dexametasone and Haloperidole; N5 - Dexametasone and Ziprasidone; N6 -control lot.We monitorised the cardiovascular function, respiration and EPS, without signaling any serious deadly adverse event. the rats were sacrificed during the 10th day and 21th day.Results:Frontal cortex and hippocamp were the most intensely affected even since the 10-th day to the N4 (haloperidole and dexametasone) lot with massive neuronal loss at the VI, V, and IV frontal cerebral layers.The lots treated with ziprasidone presented significant lesser structural changes in frontal cortex and hippocamp, comparative to haloperidole. the lots treated with dexametasone and ziprasidone (N5) are lesser affected at the cerebral structure level.Conclusions:Haloperidole has a significant decrease in neuroprotection. Ziprasidone demonstrated an neuroprotective effect.

scholarly journals Human brain harbors single nucleotide somatic variations in functionally relevant genes possibly mediated by oxidative stress

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2520 ◽  
Author(s):  
Anchal Sharma ◽  
Asgar Hussain Ansari ◽  
Renu Kumari ◽  
Rajesh Pandey ◽  
Rakhshinda Rehman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Corpus Callosum ◽  
Human Brain ◽  
Frontal Cortex ◽  
Oxidative Stress Marker ◽  
Somatic Variation ◽  
Single Nucleotide ◽  
Normal Human Brain ◽  
Normal Human ◽  
The Brain

Somatic variation in DNA can cause cells to deviate from the preordained genomic path in both disease and healthy conditions. Here, using exome sequencing of paired tissue samples, we show that the normal human brain harbors somatic single base variations measuring up to 0.48% of the total variations. Interestingly, about 64% of these somatic variations in the brain are expected to lead to non-synonymous changes, and as much as 87% of these represent G:C>T:A transversion events. Further, the transversion events in the brain were mostly found in the frontal cortex, whereas the corpus callosum from the same individuals harbors the reference genotype. We found a significantly higher amount of 8-OHdG (oxidative stress marker) in the frontal cortex compared to the corpus callosum of the same subjects (p<0.01), correlating with the higher G:C>T:A transversions in the cortex. We found significant enrichment for axon guidance and related pathways for genes harbouring somatic variations. This could represent either a directed selection of genetic variations in these pathways or increased susceptibility of some loci towards oxidative stress. This study highlights that oxidative stress possibly influence single nucleotide somatic variations in normal human brain.

scholarly journals Evaluation of Genotype-Based Gene Expression Model Performance: A Cross-Framework and Cross-Dataset Study

Genes ◽  
2021 ◽  
Vol 12 (10) ◽  
pp. 1531
Author(s):  
Vânia Tavares ◽  
Joana Monteiro ◽  
Evangelos Vassos ◽  
Jonathan Coleman ◽  
Diana Prata
Keyword(s):  
Gene Expression ◽  
Frontal Cortex ◽  
Model Performance ◽  
Variation Method ◽  
Expression Model ◽  
The Brain ◽  
Gene Expression Model ◽  
And Training ◽  
Predict Gene Expression ◽  
Fold Cross Validation

Predicting gene expression from genotyped data is valuable for studying inaccessible tissues such as the brain. Herein we present eGenScore, a polygenic/poly-variation method, and compare it with PrediXcan, a method based on regularized linear regression using elastic nets. While both methods have the same purpose of predicting gene expression based on genotype, they carry important methodological differences. We compared the performance of expression quantitative trait loci (eQTL) models to predict gene expression in the frontal cortex, comparing across these frameworks (eGenScore vs. PrediXcan) and training datasets (BrainEAC, which is brain-specific, vs. GTEx, which has data across multiple tissues). In addition to internal five-fold cross-validation, we externally validated the gene expression models using the CommonMind Consortium database. Our results showed that (1) PrediXcan outperforms eGenScore regardless of the training database used; and (2) when using PrediXcan, the performance of the eQTL models in frontal cortex is higher when trained with GTEx than with BrainEAC.

Decoding the sense of smell: understanding the structural organization within the brain

2020 ◽  
Vol 2 (7) ◽  
pp. 4-9
Author(s):  
Shripriya Singh
Keyword(s):  
Neural Activity ◽  
Structural Organization ◽  
Piriform Cortex ◽  
Molecular Structures ◽  
The Other ◽  
Multiphoton Imaging ◽  
Sensory Inputs ◽  
Correlated Patterns ◽  
Olfactory Sense ◽  
The Brain

The olfactory sense is a potent sensory tool which helps us perceive our environment much better. However, smells despite being similar have different impacts on individuals. What makes one odor categorically different from the other and why do people have a unique and personalized experience with smell is an answer that needs to be addressed. In the present article we have discussed the research in which neuroscientists have decoded and described how the relationships between different odors are encoded in the brain. How the brain transforms information about odor chemistry into the perception of smell is a major highlight of this publication. Carefully selected odors with defined molecular structures were delivered in mice and the neural activity was analyzed. It was observed that neuronal representations of smell in the cortex reflected chemical similarities between odors, thus allowing the brain to categorize scents. The study has employed chemo informatics and multiphoton imaging in the mouse to demonstrate both the piriform cortex and its sensory inputs from the olfactory bulb represent chemical odor relationships through correlated patterns of activity. The research has given us cues in the direction of how the brain translates odor chemistry into neurochemistry and eventually perception of smell.

Cerebral metabolic and histological effects of thioacetamide-induced liver failure

1993 ◽  
Vol 265 (3) ◽  
pp. G572-G578 ◽  
Author(s):  
J. Peeling ◽  
L. Shoemaker ◽  
T. Gauthier ◽  
A. Benarroch ◽  
G. R. Sutherland ◽  
...  
Keyword(s):  
Liver Failure ◽  
Frontal Cortex ◽  
Clinical Symptoms ◽  
Neuronal Injury ◽  
Acute Hepatic Failure ◽  
Occipital Cortex ◽  
Resonance Spectroscopy ◽  
Histopathological Analysis ◽  
Gamma Aminobutyric Acid ◽  
The Brain

Acute liver failure was induced in rats by successive administrations of thioacetamide over 3 days. At progressing stages of hepatic encephalopathy (HE), brains were fixed with microwave irradiation for analysis of metabolite levels or with formaldehyde for histopathological analysis. Metabolite levels were determined using 1H-nuclear magnetic resonance spectroscopy of perchloric acid extracts of the frontal cortex, parietal or occipital cortex, hippocampus, striatum, brain stem, and cerebellum. After thioacetamide treatment, thioacetamide and its metabolites were detected in the brains at levels that did not correlate with the stage of HE. No changes were observed in the levels of N-acetylaspartate, alanine, gamma-aminobutyric acid, aspartate, or inositol in any brain region after thioacetamide treatment. HE was accompanied by elevated glutamine, glucose, and lactate throughout the brain. At all stages of HE, taurine was decreased in the neocortex and hippocampus, and glutamate and choline compounds were decreased in the frontal cortex. None of the metabolite changes showed progression with the stage of HE. Progressing HE was accompanied by increasing neuronal injury in layer III of the neocortex, in the Purkinje cells of the cerebellum, and in the hippocampus, particularly in the CA4 sector. The similarity of this distribution of injury to that associated with excitotoxic injury suggests that metabolic abnormalities after acute hepatic failure may give rise to adverse effects at excitatory (glutamatergic) neuronal receptors, leading to neuronal injury and clinical symptoms of progressing encephalopathy in this model. However, neuronal injury and the presence of thioacetamide and its metabolites in the brain raise questions about the validity of thioacetamide-induced liver failure as a model for clinical HE.

scholarly journals Kynurenic Acid Metabolism in Various Types of Brain Pathology in HIV-1 Infected Patients

2012 ◽  
Vol 5 ◽  
pp. IJTR.S10627 ◽  
Author(s):  
H. Baran ◽  
J.A. Hainfellner ◽  
B. Kepplinger
Keyword(s):  
Frontal Cortex ◽  
Kynurenic Acid ◽  
Acid Metabolism ◽  
Excitatory Amino Acid ◽  
High Ratio ◽  
Competitive Antagonist ◽  
Kynurenine Aminotransferase ◽  
Cognition Impairment ◽  
The Brain ◽  
Hiv 1

Kynurenic acid, an intermediate metabolite of L-kynurenine, is a competitive antagonist of inotropic excitatory amino acid (EAA) receptors as well as a non competitive antagonist of 7 alpha nicotine cholinergic receptors and its involvement in memory deficit and cognition impairment has been suggested. Alterations of kynurenic acid metabolism in the brain after HIV-1 (human immunodeficiency virus type-1) infection have been demonstrated. The present study evaluates the biosynthetic machinery of kynurenic acid e.g. the content of L-kynurenine and kynurenic acid, as well as the activity of enzymes synthesizing kynurenic acid, kynurenine aminotransferase I (KAT I) and kynurenine aminotransferase II (KAT II) in the frontal cortex and cerebellum of HIV-1 infected patients in relation to different types of pathology classified as follows: HIV in brain (HIV); opportunistic infection (OPP); infarction of brain (INF); malignant lymphoma of brain (LY); and glial dystrophy (GD) and of control (CO) subjects. Of all investigated pathologies the most frequent was OPP (65%), followed by HIV (26%), LY, INF, and GD (each 22%, respectively). Further, 68% of HIV-1 patients had bronchopneumonia, the highest incidence of which, at 60%, was seen in the OPP and LY group. Kynurenic acid was increased significantly in the frontal cortex of LY (392% of CO, P < 0.001), HIV (231% of CO, P < 0.01) and GD (193% of CO, P < 0.05), as well as in the cerebellum of GD (261% of CO, P < 0.01). A significant increase of L-kynurenine was observed in the frontal cortex of LY (385% of CO, P < 0.001) and INF (206% of CO, P < 0.01), and in the cerebellum of GD, LY, OPP and HIV (between 177% and 147% of CO). The KAT I activity increased significantly in the frontal cortex of all pathological subgroups, ie OPP = 420% > INF > LY > HIV > GD = 192% of CO. In the cerebellum, too, all pathological subgroups showed marked increase of KAT I activity (OPP = 320% > LY, HIV > GD > INF = 176% of CO). On contrary, the activity of KAT II was moderately, but significantly, higher in the frontal cortex of INF and OPP; in the cerebellum of HIV, OPP and LY it was comparable to the control, while mildly reduced in INF and GD. Interestingly, normal subjects with the diagnosis of bronchopneumonia were characterized by high kynurenic acid metabolism in the brain, too. Correlation analyses between kynurenine parameters revealed association between high ratio KAT I/KAT II and increased kynurenic acid level and lower L-kynurenine in the frontal cortex and cerebellum of HIV and LY subgroups. The present study revealed a different pattern of alteration of kynurenic acid metabolism in frontal cortex and cerebellum among investigated pathological subgroups of HIV-1 infected patients. Interestingly, a marked enhancement of kynurenic acid metabolism in the brain has been found with occurrence of bronchopneumonia. This finding indicates a notable association between impaired conditions of oxygen availability and enhancement of kynurenic acid formation in the human brain. These observation(s) might have an impact on the understanding of pathological processes in the brain after HIV-1 infection involving the development of neuropsychiatric and neurological symptoms, including memory and cognition impairment.

scholarly journals What the Brain Stem Tells the Frontal Cortex. I. Oculomotor Signals Sent From Superior Colliculus to Frontal Eye Field Via Mediodorsal Thalamus

2004 ◽  
Vol 91 (3) ◽  
pp. 1381-1402 ◽  
Author(s):  
Marc A. Sommer ◽  
Robert H. Wurtz
Keyword(s):  
Superior Colliculus ◽  
Frontal Cortex ◽  
Brain Stem ◽  
Signal Transmission ◽  
Frontal Eye Field ◽  
Visual Responses ◽  
Mediodorsal Thalamus ◽  
Visual Activity ◽  
Eye Field ◽  
The Brain

Neuronal processing in cerebral cortex and signal transmission from cortex to brain stem have been studied extensively, but little is known about the numerous feedback pathways that ascend from brain stem to cortex. In this study, we characterized the signals conveyed through an ascending pathway coursing from the superior colliculus (SC) to the frontal eye field (FEF) via mediodorsal thalamus (MD). Using antidromic and orthodromic stimulation, we identified SC source neurons, MD relay neurons, and FEF recipient neurons of the pathway in Macaca mulatta. The monkeys performed oculomotor tasks, including delayed-saccade tasks, that permitted analysis of signals such as visual activity, delay activity, and presaccadic activity. We found that the SC sends all of these signals into the pathway with no output selectivity, i.e., the signals leaving the SC resembled those found generally within the SC. Visual activity arrived in FEF too late to contribute to short-latency visual responses there, and delay activity was largely filtered out in MD. Presaccadic activity, however, seemed critical because it traveled essentially unchanged from SC to FEF. Signal transmission in the pathway was fast (∼2 ms from SC to FEF) and topographically organized (SC neurons drove MD and FEF neurons having similarly eccentric visual and movement fields). Our analysis of identified neurons in one pathway from brain stem to frontal cortex thus demonstrates that multiple signals are sent from SC to FEF with presaccadic activity being prominent. We hypothesize that a major signal conveyed by the pathway is corollary discharge information about the vector of impending saccades.

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