Coding of Stimulus Frequency by Latency in Thalamic Networks Through the Interplay of GABAB-Mediated Feedback and Stimulus Shape

2006 ◽  
Vol 95 (3) ◽  
pp. 1735-1750 ◽  
Author(s):  
David Golomb ◽  
Ehud Ahissar ◽  
David Kleinfeld
Keyword(s):  
Brain Stem ◽  
Sensory Input ◽  
Feedback Inhibition ◽  
Stimulus Frequency ◽  
Period Doubling ◽  
Spike Rate ◽  
Temporal Coding ◽  
Normal Brain ◽  
Normal Brain Function ◽  
Sensory Code

A temporal sensory code occurs in posterior medial (POm) thalamus of the rat vibrissa system, where the latency for the spike rate to peak is observed to increase with increasing frequency of stimulation between 2 and 11 Hz. In contrast, the latency of the spike rate in the ventroposterior medial (VPm) thalamus is constant in this frequency range. We consider the hypothesis that two factors are essential for latency coding in the POm. The first is GABAB-mediated feedback inhibition from the reticular thalamic (Rt) nucleus, which provides delayed and prolonged input to thalamic structures. The second is sensory input that leads to an accelerating spike rate in brain stem nuclei. Essential aspects of the experimental observations are replicated by the analytical solution of a rate-based model with a minimal architecture that includes only the POm and Rt nuclei, i.e., an increase in stimulus frequency will increase the level of inhibitory output from Rt thalamus and lead to a longer latency in the activation of POm thalamus. This architecture, however, admits period-doubling at high levels of GABAB-mediated conductance. A full architecture that incorporates the VPm nucleus suppresses period-doubling. A clear match between the experimentally measured spike rates and the numerically calculated rates for the full model occurs when VPm thalamus receives stronger brain stem input and weaker GABAB-mediated inhibition than POm thalamus. Our analysis leads to the prediction that the latency code will disappear if GABAB-mediated transmission is blocked in POm thalamus or if the onset of sensory input is too abrupt. We suggest that GABAB-mediated inhibition is a substrate of temporal coding in normal brain function.

Cancer stem cells obtained from normal brain stem cells

2007 ◽  
Vol 34 (S 2) ◽  
Author(s):  
FA Siebzehnrubl ◽  
I Jeske ◽  
D Müller ◽  
M Hildebrandt ◽  
E Hahnen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Brain Stem ◽  
Normal Brain

A Survey on Detection and Classification of Brain Tumor Using Image Processing Techniques

2020 ◽  
pp. 967-973
Author(s):  
V. Deepika ◽  
T. Rajasenbagam
Keyword(s):  
Image Processing ◽  
Brain Tumor ◽  
Soft Tissues ◽  
Tumor Detection ◽  
Tumor Classification ◽  
Normal Brain ◽  
Image Processing Techniques ◽  
Normal Brain Function ◽  
Processing Techniques ◽  
The Brain

A brain tumor is an uncontrolled growth of abnormal brain tissue that can interfere with normal brain function. Although various methods have been developed for brain tumor classification, tumor detection and multiclass classification remain challenging due to the complex characteristics of the brain tumor. Brain tumor detection and classification are one of the most challenging and time-consuming tasks in the processing of medical images. MRI (Magnetic Resonance Imaging) is a visual imaging technique, which provides a information about the soft tissues of the human body, which helps identify the brain tumor. Proper diagnosis can prevent a patient's health to some extent. This paper presents a review of various detection and classification methods for brain tumor classification using image processing techniques.

The role of GABAA receptor biogenesis, structure and function in epilepsy

2006 ◽  
Vol 34 (5) ◽  
pp. 863-867 ◽  
Author(s):  
S. Mizielinska ◽  
S. Greenwood ◽  
C.N. Connolly
Keyword(s):  
Gabaa Receptor ◽  
Structure And Function ◽  
Inhibitory Synapses ◽  
Normal Brain ◽  
Synaptic Targeting ◽  
Acid Type ◽  
Normal Brain Function ◽  
And Function ◽  
The Brain

Maintaining the correct balance in neuronal activation is of paramount importance to normal brain function. Imbalances due to changes in excitation or inhibition can lead to a variety of disorders ranging from the clinically extreme (e.g. epilepsy) to the more subtle (e.g. anxiety). In the brain, the most common inhibitory synapses are regulated by GABAA (γ-aminobutyric acid type A) receptors, a role commensurate with their importance as therapeutic targets. Remarkably, we still know relatively little about GABAA receptor biogenesis. Receptors are constructed as pentameric ion channels, with α and β subunits being the minimal requirement, and the incorporation of a γ subunit being necessary for benzodiazepine modulation and synaptic targeting. Insights have been provided by the discovery of several specific assembly signals within different GABAA receptor subunits. Moreover, a number of recent studies on GABAA receptor mutations associated with epilepsy have further enhanced our understanding of GABAA receptor biogenesis, structure and function.

Impacts of Iron Metabolism Dysregulation on Alzheimer’s Disease

2021 ◽  
Vol 80 (4) ◽  
pp. 1439-1450
Author(s):  
Najla Jouini ◽  
Zakaria Saied ◽  
Samia Ben Sassi ◽  
Fatma Nebli ◽  
Taieb Messaoud ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Antioxidant System ◽  
Plasma Concentrations ◽  
Normal Brain ◽  
Cognitively Normal ◽  
Iron Trafficking ◽  
Major Species ◽  
Normal Brain Function ◽  
Calcium Magnesium

Background: Iron plays an important role in maintaining cell survival, with normal iron trafficking known to be regulated by the ceruloplasmin-transferrin (Cp-Tf) antioxidant system. Disruption to this system is thought to be detrimental to normal brain function. Objective: To determine whether an imbalance of iron and the proteins involved in its metabolism (ceruloplasmin and transferrin) are linked to Alzheimer’s disease (AD) and to the expression of amyloid-beta (Aβ) peptide 1–42 (Aβ1–42), which is a major species of Aβ, and the most toxic. Methods: We evaluated the concentrations of iron, calcium, magnesium, and Aβ1–42 in the cerebrospinal fluid (CSF) of patients with AD and cognitively normal controls. Correlations between the components of the Cp-Tf antioxidant system in plasma were studied to determine the role of peripheral blood in the onset and/or development of AD. We used commercial ELISA immunoassays to measure Aβ1–42, immunoturbidimetry to quantify ceruloplasmin and transferrin, and colorimetry to quantify iron, calcium, and magnesium. Results: We found that the AD group had lower CSF concentrations of Aβ1–42 (p < 0.001) and calcium (p < 0.001), but a higher CSF concentration of iron (p < 0.001). Significantly lower plasma concentrations of ceruloplasmin (p = 0.003), transferrin (mean, p < 0.001), and iron (p < 0.001) were observed in the AD group than in cognitively normal adults. Moreover, we found a strong interdependence between most of these components. Conclusion: Iron dyshomeostasis has a crucial role in the onset of AD and/or its development. Correcting metal misdistribution is an appealing therapeutic strategy for AD.

scholarly journals Cranioplasty Sinking Should Affect Normal Brain Function Mimicking Other Neurologic Illness: Fig 1.

2012 ◽  
Vol 33 (4) ◽  
pp. e65-e65
Author(s):  
M. del Mar Carmona Abellán ◽  
M. Murie Fernández ◽  
P. Esteve Belloch
Keyword(s):  
Brain Function ◽  
Normal Brain ◽  
Normal Brain Function

THE INSULA: ISLAND OF REIL

2015 ◽  
Vol 86 (11) ◽  
pp. e4.155-e4
Author(s):  
Ray Wynford-Thomas ◽  
Rob Powell
Keyword(s):  
Speech Processing ◽  
Brain Function ◽  
Insular Cortex ◽  
Normal Brain ◽  
Temporal Epilepsy ◽  
Normal Brain Function ◽  
Temporal Structures ◽  
Hypermotor Seizures ◽  
Posterior Insula ◽  
As Effects

Just as ‘no man is an island’, despite its misleading name, the insula is not an island. Sitting deeply within the cerebrum, the insular cortex and its connections play an important role in both normal brain function and seizure generation. Stimulating specific areas of the insula can produce somatosensory, viscerosensory, somatomotor and visceroautonomic symptoms, as well as effects on speech processing and pain. Insular onset seizures are rare, but may mimic both temporal and extra-temporal epilepsy and if not recognised, may lead to failure of epilepsy surgery. We therefore highlight the semiology of insular epilepsy by discussing three cases with different auras. Insular onset seizures can broadly be divided into three main types both anatomically and according to seizure semiology:1. Seizures originating in the antero-inferior insula present with laryngeal constriction, along with visceral and gustatory auras (similar to those originating in medial temporal structures).2. Antero-superior onset seizures can have a silent onset, but tend to propagate rapidly to motor areas causing focal motor or hypermotor seizures.3. Seizures originating in the posterior insula present with contralateral sensory symptoms.

scholarly journals What is the effect of body’s chemical messengers in the brain?

2019 ◽  
Vol 8 (3) ◽  
pp. 613-618
Keyword(s):  
Language Learning ◽  
Brain Function ◽  
Physicochemical Parameters ◽  
Active Sites ◽  
Geometry Optimization ◽  
Normal Brain ◽  
Delivery Technique ◽  
Normal Brain Function ◽  
Practical Model ◽  
The Brain

Neurochemical transmitters in the brain are fundamental to normal brain function and this investigation aims to introduce a study on the center of neuroscientific through an account of language development which conducts human speech mechanism using theoretical methods. In the process of this work, new understanding has been gained from the neurochemistry of several important neurotransmitters of dopamine (DA), epinephrine (EN), norepinephrine (NE), histamine (HA) and serotonin (ST) in brain by Monte Carlo simulation (MC) which uses the increased temperature to the potential energy of the neurochemicals in the brain considering the geometry optimization of the compounds as an additional conformational level. Moreover, the results of optimized DA, EN, NE, HA, ST neurochemical transmitters by running the physicochemical parameters as a practical model using Gaussian 09 program package can approve the twisting of language-brain due to these structures using density electron deliverers. The most stable of these compounds through the active sites of nitrogen and oxygen atoms has illustrated the best optimized position for localizing the structure through delivery technique in the brain to activate the center of learning a language as a simulated model. So, the best results with the calculated amounts conduct us to analyze the perspective of language learning process and enhancing this ability.

scholarly journals Defective Neuronal Positioning Correlates With Aberrant Motor Circuit Function in Zebrafish

2021 ◽  
Vol 15 ◽  
Author(s):  
Emilia Asante ◽  
Devynn Hummel ◽  
Suman Gurung ◽  
Yasmin M. Kassim ◽  
Noor Al-Shakarji ◽  
...  
Keyword(s):  
Neuromuscular Junctions ◽  
Larval Feeding ◽  
Normal Brain ◽  
Axon Pathfinding ◽  
Loss Of Function ◽  
Jaw Muscles ◽  
Normal Brain Function ◽  
Functional Consequences ◽  
And Migration ◽  
Circuit Function

Precise positioning of neurons resulting from cell division and migration during development is critical for normal brain function. Disruption of neuronal migration can cause a myriad of neurological disorders. To investigate the functional consequences of defective neuronal positioning on circuit function, we studied a zebrafish frizzled3a (fzd3a) loss-of-function mutant off-limits (olt) where the facial branchiomotor (FBM) neurons fail to migrate out of their birthplace. A jaw movement assay, which measures the opening of the zebrafish jaw (gape), showed that the frequency of gape events, but not their amplitude, was decreased in olt mutants. Consistent with this, a larval feeding assay revealed decreased food intake in olt mutants, indicating that the FBM circuit in mutants generates defective functional outputs. We tested various mechanisms that could generate defective functional outputs in mutants. While fzd3a is ubiquitously expressed in neural and non-neural tissues, jaw cartilage and muscle developed normally in olt mutants, and muscle function also appeared to be unaffected. Although FBM neurons were mispositioned in olt mutants, axon pathfinding to jaw muscles was unaffected. Moreover, neuromuscular junctions established by FBM neurons on jaw muscles were similar between wildtype siblings and olt mutants. Interestingly, motor axons innervating the interhyoideus jaw muscle were frequently defasciculated in olt mutants. Furthermore, GCaMP imaging revealed that mutant FBM neurons were less active than their wildtype counterparts. These data show that aberrant positioning of FBM neurons in olt mutants is correlated with subtle defects in fasciculation and neuronal activity, potentially generating defective functional outputs.

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