scholarly journals Input Statistics and Hebbian Cross-Talk Effects

2014 ◽  
Vol 26 (4) ◽  
pp. 654-692
Author(s):  
Anca Rădulescu
Keyword(s):  
Numerical Simulations ◽  
Cross Talk ◽  
Error Rate ◽  
Critical State ◽  
Hebbian Learning ◽  
Neural Mechanism ◽  
Prior Work ◽  
Learning Dynamics ◽  
Analytical Tools ◽  
The Brain

As an extension of prior work, we studied inspecific Hebbian learning using the classical Oja model. We used a combination of analytical tools and numerical simulations to investigate how the effects of synaptic cross talk (which we also refer to as synaptic inspecificity) depend on the input statistics. We investigated a variety of patterns that appear in dimensions higher than two (and classified them based on covariance type and input bias). We found that the effects of cross talk on learning dynamics and outcome is highly dependent on the input statistics and that cross talk may lead in some cases to catastrophic effects on learning or development. Arbitrarily small levels of cross talk are able to trigger bifurcations in learning dynamics, or bring the system in close enough proximity to a critical state, to make the effects indistinguishable from a real bifurcation. We also investigated how cross talk behaves toward unbiased (“competitive”) inputs and in which circumstances it can help the system productively resolve the competition. Finally, we discuss the idea that sophisticated neocortical learning requires accurate synaptic updates (similar to polynucleotide copying, which requires highly accurate replication). Since it is unlikely that the brain can completely eliminate cross talk, we support the proposal that is uses a neural mechanism that “proofreads” the accuracy of the updates, much as DNA proofreading lowers copying error rate.

Potential immunotherapy for Alzheimer disease and age-related dementia

2019 ◽  
Vol 21 (1) ◽  
pp. 21-25 ◽  
Keyword(s):  
Immune System ◽  
Alzheimer Disease ◽  
Cross Talk ◽  
Immune Checkpoint ◽  
Short Review ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
New Approach ◽  
Age Related ◽  
The Brain

Emerging results support the concept that Alzheimer disease (AD) and age-related dementia are affected by the ability of the immune system to contain the brain's pathology. Accordingly, well-controlled boosting, rather than suppression of systemic immunity, has been suggested as a new approach to modify disease pathology without directly targeting any of the brain's disease hallmarks. Here, we provide a short review of the mechanisms orchestrating the cross-talk between the brain and the immune system. We then discuss how immune checkpoint blockade directed against the PD-1/PD-L1 pathways could be developed as an immunotherapeutic approach to combat this disease using a regimen that will address the needs to combat AD.

Potential immunotherapy for Alzheimer disease and age-related dementia

2019 ◽  
Vol 21 (1) ◽  
pp. 21-25 ◽  
Keyword(s):  
Immune System ◽  
Alzheimer Disease ◽  
Cross Talk ◽  
Immune Checkpoint ◽  
Short Review ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
New Approach ◽  
Age Related ◽  
The Brain

Emerging results support the concept that Alzheimer disease (AD) and age-related dementia are affected by the ability of the immune system to contain the brain’s pathology. Accordingly, well-controlled boosting, rather than suppression of systemic immunity, has been suggested as a new approach to modify disease pathology without directly targeting any of the brain’s disease hallmarks. Here, we provide a short review of the mechanisms orchestrating the cross-talk between the brain and the immune system. We then discuss how immune checkpoint blockade directed against the PD-1/PD-L1 pathways could be developed as an immunotherapeutic approach to combat this disease using a regimen that will address the needs to combat AD.

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)

scholarly journals Targeting neuro–immune communication in neurodegeneration: Challenges and opportunities

2018 ◽  
Vol 215 (11) ◽  
pp. 2702-2704 ◽  
Author(s):  
Aleksandra Deczkowska ◽  
Michal Schwartz
Keyword(s):  
Immune System ◽  
Cross Talk ◽  
Immune Cells ◽  
Therapeutic Approach ◽  
Neurological Diseases ◽  
Challenges And Opportunities ◽  
The Cross ◽  
The Brain

Immune cells patrol the brain and can support its function, but can we modulate brain–immune communication to fight neurological diseases? Here, we briefly discuss the mechanisms orchestrating the cross-talk between the brain and the immune system and describe how targeting this interaction in a well-controlled manner could be developed as a universal therapeutic approach to treat neurodegeneration.

NEUROECONOMICS, NEUROPHYSIOLOGY AND THE COMMON CURRENCY HYPOTHESIS

2008 ◽  
Vol 24 (3) ◽  
pp. 419-429 ◽  
Author(s):  
Anthony Landreth ◽  
John Bickle
Keyword(s):  
Rational Choice ◽  
Dopamine Release ◽  
Research Programme ◽  
Neural Mechanism ◽  
The Other ◽  
Common Currency ◽  
The Common ◽  
The Brain ◽  
Electrophysiological Methods

We briefly describe ways in which neuroeconomics has made contributions to its contributing disciplines, especially neuroscience, and a specific way in which it could make future contributions to both. The contributions of a scientific research programme can be categorized in terms of (1) description and classification of phenomena, (2) the discovery of causal relationships among those phenomena, and (3) the development of tools to facilitate (1) and (2). We consider ways in which neuroeconomics has advanced neuroscience and economics along each line. Then, focusing on electrophysiological methods, we consider a puzzle within neuroeconomics whose solution we believe could facilitate contributions to both neuroscience and economics, in line with category (2). This puzzle concerns how the brain assigns reward values to otherwise incomparable stimuli. According to the common currency hypothesis, dopamine release is a component of a neural mechanism that solves comparability problems. We review two versions of the common currency hypothesis, one proposed by Read Montague and colleagues, the other by William Newsome and colleagues, and fit these hypotheses into considerations of rational choice.

scholarly journals Pre-stimulus phase and amplitude regulation of phase-locked responses are maximized in the critical state

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Arthur-Ervin Avramiea ◽  
Richard Hardstone ◽  
Jan-Matthis Lueckmann ◽  
Jan Bím ◽  
Huibert D Mansvelder ◽  
...  
Keyword(s):  
Computational Model ◽  
Critical State ◽  
Global Dynamics ◽  
Critical Dynamics ◽  
Neuronal Responses ◽  
Scale Free ◽  
Stimulus Response ◽  
Functional States ◽  
The Brain

Understanding why identical stimuli give differing neuronal responses and percepts is a central challenge in research on attention and consciousness. Ongoing oscillations reflect functional states that bias processing of incoming signals through amplitude and phase. It is not known, however, whether the effect of phase or amplitude on stimulus processing depends on the long-term global dynamics of the networks generating the oscillations. Here, we show, using a computational model, that the ability of networks to regulate stimulus response based on pre-stimulus activity requires near-critical dynamics—a dynamical state that emerges from networks with balanced excitation and inhibition, and that is characterized by scale-free fluctuations. We also find that networks exhibiting critical oscillations produce differing responses to the largest range of stimulus intensities. Thus, the brain may bring its dynamics close to the critical state whenever such network versatility is required.

Abstract 1375: Brain Renin Angiotensin Blockade Attenuates Cytokines and Oxidative Stress in the Paraventricular Nucleus of Hypothalamus and Decreases Sympathoexcitation in Heart Failure Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Ying Ma ◽  
Yu-Ming Kang* ◽  
Zhi-Ming Yang ◽  
Joseph Francis*
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Paraventricular Nucleus ◽  
Cross Talk ◽  
Renin Angiotensin System ◽  
Heart Weight ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain ◽  
And Oxidative Stress

Introduction: Neurohumoral mechanisms play an important role in the pathophysiology of congestive heart failure (HF). Recent studies suggest that the brain renin angiotensin system (RAS) plays an important role in regulating body fluids and sympathetic drive in HF. In addition, it has been shown that there is cross talk between cytokines and RAS in cardiovascular disease. In this study we determined whether blockade of brain RAS attenuate inflammatory cytokines and oxidative stress in HF rats. Methods and Results: Adult male Sprague-Dawley rats were implanted with intracerebroventricular (ICV) cannulae and subjected to coronary artery ligation to induce HF and confirmed by echocardiography. Rats were treated with an angiotensin type 1 receptors (AT1-R) antagonist losartan (LOS, 20 μg/hr, ICV) or vehicle (VEH) for 4 weeks. At the end of the study, left ventricular (LV) function was measured by echocardiography and rats were sacrificed, and brain and plasma samples were collected for measurements of cytokines and superoxide using immunohistochemistry, Western blot and real time RT-PCR. HF rats induced significant increases in Nuclear Factor-kappaB (NF-κB) p50-positive neurons and activated microglia in the paraventricular nucleus (PVN) of hypothalamus, and TNF-α, IL-1β, IL-6 and NF-κB p50 in hypothalamus when compared with sham rats. These animals also had increased staining for dihydroethidium (DHE) and plasma levels of norepinephrine (NE), an indirect indicator of sympathetic activity. In contrast, ICV treatment with LOS attenuated cytokine expression and oxidative stress in the PVN and hypothalamus when compared with VEH treated HF rats. ICV treatment with LOS also reduced plasma NE levels, and proinflammatory cytokine, heart weight to body weight ratio with decreased LV end-diastolic pressure. Conclusions : These findings suggest the cross talk between the cytokines and renin angiotensin system within the brain contribute to sympatho-excitation in HF.

Plasticity: Cells, Circuits, Brains, and Behavior

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.

Difficulties with synaptic theory of learning and memory and possible remedies

2000 ◽  
Vol 23 (4) ◽  
pp. 550-551
Author(s):  
Mikhail N. Zhadin
Keyword(s):  
Cerebral Cortex ◽  
Associative Learning ◽  
Learning And Memory ◽  
Hebbian Learning ◽  
Behavioral Responses ◽  
Learning Rules ◽  
The Brain

The absence of a clear influence of an animal's behavioral responses to Hebbian associative learning in the cerebral cortex requires some changes in the Hebbian learning rules. The participation of the brain monoaminergic systems in Hebbian associative learning is considered.

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