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1 |
Graph-theoretical derivation of brain structural connectivity
استخراج نمودار نظری از اتصال ساختاری مغز-2020 Brain connectivity at the single neuron level can provide fundamental insights into how information is integrated and propagated within and between brain regions. However, it is almost impossible to adequately study this problem experimentally and, despite intense ef- forts in the field, no mathematical description has been obtained so far. Here, we present a mathematical framework based on a graph-theoretical approach that, starting from exper- imental data obtained from a few small subsets of neurons, can quantitatively explain and predict the corresponding full network properties. This model also changes the paradigm with which large-scale model networks can be built, from using probabilistic/empiric con- nections or limited data, to a process that can algorithmically generate neuronal networks connected as in the real system. Keywords: Connectome | Neuronal networks | Random graphs |
مقاله انگلیسی |
2 |
Short-term neuronal effects of Fumonisin B1 on neuronal activity in rodents
اثرات عصبی کوتاه مدت Fumonisin B1 بر فعالیت عصبی در جوندگان-2020 Fumonisin B1 (FB1) is a mycotoxin produced by microscopic fungi (mostly Fusarium
species), which may infect our major crops. The toxin inhibits the development of these plants
and may also have harmful effects on animals and humans consuming the infected crops.
FB1 inhibits sphingolipid biosynthesis which leads to altered membrane characteristics and
consequently, altered cellular functions. There are some indications that the toxin has
inhibitory effects on neuronal activity in case of repeated consumption, presumably due to
sphingolipid depletion. However, according to new literature data, FB1 may have acute
excitatory neural effects, too, via different mechanisms of action. Therefore, in the present
study, we addressed the neuronal network effects of FB1 following acute treatment, using
different electrophysiological techniques in vitro and in vivo.
Acute treatments with FB1 (10-100 μM) were carried out on brain slices, tissue cultures and
live animals. After direct treatment of samples, electrically evoked or spontaneous field
potentials were examined in the hippocampus and the neocortex of rat brain slices and in
hippocampal cell cultures. In the hippocampus, a short-term increase in the excitability of
neuronal networks and individual cells was observed in response to FB1 treatment. In some
cases, the initially enhanced excitation was reversed presumably due to overactivation of
neuronal networks. Normal spontaneous activity was found to be stimulated in hippocampal
cell cultures. Seizure susceptibility was not affected in the neocortex of brain slices.
For the verification of the results caused by direct treatment, effects of systemic
administration of FB1 (7.5 mg/kg, i.p.) were also examined. Evoked field potentials recorded
in vivo from the somatosensory cortex and cell activation measured by the c-fos technique in hippocampus and somatosensory cortex were analyzed. However, the hippocampal and cortical stimulatory effect detected in vitro could not be demonstrated by these in vivo assays.
Altogether, the toxin enhanced the basic excitability of neurons and neuronal networks after
direct treatment but there were no effects on the given brain areas after systemic treatment in
vivo. Based on the observed in vitro FB1 effects and the lack of data on the penetration of
FB1 across the blood-brain barrier, we assume that in vivo consequences of FB1
administration can be more prominent in case of perturbed blood-brain barrier functions. Keywords: neurotoxicity | electrophysiology | c-Fos, mycotoxin | field potential | brain slice | tissue culture |
مقاله انگلیسی |
3 |
Effects of electromagnetic induction on vibrational resonance in single neurons and neuronal networks
اثرات القایی الکترومغناطیسی بر تشدید ارتعاش در سلولهای عصبی تنها و شبکه های عصبی-2020 In this paper, Vibrational Resonance (VR), in which the response of some dynamical
systems to a weak, low frequency signal can be enhanced by the optimal amplitude
of high frequency signal, is investigated under the effects of electromagnetic induction
in both single neurons and small-world networks. We find that the occurrence of VR
in single neurons requires less energy in the presence of electromagnetic induction,
although the resonant peak of the response reduces. Besides, VR can be obtained in
small-world networks both with and without electromagnetic induction. In small-world
neuronal networks, the highest resonance peak of VR enhances with an increase in the
probability of adding link in case of without electromagnetic induction. On the other
hand, with the increasing of the probability of adding link, VR disappears in the presence
of relatively strong electromagnetic induction, while it enhances in the presence of
relatively weak electromagnetic induction Keywords: Electromagnetic induction | Vibrational resonance | Hodgkin–Huxley neuron |
مقاله انگلیسی |
4 |
Sparsity through evolutionary pruning prevents neuronal networks from overfitting
Sparsity از طریق هرس تکاملی شبکه های عصبی جلوگیری می از Over-fitting-2020 Modern Machine learning techniques take advantage of the exponentially rising calculation power in
new generation processor units. Thus, the number of parameters which are trained to solve complex
tasks was highly increased over the last decades. However, still the networks fail – in contrast to our
brain – to develop general intelligence in the sense of being able to solve several complex tasks with
only one network architecture. This could be the case because the brain is not a randomly initialized
neural network, which has to be trained from scratch by simply investing a lot of calculation power, but
has from birth some fixed hierarchical structure. To make progress in decoding the structural basis of
biological neural networks we here chose a bottom-up approach, where we evolutionarily trained small
neural networks in performing a maze task. This simple maze task requires dynamic decision making
with delayed rewards. We were able to show that during the evolutionary optimization random
severance of connections leads to better generalization performance of the networks compared to fully
connected networks. We conclude that sparsity is a cent Keywords: Evolution | Artificial neural networks | Maze task | Evolutionary algorithm | Overfitting | Biological plausibility |
مقاله انگلیسی |
5 |
Time delayed chemical synapses and synchronization in multilayer neuronal networks with ephaptic inter-layer coupling
تأخیر زمان در سیناپسهای شیمیایی و هماهنگ سازی در شبکه های عصبی چند لایه با اتصال بین لایه ای ephaptic -2020 In this paper, a three-layer neuronal network is studied to consider different com plex con- nections between the neurons. In the nervous system, the communication between the neurons is mostly based on the electrical and chemical synapses. However, extracellular electric fields can induce a magnetic flux which can lead to indirect neural communica- tions, by means of electromagnetic induction. This mode of coupling is called ephaptic coupling, which here is used between the layer. To describe the coupling within the lay- ers, the electrical and chemical synapses are defined. We also take into account the par- tial time delays, to reflect the required time for information transmission through chem- ical synapses. Particularly, we consider partial and full time delays, as well as strong and weak coupling strengths. It is shown that three layers typically have opposite synchroniza- tion properties in the strong and weak coupling regimes. Specifically, when the coupling is strong, the top and bottom layers are synchronous, while the middle layer is desyn- chronous. But when the coupling is weak, the middle layer is synchronous, while the top and bottom layers are desynchronous. In overall, the most synchrony is obtained when the weak coupling is accompanied with partial time delays in chemical communications. Our research sheds new light on the complex interplay between the time delay, the ephaptic coupling, and the synchronization in neuronal networks. Keywords: Multilayer network | Ephaptic coupling | Time delay | Synchronization |
مقاله انگلیسی |
6 |
Long-Range Optogenetic Control of Axon Guidance Overcomes Developmental Boundaries and Defects
کنترل بینایی زاویه دار راهنمایی آکسون بر مرزها و نقص های توسعه غلبه می کند-2020 Axons connect neurons together, establishing the wiring architecture of neuronal networks. Axonal connectivity
is largely built during embryonic development through highly constrained processes of axon guidance,
which have been extensively studied. However, the inability to control axon guidance, and thus neuronal
network architecture, has limited investigation of how axonal connections influence subsequent development
and function of neuronal networks. Here, weuse zebrafish motor neurons expressing a photoactivatable Rac1
to co-opt endogenous growth cone guidance machinery to precisely and non-invasively direct axon growth
using light. Axons can be guided over large distances, within complex environments of living organisms, overriding
competing endogenous signals and redirecting axons across potent repulsive barriers to construct
novel circuitry. Notably, genetic axon guidance defects can be rescued, restoring functional connectivity.
These data demonstrate that intrinsic growth cone guidance machinery can be co-opted to non-invasively
build new connectivity, allowing investigation of neural network dynamics in intact living organisms. |
مقاله انگلیسی |
7 |
Distinct Pathogenic Genes Causing Intellectual Disability and Autism Exhibit a Common Neuronal Network Hyperactivity Phenotype
ژنهای پاتوژن مشخص متمایز کننده ناتوانی ذهنی و اوتیسم از فنوتیپ بیش فعالی شبکه عصبی مشترک-2020 Pathogenic mutations in either one of the epigenetic
modifiers EHMT1, MBD5, MLL3, or SMARCB1 have
been identified to be causative for Kleefstra syndrome
spectrum (KSS), a neurodevelopmental disorder
with clinical features of both intellectual disability
(ID) and autism spectrum disorder (ASD). To understand
how these variants lead to the phenotypic
convergence in KSS, we employ a loss-of-function
approach to assess neuronal network development
at the molecular, single-cell, and network activity
level. KSS-gene-deficient neuronal networks all
develop into hyperactive networks with altered
network organization and excitatory-inhibitory balance.
Interestingly, even though transcriptional
data reveal distinct regulatory mechanisms, KSS
target genes share similar functions in regulating
neuronal excitability and synaptic function, several
of which are associated with ID and ASD. Our results
show that KSS genes mainly converge at the level of
neuronal network communication, providing insights
into the pathophysiology of KSS and phenotypically
congruent disorders. |
مقاله انگلیسی |
8 |
m:3243A > G-Induced Mitochondrial Dysfunction Impairs Human Neuronal Development and Reduces Neuronal Network Activity and Synchronicity
m:3243A > G-Induced Mitochondrial Dysfunction Impairs Human Neuronal Development and Reduces Neuronal Network Activity and Synchronicity-2020 Epilepsy, intellectual and cortical sensory deficits,
and psychiatric manifestations are the most frequent
manifestations of mitochondrial diseases. How mitochondrial
dysfunction affects neural structure and
function remains elusive, mostly because of a lack
of proper in vitro neuronal model systems with mitochondrial
dysfunction. Leveraging induced pluripotent
stem cell technology, we differentiated excitatory
cortical neurons (iNeurons) with normal (low
heteroplasmy) and impaired (high heteroplasmy)
mitochondrial function on an isogenic nuclear DNA
background from patients with the common pathogenic
m.3243A > G variant of mitochondrial encephalomyopathy,
lactic acidosis, and stroke-like episodes
(MELAS). iNeurons with high heteroplasmy
exhibited mitochondrial dysfunction, delayed neural
maturation, reduced dendritic complexity, and fewer
excitatory synapses. Micro-electrode array recordings
of neuronal networks displayed reduced
network activity and decreased synchronous
network bursting. Impaired neuronal energy metabolism
and compromised structural and functional
integrity of neurons and neural networks could be
the primary drivers of increased susceptibility to
neuropsychiatric manifestations of mitochondrial
disease. |
مقاله انگلیسی |