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1 |
Computational analysis of NIRS and BOLD signal from neurovascular coupling with three neuron-system feedforward inhibition network
تجزیه و تحلیل محاسباتی سیگنال های NIRS و BOLD از اتصال جفت عصبی عروقی با سه شبکه مهار کننده تغذیه ای سیستم عصبی-2020 Several neurological disorders occur due to hypoxic condition in brain arising from impairment of cere- bral functionality, which can be controlled by neural stimulation driven vasoactive response mediated through biological response in astrocyte, a phenomenon known as neurovascular coupling. Brain can ad- just with the problem of hypoxic condition by causing vasodilation with the help of this mechanism. To deduce the mechanism behind vasodilation of blood vessel caused by neuronal stimulus, current study articulates a mathematical model involving neuronal system feedforward inhibition network model (FFI) with two other functional components of neurovascular coupling, i.e. astrocyte and smooth muscle cell lining blood vessel. This study includes the neural inhibition network system where glutamatergic pyra- midal neuron and GABAergic interneuron act antagonistically with each other. The proposed model suc- cessfully includes the implication of the inhibition system to design mathematical model for neurovas- cular coupling. Result of the proposed model shows that the increase in neuronal stimulus from 20 to 60 μA/cm 2 has the ability to increase the vasodilatory activity of blood tissue vasculature. Oxygenation level and hemodynamic response due to input synaptic stimulation has been calculated by regional cere- bral oxygenation level (rS0 2 ) and blood oxygen level dependent (BOLD) imaging signal which supports vasodilation of blood vessel with increase in synaptic input stimulus. Keywords: Neurovascular coupling unit | Hodgkin-Huxley model | Neurotransmitter | Feedforward-inhibition network | Regional cerebral oxygen saturation |
مقاله انگلیسی |
2 |
Assemblies of Perisomatic GABAergic Neurons in the Developing Barrel Cortex
مجامع سلولهای عصبی گاباژیک پریسوماتیک در توسعه قشر بارل-2020 The developmental journey of cortical interneurons
encounters several activity-dependent milestones.
During the early postnatal period in developing
mice, GABAergic neurons are transient preferential
recipients of thalamic inputs and undergo activitydependent
migration arrest, wiring, and programmed
cell-death. Despite their importance for
the emergence of sensory experience and the role
of activity in their integration into cortical networks,
the collective dynamics of GABAergic neurons during
that neonatal period remain unknown. Here, we
study coordinated activity in GABAergic cells of the
mouse barrel cortex using in vivo calcium imaging.
We uncover a transient structure in GABAergic
population dynamics that disappears in a sensorydependent
process. Its building blocks are anatomically
clustered GABAergic assemblies mostly
composed by prospective parvalbumin-expressing
cells. These progressively widen their territories until
forming a uniform perisomatic GABAergic network.
Such transient patterning of GABAergic activity is a
functional scaffold that links the cortex to the
external world prior to active exploration |
مقاله انگلیسی |
3 |
Pathological high frequency oscillations associate with increased GABA synaptic activity in pediatric epilepsy surgery patients
نوسانات فرکانس پاتولوژیک با افزایش فعالیت سیناپسی GABA در بیماران جراحی صرع کودکان ارتباط دارد-2020 Pathological high-frequency oscillations (HFOs), specifically fast ripples (FRs,>250 Hz), are pathognomonic of
an active epileptogenic zone. However, the origin of FRs remains unknown. Here we explored the correlation
between FRs recorded with intraoperative pre-resection electrocorticography (ECoG) and spontaneous synaptic
activity recorded ex vivo from cortical tissue samples resected for the treatment of pharmacoresistant epilepsy.
The cohort included 47 children (ages 0.22–9.99 yr) with focal cortical dysplasias (CD types I and II), tuberous
sclerosis complex (TSC) and non-CD pathologies. Whole-cell patch clamp recordings were obtained from pyramidal
neurons and interneurons in cortical regions that were positive or negative for pathological HFOs, defined
as FR band oscillations (250–500 Hz) at ECoG. The frequency of spontaneous excitatory and inhibitory
postsynaptic currents (sEPSCs and IPSCs, respectively) was compared between HFO+ and HFO- regions.
Regardless of pathological substrate, regions positive for FRs displayed significantly increased frequencies of
sIPSCs compared with regions negative for FRs. In contrast, the frequency of sEPSCs was similar in both regions.
In about one third of cases (n=17), pacemaker GABA synaptic activity (PGA) was observed. In the vast majority
(n=15), PGA occurred in HFO+ areas. Further, fast-spiking interneurons displayed signs of hyperexcitability
exclusively in HFO+ areas. These results indicate that, in pediatric epilepsy patients, increased GABA synaptic
activity is associated with interictal FRs in the epileptogenic zone and suggest an active role of GABAergic
interneurons in the generation of pathological HFOs. Increased GABA synaptic activity could serve to dampen
excessive excitability of cortical pyramidal neurons in the epileptogenic zone, but it could also promote neuronal
network synchrony. Keywords: Fast ripples | Cortical dysplasia | GABA | Electrophysiology | Slice | Synaptic activity |
مقاله انگلیسی |
4 |
Deficiency of anti-inflammatory cytokine IL-4 leads to neural hyperexcitability and aggravates cerebral ischemia–reperfusion injury
کمبود سیتوکین ضد التهاب IL-4 منجر به فشار بیش از حد عصبی شده و آسیب به ایسکمی مغزی - مجدد جریان خون را تشدید می کند.-2020 Systematic administration of anti-inflammatory cytokine interleukin 4 (IL-4) has been
shown to improve recovery after cerebral ischemic stroke. However, whether IL-4 affects
neuronal excitability and how IL-4 improves ischemic injury remain largely unknown. Here we
report the neuroprotective role of endogenous IL-4 in focal cerebral ischemia–reperfusion (I/R)
injury. In multi-electrode array (MEA) recordings, IL-4 reduces spontaneous firings and network
activities of mouse primary cortical neurons. IL-4 mRNA and protein expressions are
upregulated after I/R injury. Genetic deletion of Il-4 gene aggravates I/R injury in vivo and
exacerbates oxygen-glucose deprivation (OGD) injury in cortical neurons. Conversely,
supplemental IL-4 protects Il-4–/– cortical neurons against OGD injury. Mechanistically, cortical
pyramidal and stellate neurons common for ischemic penumbra after I/R injury exhibit intrinsic
hyperexcitability and enhanced excitatory synaptic transmissions in Il-4–/– mice. Furthermore, upregulation of Nav1.1 channel, and downregulations of KCa3.1 channel and α6 subunit of GABAA receptors are detected in the cortical tissues and primary cortical neurons from Il-4–/–
mice. Taken together, our findings demonstrate that IL-4 deficiency results in neural
hhoottppaappeerr..nneett hyperexcitability and aggravates I/R injury, thus activation of IL-4 signaling may protect the
brain against the development of permanent damage and help recover from ischemic injury after
stroke. KEY WORDS Anoxic depolarization | IL-4 | Ischemia–reperfusion injury | Neuronal excitability | Synaptic transmissions |
مقاله انگلیسی |
5 |
In Vitro Differentiated Human Stem Cell-Derived Neurons Reproduce Synaptic Synchronicity Arising during Neurodevelopment
سلولهای عصبی مشتق شده از سلولهای بنیادی سلولهای بنیادی بدن در شرایط in vitro تولید مثل سینکروتیک سیناپسی ناشی از توسعه عصبی-2020 Neurons differentiated from induced pluripotent stem cells (iPSCs) typically show regular spiking and synaptic activity but lack more
complex network activity critical for brain development, such as periodic depolarizations including simultaneous involvement of glutamatergic
and GABAergic neurotransmission.We generated human iPSC-derived neurons exhibiting spontaneous oscillatory activity after
cultivation of up to 6 months, which resembles early oscillations observed in rodent neurons. This behavior was found in neurons
generated using a more ‘‘native’’ embryoid body protocol, in contrast to a ‘‘fast’’ protocol based on NGN2 overexpression. A comparison
with published data indicates that EB-derived neurons reach the maturity of neurons of the third trimester and NGN2-derived neurons of
the second trimester of human gestation. Co-culturing NGN2-derived neurons with astrocytes only led to a partial compensation and did
not reliably induce complex network activity. Our data will help selection of the appropriate iPSC differentiation assay to address specific
questions related to neurodevelopmental disorders |
مقاله انگلیسی |
6 |
Targeted viral vector transduction of relaxin-3 neurons in the rat nucleus incertus using a novel cell-type specific promoter
انتقال بردار ویروسی هدفمند از سلولهای عصبی ریلسین -3 در هسته موش با استفاده از یک پروموتر خاص از نوع سلول جدید-2020 Modern neuroscience utilizes transgenic techniques extensively to study the activity and function of brain neural
networks. A key feature of this approach is its compatibility with molecular methods for selective transgene
expression in neuronal circuits of interest. Until now, such targeted transgenic approaches have not been applied
to the extensive circuitry involving the neuropeptide, relaxin-3. Pharmacological and gene knock-out studies
have revealed relaxin-3 signalling modulates interrelated behaviours and cognitive processes, including stress
and anxiety, food and alcohol consumption, and spatial and social memory, highlighting the potential of this
system as a therapeutic target. In the present study, we aimed to identify a promoter sequence capable of
regulating cell-type specific transgene expression from an adeno-associated viral (AAV) vector in relaxin-3
neurons of the rat nucleus incertus (NI). In parallel to relaxin-3 promoter sequences, we also tested an AAV vector
containing promoter elements for the tropomyosin receptor kinase A (TrkA) gene, as TrkA is co-expressed with
relaxin-3 in rat NI neurons. Stereotaxic injection of an mCherry-expressing AAV vector revealed widespread nonspecific
TrkA promoter (880 bp) activity in and adjacent to the NI at 8 weeks post-treatment. In contrast,
mCherry expression was successfully restricted to relaxin-3 NI neurons with 98% specificity using a 1736 bp
relaxin-3 promoter. In addition to detailed anatomical mapping of NI relaxin-3 networks, illustrated here in
association with GABAergic medial septum neurons, this method for targeted transgene delivery offers a versatile
tool for ongoing preclinical studies of relaxin-3 circuitry. Keywords: Adeno-associated viral (AAV) vector | Cell-type specific promoter | Medial septum | Nucleus incertus | Relaxin-3 | Tropomyosin receptor kinase A (TrkA) |
مقاله انگلیسی |
7 |
Plasticity of Synaptic Transmission in Human Stem Cell-Derived Neural Networks
انعطاف پذیری انتقال سیناپسی در شبکه های عصبی مشتق از سلولهای بنیادی انسان-2020 Long-term potentiation and depression, inferred from analysis on brain slices, are considered the
cellular processes underlying learning and memory formation. They have not so far been demonstrated
in human stem cell-derived neurons. By expressing channelrhodopsin in hESCs-derived glutamate
neurons and co-culturing them with GABA neurons, we found that blue light stimulation
increased the frequency of miniature excitatory postsynaptic currents (mEPSCs) and decreased the
ratio of paired pulse facilitation (PPF) in non-ChR2-expressing GABA neurons, indicating a facilitating
action at the presynaptic terminals. When paired with postsynaptic depolarization, the repetitive
stimulation significantly increased the amplitude of light-evoked EPSCs that persisted during the
period, indicating long-term potentiation (LTP). In contrast, low-frequency light stimulation induced
long-term depression (LTD). These effects were blocked by N-methyl-D-aspartic acid (NMDA) receptor
antagonists, suggesting NMDA receptor-mediated synaptic plasticity in human neural networks.
Furthermore, induced pluripotent stem cell (iPSC)-derived neurons of patient with Down syndrome
showed absence of LTP or LTD. Thus, our platformoffers a versatile model for assessing human neural
plasticity under physiological and pathological conditions |
مقاله انگلیسی |
8 |
Immature Dentate Granule Cells Require Ntrk2/Trkb for the Formation of Functional Hippocampal Circuitry
سلولهای گرانول دندانی دفع نشده مورد نیاز به Ntrk2 / Trkb برای تشکیل مدار عملکردی هیپوکامپ -2020 Early in brain development, impaired neuronal signaling during time-sensitive
windows triggers the onset of neurodevelopmental disorders. GABA, through
its depolarizing and excitatory actions, drives early developmental events
including neuronal circuit formation and refinement. BDNF/TrkB signaling cooperates
with GABA actions. How these developmental processes influence the formation
of neural circuits and affect adult brain function is unknown. Here, we
show that early deletion of Ntrk2/Trkb from immature mouse hippocampal dentate
granule cells (DGCs) affects the integration and maturation of newly formed
DGCs in the hippocampal circuitry and drives a premature shift from depolarizing
to hyperpolarizing GABAergic actions in the target of DGCs, the CA3 principal
cells of the hippocampus, by reducing the expression of the cation-chloride
importer Nkcc1. These changes lead to the disruption of early synchronized
neuronal activity at the network level and impaired morphological maturation
of CA3 pyramidal neurons, ultimately contributing to altered adult hippocampal
synaptic plasticity and cognitive processes. |
مقاله انگلیسی |
9 |
Prefrontal cortical alterations of glutamate and GABA neurotransmission in schizophrenia: Insights for rational biomarker development
تغییرات قشر جلوی مغزی گلوتامات و انتقال عصبی گابا در اسکیزوفرنی : بینش برای توسعه علامت تجاری زیستی منطقی-2020 Certain cognitive deficits in schizophrenia, such as impaired working memory, are thought to reflect alterations in
the neural circuitry of the dorsolateral prefrontal cortex (DLPFC). Gamma oscillations in the DLPFC appear to be a
neural corollary of working memory function, and the power of these oscillations during working memory tasks is
lower in individuals with schizophrenia. Thus, gamma oscillations represent a potentially useful biomarker to index
dysfunction in the DLPFC circuitry responsible for working memory in schizophrenia. Postmortem studies, by
identifying the cellular basis of DLPFC dysfunction, can help inform the utility of biomarker measures obtained in
vivo. Given that gamma oscillations reflect network activity of excitatory pyramidal neurons and inhibitory GABA
neurons, we review postmortem findings of alterations to both cell types in the DLPFC and discuss how these findings
might inform future biomarker development and use. Keywords: GABA | gamma oscillations | Glutamate | Cognition | Working memory | Schizophrenia |
مقاله انگلیسی |
10 |
Spiking pattern recognition using informative signal of image and unsupervised biologically plausible learning
تشخیص الگوی Spiking با استفاده از سیگنال آموزنده تصویر و یادگیری بیولوژیکی غیرقابل کنترل-2019 The recent progress of low-power neuromorphic hardware provides exceptional conditions for applica- tions where their focus is more on saving power. However, the design of spiking neural networks (SNN) to recognize real-world patterns on such hardware remains a major challenge ahead of the researchers. In this paper, SNN inspired by the model of local cortical population as a biological neuro-computing resource for digit recognition was presented. SNN was equipped with spike-based unsupervised weight optimization based on the dynamical behavior of the excitatory (AMPA) and inhibitory (GABA) synapses using Spike Timing Dependent Plasticity (STDP). This biologically plausible learning enables neurons to make decisions and learns the structure of the input examples. There are two main reasons why this structure is state of the art compared to previous works: learning process is compatible with many ex- perimental observations on induction of long-term potentiation and long-term depression, image to sig- nal mapping created an informative signal of the image based on sequences of prolate spheroidal wave functions (PSWFs). The proposed image mapping translates the pixels attributes to the frequency, phase, and amplitude of a sinusoidal signal. This mapping enables the SNN to generalize better to the realis- tic sized images and significantly decreases the size of the input layer. Cortical SNN compared to earlier related studies recognized MNIST digits more accurate and achieved 96.1% classification accuracy with unsupervised learning based on sparse spike activity Keywords: Spiking neural network | STDP, AMPA and GABA current | Digit Recognition | Image coding |
مقاله انگلیسی |