scholarly journals Growth rules for the repair of Asynchronous Irregular neuronal networks after peripheral lesions

2021 ◽  
Vol 17 (6) ◽  
pp. e1008996
Author(s):  
Ankur Sinha ◽  
Christoph Metzner ◽  
Neil Davey ◽  
Roderick Adams ◽  
Michael Schmuker ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Network Model ◽  
Low Frequency ◽  
Structural Plasticity ◽  
Network Activity ◽  
Activity Levels ◽  
Dependent Growth ◽  
Underlying Mechanisms ◽  
Activity Dependent ◽  
The Brain

Several homeostatic mechanisms enable the brain to maintain desired levels of neuronal activity. One of these, homeostatic structural plasticity, has been reported to restore activity in networks disrupted by peripheral lesions by altering their neuronal connectivity. While multiple lesion experiments have studied the changes in neurite morphology that underlie modifications of synapses in these networks, the underlying mechanisms that drive these changes are yet to be explained. Evidence suggests that neuronal activity modulates neurite morphology and may stimulate neurites to selective sprout or retract to restore network activity levels. We developed a new spiking network model of peripheral lesioning and accurately reproduced the characteristics of network repair after deafferentation that are reported in experiments to study the activity dependent growth regimes of neurites. To ensure that our simulations closely resemble the behaviour of networks in the brain, we model deafferentation in a biologically realistic balanced network model that exhibits low frequency Asynchronous Irregular (AI) activity as observed in cerebral cortex. Our simulation results indicate that the re-establishment of activity in neurons both within and outside the deprived region, the Lesion Projection Zone (LPZ), requires opposite activity dependent growth rules for excitatory and inhibitory post-synaptic elements. Analysis of these growth regimes indicates that they also contribute to the maintenance of activity levels in individual neurons. Furthermore, in our model, the directional formation of synapses that is observed in experiments requires that pre-synaptic excitatory and inhibitory elements also follow opposite growth rules. Lastly, we observe that our proposed structural plasticity growth rules and the inhibitory synaptic plasticity mechanism that also balances our AI network both contribute to the restoration of the network to pre-deafferentation stable activity levels.

scholarly journals Growth Rules for the Repair of Asynchronous Irregular Neuronal Networks after Peripheral Lesions

2019 ◽  
Author(s):  
Ankur Sinha ◽  
Christoph Metzner ◽  
Neil Davey ◽  
Roderick Adams ◽  
Michael Schmuker ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Network Model ◽  
Neuronal Networks ◽  
Structural Plasticity ◽  
Activity Levels ◽  
Peripheral Lesion ◽  
Simulation Results ◽  
Dependent Growth ◽  
Activity Dependent ◽  
The Brain

AbstractSeveral homeostatic mechanisms enable the brain to maintain desired levels of neuronal activity. One of these, homeostatic structural plasticity, has been reported to restore activity in networks disrupted by peripheral lesions by altering their neuronal connectivity. While multiple lesion experiments have studied the changes in neurite morphology that underlie modifications of synapses in these networks, the underlying mechanisms that drive these changes are yet to be explained. Evidence suggests that neuronal activity modulates neurite morphology and may stimulate neurites to selective sprout or retract to restore network activity levels. We developed a new spiking network model, simulations of which accurately reproduce network rewiring after peripheral lesions as reported in experiments, to study these activity dependent growth regimes of neurites. To ensure that our simulations closely resemble the behaviour of networks in the brain, we deafferent a biologically realistic network model that exhibits low frequency Asynchronous Irregular (AI) activity as observed in cerebral cortex.Our simulation results indicate that the re-establishment of activity in neurons both within and outside the deprived region, the Lesion Projection Zone (LPZ), requires opposite activity dependent growth rules for excitatory and inhibitory post-synaptic elements. Analysis of these growth regimes indicates that they also contribute to the maintenance of activity levels in individual neurons. Furthermore, in our model, the directional formation of synapses that is observed in experiments requires that pre-synaptic excitatory and inhibitory elements also follow opposite growth rules. Lastly, we observe that our proposed model of homeostatic structural plasticity and the inhibitory synaptic plasticity mechanism that also balances our AI network are both necessary for successful rewiring of the network.Author summaryAn accumulating body of evidence suggests that our brain can compensate for peripheral lesions by adaptive rewiring of its neuronal circuitry. The underlying process, structural plasticity, can modify the connectivity of neuronal networks in the brain, thus affecting their function. To better understand the mechanisms of structural plasticity in the brain, we have developed a novel model of peripheral lesions and the resulting activity-dependent rewiring in a simplified cortical network model that exhibits biologically realistic asynchronous irregular activity. In order to accurately reproduce the directionality and time course of rewiring after injury that is observed in peripheral lesion experiments, we derive activity dependent growth rules for different synaptic elements: dendritic and axonal contacts. Our simulation results suggest that excitatory and inhibitory synaptic elements have to react to changes in neuronal activity in opposite ways. We show that these rules result in a homeostatic stabilisation of activity in individual neurons. In our simulations, both synaptic and structural plasticity mechanisms are necessary for network repair. Furthermore, our simulations indicate that while activity is restored in neurons deprived by the peripheral lesion, the temporal firing characteristics of the network can be changed by the rewiring process.

scholarly journals Vibration Isolation Critical to Measuring Neuronal Patterns in the Brain

2009 ◽  
Vol 17 (3) ◽  
pp. 12-15
Author(s):  
David L. Platus
Keyword(s):  
Neuronal Activity ◽  
Vibration Isolation ◽  
Medical Center ◽  
Low Frequency ◽  
Vibration Isolators ◽  
Low Frequency Vibration ◽  
Conducting Research ◽  
Neuronal Patterns ◽  
Isolation Systems ◽  
The Brain

Researchers at Georgetown University's Department of Physiology and Biophysics use negative-stiffness vibration isolators to help measure micron-level patterns of neuronal activity in the mammalian neocortex. The research is shedding new light into brain sensory and motor processing functions relating to cardiac fibrillation and epilepsy.Isolating a laboratory's sensitive microscopy equipment against low-frequency vibration has become increasingly more vital to maintaining imaging quality and data integrity for neurobiology researches. Ever more frequently, laboratory researchers are discovering that conventional air tables and the more recent active (electronic) vibration isolation systems are not able to adequately cancel out the lower frequency perturbations derived from air conditioning systems, outside vehicular movements and ambulatory personnel. Such was the case with the Department of Physiology and Biophysics at Georgetown University Medical Center, where Professor Jian-Young Wu has been conducting research on waves of neuronal activity in the neocortex of the brain.

scholarly journals Respiration competes with theta for modulating parietal cortex neurons

2019 ◽  
Author(s):  
Felix Jung ◽  
Yevgenij Yanovsky ◽  
Jurij Brankačk ◽  
Adriano BL Tort ◽  
Andreas Draguhn
Keyword(s):  
Neuronal Activity ◽  
Parietal Cortex ◽  
Field Potential ◽  
Anterior Cingulate ◽  
Theta Oscillations ◽  
Network Activity ◽  
Coupled Oscillations ◽  
Neuronal Network Activity ◽  
Posterior Parietal ◽  
The Brain

AbstractRecent work has shown that nasal respiration entrains local field potential (LFP) and neuronal activity in widespread regions of the brain. This includes non-olfactory regions where respiration-coupled oscillations have been described in different mammals, such as rodents, cats and humans. They may, thus, constitute a global signal aiding interregional communication. Nevertheless, the brain produces other widespread slow rhythms, such as theta oscillations, which also mediate long-range synchronization of neuronal activity. It is completely unknown how these different signals interact to control neuronal network activity. In this work, we characterized respiration- and theta-coupled activity in the posterior parietal cortex of mice. Our results show that respiration-coupled and theta oscillations have different laminar profiles, in which respiration preferentially entrains LFPs and units in more superficial layers, whereas theta modulation does not differ across the parietal cortex. Interestingly, we find that the percentage of theta-modulated units increases in the absence of respiration-coupled oscillations, suggesting that both rhythms compete for modulating parietal cortex neurons. We further show through intracellular recordings that synaptic inhibition is likely to play a role in generating respiration-coupled oscillations at the membrane potential level. Finally, we provide anatomical and electrophysiological evidence of reciprocal monosynaptic connections between the anterior cingulate and posterior parietal cortices, suggesting a possible source of respiration-coupled activity in the parietal cortex.

Activity-Dependent Development of Axonal and Dendritic Delays, or, Why Synaptic Transmission Should Be Unreliable

2002 ◽  
Vol 14 (3) ◽  
pp. 583-619 ◽  
Author(s):  
Walter Senn ◽  
Martin Schneider ◽  
Berthold Ruf
Keyword(s):  
Selection Process ◽  
Learning Rule ◽  
Network Activity ◽  
Direct Modification ◽  
Evolutionary Advantage ◽  
Neural Growth ◽  
Asymmetric Learning ◽  
Temporally Correlated ◽  
Activity Dependent ◽  
The Brain

Systematic temporal relations between single neuronal activities or population activities are ubiquitous in the brain. No experimental evidence, however, exists for a direct modification of neuronal delays during Hebbian-type stimulation protocols. We show that in fact an explicit delay adaptation is not needed if one assumes that the synaptic strengths are modified according to the recently observed temporally asymmetric learning rule with the downregulating branch dominating the upregulating branch. During development, slow, unbiased fluctuations in the transmission time, together with temporally correlated network activity, may control neural growth and implicitly induce drifts in the axonal delays and dendritic latencies. These delays and latencies become optimally tuned in the sense that the synaptic response tends to peak in the soma of the postsynaptic cell if this is most likely to fire. The nature of the selection process requires unreliable synapses in order to give successful synapses an evolutionary advantage over the others. The width of the learning function also determines the preferred dendritic delay and the preferred width of the postsynaptic response. Hence, it may implicitly determine whether a synaptic connection provides a precisely timed or a broadly tuned “contextual” signal.

scholarly journals In Vivo Optogenetic Modulation with Simultaneous Neural Detection Using Microelectrode Array Integrated with Optical Fiber

Sensors ◽  
2020 ◽  
Vol 20 (16) ◽  
pp. 4526
Author(s):  
Penghui Fan ◽  
Yilin Song ◽  
Shengwei Xu ◽  
Yuchuan Dai ◽  
Yiding Wang ◽  
...  
Keyword(s):  
Optical Fiber ◽  
Neuronal Activity ◽  
Microelectrode Array ◽  
Adhesive Bonding ◽  
Neural Circuit ◽  
Low Frequency ◽  
Depth Range ◽  
Light Power ◽  
The Brain

The detection of neuroelectrophysiology while performing optogenetic modulation can provide more reliable and useful information for neural research. In this study, an optical fiber and a microelectrode array were integrated through hot-melt adhesive bonding, which combined optogenetics and electrophysiological detection technology to achieve neuromodulation and neuronal activity recording. We carried out the experiments on the activation and electrophysiological detection of infected neurons at the depth range of 900–1250 μm in the brain which covers hippocampal CA1 and a part of the upper cortical area, analyzed a possible local inhibition circuit by combining opotogenetic modulation and electrophysiological characteristics and explored the effects of different optical patterns and light powers on the neuromodulation. It was found that optogenetics, combined with neural recording technology, could provide more information and ideas for neural circuit recognition. In this study, the optical stimulation with low frequency and large duty cycle induces more intense neuronal activity and larger light power induced more action potentials of neurons within a certain power range (1.032 mW–1.584 mW). The present study provided an efficient method for the detection and modulation of neurons in vivo and an effective tool to study neural circuit in the brain.

scholarly journals Activity- and Ca2+-Dependent Modulation of Surface Expression of Brain-Derived Neurotrophic Factor Receptors in Hippocampal Neurons

2000 ◽  
Vol 150 (6) ◽  
pp. 1423-1434 ◽  
Author(s):  
Jing Du ◽  
Linyin Feng ◽  
Feng Yang ◽  
Bai Lu
Keyword(s):  
Neuronal Activity ◽  
Neurotrophic Factor ◽  
High Frequency ◽  
Hippocampal Neurons ◽  
Electric Stimulation ◽  
Low Frequency ◽  
Brain Derived Neurotrophic Factor ◽  
Dependent Manner ◽  
Tetanic Stimulation ◽  
Activity Dependent

Brain-derived neurotrophic factor (BDNF) has been shown to regulate neuronal survival and synaptic plasticity in the central nervous system (CNS) in an activity-dependent manner, but the underlying mechanisms remain unclear. Here we report that the number of BDNF receptor TrkB on the surface of hippocampal neurons can be enhanced by high frequency neuronal activity and synaptic transmission, and this effect is mediated by Ca2+ influx. Using membrane protein biotinylation as well as receptor binding assays, we show that field electric stimulation increased the number of TrkB on the surface of cultured hippocampal neurons. Immunofluorescence staining suggests that the electric stimulation facilitated the movement of TrkB from intracellular pool to the cell surface, particularly on neuronal processes. The number of surface TrkB was regulated only by high frequency tetanic stimulation, but not by low frequency stimulation. The activity dependent modulation appears to require Ca2+ influx, since treatment of the neurons with blockers of voltage-gated Ca2+ channels or NMDA receptors, or removal of extracellular Ca2+, severely attenuated the effect of electric stimulation. Moreover, inhibition of Ca2+/calmodulin-dependent kinase II (CaMKII) significantly reduced the effectiveness of the tetanic stimulation. These findings may help us to understand the role of neuronal activity in neurotrophin function and the mechanism for receptor tyrosine kinase signaling.

­­­Neuron-astrocyte networking: Astrocytes orchestrate and respond to changes in neuronal network activity across brain states and behaviors

2021 ◽  
Author(s):  
Marion R Van Horn ◽  
Nicholas J Benfey ◽  
Colleen Ann Shikany ◽  
Liza J Severs ◽  
Tara Deemyad
Keyword(s):  
Neuronal Activity ◽  
Brain Function ◽  
Network Activity ◽  
Brain State ◽  
Neuronal Network Activity ◽  
The Status ◽  
Brain States ◽  
Sleep Arousal ◽  
Respiratory Rhythms ◽  
The Brain

Astrocytes are known to play many important roles in brain function. However, research underscoring the extent to which astrocytes modulate neuronal activity is still underway. Here we review the latest evidence regarding the contribution of astrocytes to neuronal oscillations across the brain, with a specific focus on how astrocytes respond to changes in brain state (e.g., sleep, arousal, stress). We then discuss the general mechanisms by which astrocytes signal to neurons to modulate neuronal activity, ultimately driving changes in behavior, followed by a discussion of how astrocytes contribute to respiratory rhythms in the medulla. Lastly, we contemplate the possibility that brainstem astrocytes could modulate brain-wide oscillations by communicating the status of oxygenation to higher cortical areas.

scholarly journals Astrocytes regulate brain extracellular pH via a neuronal activity-dependent bicarbonate shuttle

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Shefeeq M. Theparambil ◽  
Patrick S. Hosford ◽  
Iván Ruminot ◽  
Olga Kopach ◽  
James R. Reynolds ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Extracellular Ph ◽  
Ph Homeostasis ◽  
Sodium Bicarbonate Cotransporter ◽  
Highly Sensitive ◽  
Activity Dependent ◽  
The Brain ◽  
Local Brain

Abstract Brain cells continuously produce and release protons into the extracellular space, with the rate of acid production corresponding to the levels of neuronal activity and metabolism. Efficient buffering and removal of excess H+ is essential for brain function, not least because all the electrogenic and biochemical machinery of synaptic transmission is highly sensitive to changes in pH. Here, we describe an astroglial mechanism that contributes to the protection of the brain milieu from acidification. In vivo and in vitro experiments conducted in rodent models show that at least one third of all astrocytes release bicarbonate to buffer extracellular H+ loads associated with increases in neuronal activity. The underlying signalling mechanism involves activity-dependent release of ATP triggering bicarbonate secretion by astrocytes via activation of metabotropic P2Y1 receptors, recruitment of phospholipase C, release of Ca2+ from the internal stores, and facilitated outward HCO3− transport by the electrogenic sodium bicarbonate cotransporter 1, NBCe1. These results show that astrocytes maintain local brain extracellular pH homeostasis via a neuronal activity-dependent release of bicarbonate. The data provide evidence of another important metabolic housekeeping function of these glial cells.

scholarly journals CA 10 and CA 11 negatively regulate neuronal activity‐dependent growth of gliomas

2019 ◽  
Vol 13 (5) ◽  
pp. 1018-1032
Author(s):  
Bangbao Tao ◽  
Yiqun Ling ◽  
Youyou Zhang ◽  
Shu Li ◽  
Ping Zhou ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Dependent Growth ◽  
Activity Dependent

Reversible alterations of the neuronal activity in spontaneous intracranial hypotension

Cephalalgia ◽  
2015 ◽  
Vol 36 (2) ◽  
pp. 162-171 ◽  
Author(s):  
Shiori Amemiya ◽  
Koichi Takahashi ◽  
Tatsuo Mima ◽  
Naoki Yoshioka ◽  
Soichiro Miki ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Neuronal Activity ◽  
Intracranial Hypotension ◽  
Linear Regression Analysis ◽  
Spontaneous Intracranial Hypotension ◽  
Low Frequency ◽  
Network Activity ◽  
Performance Change ◽  
Spontaneous Neuronal Activity ◽  
The Right

Aim The aim of this article is to investigate the pathophysiology underlying the alternation of the cognitive function and neuronal activity in spontaneous intracranial hypotension (SIH). Methods Fifteen patients with SIH underwent resting-state functional magnetic resonance imaging and working-memory (WM) test one day before and one month after a surgical operation. Alternation of the cognitive function and spontaneous neuronal activity measured as amplitude of the low-frequency fluctuations (ALFF) and the functional connectivity of the default-mode network (DMN) and frontoparietal networks (FPNs) were evaluated. Results WM performance significantly improved post-operatively. Whole-brain linear regression analysis of the ALFF revealed a positive correlation between cognitive performance change and ALFF change in the precuneus while a negative correlation was found in the bilateral orbitofrontal cortices (OFCs) and right medial frontal cortex (MFC). The ALFF changes normalised with the WM performance improvement post-operatively. The FPN activity in the right OFC was also increased pre-operatively. Partial correlation analysis revealed a significant correlation between WM performance and right OFC activity controlled for right FPN activity. Conclusions The abnormal activity of the OFCs and MFC that is not originating from the synchronous intrinsic network activity, together with the decreased activity of the central node of the DMN, could lead to cognitive impairment in SIH that is reversible through restoration of the cerebrospinal fluid.

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