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 Signal-to-noise ratio in the membrane potential of the owl's auditory coincidence detectors

2012 ◽  
Vol 108 (10) ◽  
pp. 2837-2845 ◽  
Author(s):  
Go Ashida ◽  
Kazuo Funabiki ◽  
Paula T. Kuokkanen ◽  
Richard Kempter ◽  
Catherine E. Carr
Keyword(s):  
Neural Circuit ◽  
Signal To Noise Ratio ◽  
Phase Locking ◽  
Low Frequency ◽  
Membrane Potentials ◽  
Signal To Noise ◽  
Theoretical Predictions ◽  
Noise Ratio ◽  
Band Limited

Owls use interaural time differences (ITDs) to locate a sound source. They compute ITD in a specialized neural circuit that consists of axonal delay lines from the cochlear nucleus magnocellularis (NM) and coincidence detectors in the nucleus laminaris (NL). Recent physiological recordings have shown that tonal stimuli induce oscillatory membrane potentials in NL neurons (Funabiki K, Ashida G, Konishi M. J Neurosci 31: 15245–15256, 2011). The amplitude of these oscillations varies with ITD and is strongly correlated to the firing rate. The oscillation, termed the sound analog potential, has the same frequency as the stimulus tone and is presumed to originate from phase-locked synaptic inputs from NM fibers. To investigate how these oscillatory membrane potentials are generated, we applied recently developed signal-to-noise ratio (SNR) analysis techniques (Kuokkanen PT, Wagner H, Ashida G, Carr CE, Kempter R. J Neurophysiol 104: 2274–2290, 2010) to the intracellular waveforms obtained in vivo. Our theoretical prediction of the band-limited SNRs agreed with experimental data for mid- to high-frequency (>2 kHz) NL neurons. For low-frequency (≤2 kHz) NL neurons, however, measured SNRs were lower than theoretical predictions. These results suggest that the number of independent NM fibers converging onto each NL neuron and/or the population-averaged degree of phase-locking of the NM fibers could be significantly smaller in the low-frequency NL region than estimated for higher best-frequency NL.

scholarly journals Microglia motility depends on neuronal activity and promotes structural plasticity in the hippocampus

2019 ◽  
Author(s):  
Felix C. Nebeling ◽  
Stefanie Poll ◽  
Lena C. Schmid ◽  
Manuel Mittag ◽  
Julia Steffen ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Dendritic Spines ◽  
Synapse Formation ◽  
Brain Parenchyma ◽  
Two Photon ◽  
Contact Rates ◽  
Health And Disease ◽  
The Impact ◽  
The Brain

AbstractMicroglia, the resident immune cells of the brain, play a complex role in health and disease. They actively survey the brain parenchyma by physically interacting with other cells and structurally shaping the brain. Yet, the mechanisms underlying microglia motility and their significance for synapse stability, especially during adulthood, remain widely unresolved. Here we investigated the impact of neuronal activity on microglia motility and its implication for synapse formation and survival. We used repetitive two-photon in vivo imaging in the hippocampus of awake mice to simultaneously study microglia motility and their interaction with synapses. We found that microglia process motility depended on neuronal activity. Simultaneously, more dendritic spines emerged in awake compared to anesthetized mice. Interestingly, microglia contact rates with individual dendritic spines were associated with their stability. These results suggest that microglia are not only sensing neuronal activity, but participate in synaptic rewiring of the hippocampus during adulthood, which has profound relevance for learning and memory processes.

Biophysical basis of brain activity: implications for neuroimaging

2002 ◽  
Vol 35 (3) ◽  
pp. 287-325 ◽  
Author(s):  
Robert G. Shulman ◽  
Fahmeed Hyder ◽  
Douglas L. Rothman
Keyword(s):  
Energy Consumption ◽  
Magnetic Resonance ◽  
Neuronal Activity ◽  
Glucose Oxidation ◽  
Activity Level ◽  
Quantitative Relation ◽  
Cerebral Function ◽  
Level Of Activity ◽  
The Brain

1. Summary 2882. Introduction 2883. Relationship between neuroenergetics and neurotransmitter flux 2944. A model of coupling between neuroenergetics and neurotransmission 2965. Relationship between neuroenergetics and neural spiking frequency 2976. Comparison with previous electrophysiological and fMRI measurements 2987. Contributions of non-oxidative energetics to a primarily oxidative brain 2998. Possible explanation for non-oxidative energetics contributions 3009. A model of total neuronal activity to support cerebral function 30210. Implications for interpretation of fMRI studies 30511. The restless brain 30612. Acknowledgements 31013. Appendix A. CMRO2by13C-MRS 31014. Appendix B.Vcycand test of model 31315. Appendix C. CMRO2by calibrated BOLD 31616. Appendix D. Comparison of spiking activity of a neuronal ensemble with CMRO231817. References 320In vivo13C magnetic resonance spectroscopy (MRS) studies of the brain have quantitatively assessed rates of glutamate–glutamine cycle (Vcyc) and glucose oxidation (CMRGlc(ox)) by detecting 13C label turnover from glucose to glutamate and glutamine. Contrary to expectations from in vitro and ex vivo studies, the in vivo13C-MRS results demonstrate that glutamate recycling is a major metabolic pathway, inseparable from its actions of neurotransmission. Furthermore, both in the awake human and in the anesthetized rat brain, Vcyc and CMRGlc(ox) are stoichiometrically related, where more than two thirds of the energy from glucose oxidation supports events associated with glutamate neurotransmission. The high energy consumption of the brain measured at rest and its quantitative relation to neurotransmission reflects a sizeable activity level for the resting brain. The high activity of the non-stimulated brain, as measured by cerebral metabolic rate of oxygen use (CMRO2), establishes a new neurophysiological basis of cerebral function that leads to reinterpreting functional imaging data because the large baseline signal is commonly discarded in cognitive neuroscience paradigms. Changes in energy consumption (ΔCMRO2%) can also be obtained from magnetic resonance imaging (MRI) experiments, using the blood oxygen level- dependent (BOLD) image contrast, provided that all the separate parameters contributing to the functional MRI (fMRI) signal are measured. The BOLD-derived ΔCMRO2% when compared with alterations in neuronal spiking rate (Δν%) during sensory stimulation in the rat reveals a stoichiometric relationship, in good agreement with 13C-MRS results. Hence fMRI when calibrated so as to provide ΔCMRO2% can provide high spatial resolution evaluation of neuronal activity. Our studies of quantitative measurements of changes in neuroenergetics and neurotransmission reveal that a stimulus does not provoke an arbitrary amount of activity in a localized region, rather a total level of activity is required where the increment is inversely related to the level of activity in the non-stimulated condition. These biophysical experiments have established relationships between energy consumption and neuronal activity that provide novel insights into the nature of brain function and the interpretation of fMRI data.

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 Latrophilin GPCR Signaling Mediates Synapse Formation

2021 ◽  
Author(s):  
Richard Sando ◽  
Thomas C. Südhof
Keyword(s):  
Synapse Formation ◽  
Neural Circuit ◽  
Gpcr Signaling ◽  
Synapse Loss ◽  
Ca1 Region ◽  
In Trans ◽  
Synaptic Complexes ◽  
Camp Levels ◽  
The Brain

ABSTRACTNeural circuit assembly in the brain requires precise establishment of synaptic connections, but the mechanisms of synapse assembly remain incompletely understood. Latrophilins are postsynaptic adhesion-GPCRs that engage in trans-synaptic complexes with presynaptic teneurins and FLRTs. In CA1-region neurons, Latrophilin-2 and Latrophilin-3 are essential for formation of entorhinal-cortex-derived and Schaffer-collateral-derived synapses, respectively. However, it is unknown whether latrophilins function as GPCRs in synapse formation. Here, we show that Latrophilin-2 and Latrophilin-3 exhibit constitutive GPCR activity that increases cAMP levels, which was blocked by a mutation interfering with G-protein and arrestin interactions of GPCRs. The same mutation impaired the ability of Latrophilin-2 and Latrophilin-3 to rescue the synapse-loss phenotype in Latrophilin-2 and Latrophilin-3 knockout neurons in vivo. Our results suggest that Latrophilin-2 and Latrophilin-3 require GPCR signaling in synapse formation, indicating that latrophilins promote synapse formation in the hippocampus by activating a classical GPCR-signaling pathway.

scholarly journals Protein lactylation induced by neural excitation

2021 ◽  
Author(s):  
Hideo Hagihara ◽  
Hirotaka Shoji ◽  
Hikari Otabi ◽  
Atsushi Toyoda ◽  
Kaoru Katoh ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Monocarboxylate Transporter ◽  
Brain Cells ◽  
Post Translational Modification ◽  
High Potassium ◽  
Neural Excitation ◽  
Lactate Levels ◽  
The Brain ◽  
Prefrontal Cortices

AbstractLactate is known to have diverse roles in the brain at the molecular and behavioral levels under both physiological and pathophysiological conditions, such as learning and memory and regulation of mood. Recently, a novel post-translational modification called lysine lactylation has been found in histone H3 of mouse macrophages, and the lactylation levels paralleled the intracellular lactate levels1. However, it is unknown whether lysine lactylation occurs in brain cells, and if it does, whether lactylation is induced by the stimuli that accompany changes in lactate levels. Herein, we reveal that lysine lactylation in brain cells is regulated by systemic changes in lactate levels, neural excitation, and behaviorally relevant stimuli. Lysine lactylation levels were increased by lactate treatment and by high-potassium-induced depolarization in cultured primary neurons; these increases were attenuated by pharmacological inhibition of monocarboxylate transporter 2 and lactate dehydrogenase, respectively, suggesting that both cell-autonomous and non-cell-autonomous neuronal mechanisms are involved in overall lysine lactylation. In vivo, electroconvulsive stimulation increased lysine lactylation levels in the prefrontal cortices of mice, and its levels were positively correlated with the expression levels of the neuronal activity marker c-Fos on an individual cell basis. In the social defeat stress model of depression in which brain lactate levels increase, lactylation levels were increased in the prefrontal cortices of the defeated mice, which was accompanied by increased c-Fos expression, decreased social behaviors, and increased anxiety-like behaviors, suggesting that stress-induced neuronal excitation may induce lysine lactylation, thereby affecting mood-related behaviors. Further, we identified 63 candidate lysine-lactylated proteins in the mouse cortex and found that lactylation levels in histone H1 increased in response to defeat stress. This study may open up an avenue for exploration of a novel role of neuronal activity-induced lactate mediated by protein lactylation in the brain.

scholarly journals Brain Endothelial Cell TRPA1 Channels Initiate Neurovascular Coupling

2020 ◽  
Author(s):  
Pratish Thakore ◽  
Michael G. Alvarado ◽  
Sher Ali ◽  
Amreen Mughal ◽  
Paulo W. Pires ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Neuronal Activity ◽  
Transient Receptor Potential ◽  
Neurovascular Coupling ◽  
Laser Scanning Microscopy ◽  
K Channel ◽  
Transitional Region ◽  
Capillary Endothelial Cells ◽  
The Brain

Blood flow regulation in the brain is dynamically regulated to meet the metabolic demands of active neuronal populations. Recent evidence has demonstrated that capillary endothelial cells are essential mediators of neurovascular coupling that sense neuronal activity and generate a retrograde, propagating, hyperpolarizing signal that dilates upstream arterioles. Here, we tested the hypothesis that transient receptor potential ankyrin 1 (TRPA1) channels in capillary endothelial cells are significant contributors to functional hyperemic responses that underlie neurovascular coupling in the brain. Using an integrative ex vivo and in vivo approach, we demonstrate the functional presence of TRPA1 channels in brain capillary endothelial cells, and show that activation of these channels within the capillary bed, including the post-arteriole transitional region covered by ensheathing mural cells, initiates a retrograde signal that dilates upstream parenchymal arterioles. Notably, this signaling exhibits a unique biphasic mode of propagation that begins within the capillary network as a short-range, Ca2+ signal dependent on endothelial pannexin-1 channel/purinergic P2X receptor communication pathway and then is converted to a rapid, inward-rectifying K+ channel-mediated electrical signal in the post-arteriole transitional region that propagates upstream to parenchymal arterioles. Two-photon laser-scanning microscopy further demonstrated that conductive vasodilation occurs in vivo, and that TRPA1 is necessary for functional hyperemia within the somatosensory cortex of mice. Together, these data establish a role for endothelial TRPA1 channels as sensors of neuronal activity and show that they respond accordingly by initiating a vasodilatory response that redirects blood to regions of metabolic demand.

Abstract 82: In Vivo Memri Reveals Persistent Activation of the Pvn by an Acute Systemic Angiotensin Ii Injection

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Jasenka Zubcevic ◽  
Pablo D Perez ◽  
Jessica Marulanda Carvajal ◽  
Mohan K Raizada ◽  
Marcelo Febo
Keyword(s):  
Neuronal Activity ◽  
Spontaneously Hypertensive Rat ◽  
Pressor Response ◽  
Neuronal Response ◽  
Neuronal Activation ◽  
Brain Areas ◽  
Neurogenic Hypertension ◽  
Wistar Kyoto ◽  
The Brain

Introduction: An overactive brain renin-angiotensin system is a major factor in the establishment of neurogenic hypertension in the spontaneously hypertensive rat (SHR). However, there is no concrete evidence to indicate that this is associated with enhanced neuronal activity in the brain. The objective here was to use the MRI to establish the effect of ANGII on neuronal activity in the autonomic brain areas. We propose that a single ANGII injection will cause a long-lasting neuronal response in the autonomic brain areas, which will be exaggerated in the SHR. Methods: In vivo basal and ANGII-evoked neuronal activity was measured in the Wistar-Kyoto (WKY) rat and the SHR using manganese-enhanced MRI (MEMRI) at 4.7Tesla. Rats were treated with manganese chloride (MnCl 2 30 mM solution, i.p .;16-20 hrs prior to the MRI), which labels active neurons. T 1 -weighted images were obtained 16-20 hrs after a single ANGII injection (0.32μg/kg i.p.). Coronal slice scans (caudally from end of the cerebellum towards the hypothalamus) were processed using itkSNAP, and data analyzed for normalized signal intensity. Results: Acute ANGII injection caused an immediate pressor response in the WKY (ΔSBP=∼20mmHg), normalizing within 2 hours. Despite this, ANGII evoked a persistent PVN neuronal activation, which was elevated by 22±4% in the WKY, and by 187±45% in the PVN of SHR. As a result, there was a ∼8.5fold increase in the ANGII-dependent neuronal activity in the PVN of SHR compared to WKY. Furthermore, there was a ∼2.5fold decrease in the NTS neuronal activity in the SHR compared to WKY. Conclusion: The present study shows for the first time the correlation between ANGII and autonomic neuronal activation. Even a single systemic ANGII injection results in a lasting effect on the brain. This is particularly apparent in the SHR, which exhibited an exaggerated neuronal response to the ANGII stimulus, reflected in the elevated PVN neuronal activation corresponding to the enhanced sympathetic drive, and in the depressed NTS activation corresponding to the dysfunction in the barorereflex processing. Thus, repeated pro-hypertensive stimuli in the autonomic brain areas may lead to pre-sympathetic neuronal plasticity, resulting in heightened sympathetic drive and hypertension.

scholarly journals Reduction of neuronal activity mediated by blood-vessel regression in the brain

2020 ◽  
Author(s):  
Xiaofei Gao ◽  
Jun-Liszt Li ◽  
Xingjun Chen ◽  
Bo Ci ◽  
Fei Chen ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Neuronal Activity ◽  
Leukocyte Adhesion ◽  
Adult Brain ◽  
Brain Vasculature ◽  
Vessel Regression ◽  
Blood Flow Occlusion ◽  
Human Brains ◽  
The Brain

SummaryThe brain vasculature supplies neurons with glucose and oxygen, but little is known about how vascular plasticity contributes to brain function. Using longitudinal in vivo imaging, we reported that a substantial proportion of blood vessels in the adult brain sporadically occluded and regressed. Their regression proceeded through sequential stages of blood-flow occlusion, endothelial cell collapse, relocation or loss of pericytes, and retraction of glial endfeet. Regressing vessels were found to be widespread in mouse, monkey and human brains. Both brief occlusions of the middle cerebral artery and lipopolysaccharide-mediated inflammation induced an increase of vessel regression. Blockage of leukocyte adhesion to endothelial cells alleviated LPS-induced vessel regression. We further revealed that blood vessel regression caused a reduction of neuronal activity due to a dysfunction in mitochondrial metabolism and glutamate production. Our results elucidate the mechanism of vessel regression and its role in neuronal function in the adult brain.

scholarly journals Electroacupuncture Treatment Alleviates the Remifentanil-Induced Hyperalgesia by Regulating the Activities of the Ventral Posterior Lateral Nucleus of the Thalamus Neurons in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Hong-Yan Zhao ◽  
Ling-Yu Liu ◽  
Jie Cai ◽  
Yan-Jun Cui ◽  
Guo-Gang Xing
Keyword(s):  
Neuronal Activity ◽  
Field Potential ◽  
Low Frequency ◽  
Thermal Hyperalgesia ◽  
Neuronal Firing ◽  
Mechanical Stimuli ◽  
Theta Band ◽  
Spontaneous Neuronal Activity ◽  
Lateral Nucleus

Mechanisms underlying remifentanil- (RF-) induced hyperalgesia, a phenomenon that is generally named as opioid-induced hyperalgesia (OIH), still remain elusive. The ventral posterior lateral nucleus (VPL) of the thalamus, a key relay station for the transmission of nociceptive information to the cerebral cortex, is activated by RF infusion. Electroacupuncture (EA) is an effective method for the treatment of pain. This study aimed to explore the role of VPL in the development of OIH and the effect of EA treatment on OIH in rats. RF was administered to rats via the tail vein for OIH induction. Paw withdrawal threshold (PWT) in response to mechanical stimuli and paw withdrawal latency (PWL) to thermal stimulation were tested in rats for the assessment of mechanical allodynia and thermal hyperalgesia, respectively. Spontaneous neuronal activity and local field potential (LFP) in VPL were recorded in freely moving rats using the in vivo multichannel recording technique. EA at 2 Hz frequency (pulse width 0.6 ms, 1–3 mA) was applied to the bilateral acupoints “Zusanli” (ST.36) and “Sanyinjiao” (SP.6) in rats. The results showed that both the PWT and PWL were significantly decreased after RF infusion to rats. Meanwhile, both the spontaneous neuronal firing rate and the theta band oscillation in VPL LFP were increased on day 3 post-RF infusion, indicating that the VPL may promote the development of RF-induced hyperalgesia by regulating the pain-related cortical activity. Moreover, 2 Hz-EA reversed the RF-induced decrease both in PWT and PWL of rats and also abrogated the RF-induced augmentation of the spontaneous neuronal activity and the power spectral density (PSD) of the theta band oscillation in VPL LFP. These results suggested that 2 Hz-EA attenuates the remifentanil-induced hyperalgesia via reducing the excitability of VPL neurons and the low-frequency (theta band) oscillation in VPL LFP.

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