Measurement of neuronal activity of individual neurons after stroke in the rat using a microwire electrode array

Zhang, Xueguo; Zhang, Rui Lan; Zhang, Zheng Gang; Chopp, Michael

doi:10.1016/j.jneumeth.2006.12.012

Cited by 15 publications

(10 citation statements)

References 29 publications

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“…This hyperactivity recovered to normal level again at 7 days, and then became hyperexcitability again at 14 days post-CCI ( Figure 4). A similar pattern of changes in neuronal activity in vivo has been reported in a middle cerebral artery occlusion model of brain ischemia in rats, in which neuronal activity was significantly reduced within the first day following injury, recovered to about normal level at 2 days postischemia, but reduced again at 7 days 8 . In the undercut model of brain injury in cats in vivo, there is an increased efficacy of excitatory …”

Section: Journal Of Neurotraumasupporting

confidence: 79%

“…An early decrease in neuronal activity has been documented as depressed excitatory transmission and network activity after injury in acute slice or organotypic slice culture 1-2 , as reduced action potential firing or multiunit activity in models of TBI in rats or cats [3][4] , and as reduced spontaneous multiunit activity and suppressed evoked potential in TBI patients 3,5 . Similarly, reductions in action potential firing and evoked potentials occur in neurons of the peri-infarct region immediately after ischemic stroke, and last for hours to days [6][7][8] .…”

Section: Introductionmentioning

confidence: 99%

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Transition from Initial Hypoactivity to Hyperactivity in Cortical Layer V Pyramidal Neurons after Traumatic Brain Injury In Vivo

Ping

Jin

2016

Journal of Neurotrauma

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Traumatic brain injury (TBI) often results in structural damage and a loss of neurons that is commonly accompanied by early changes in neuronal electrical activity. Loss of neuronal activity has been hypothesized to contribute to post-traumatic epileptogenesis through the regulation of homeostatic plasticity. The existence of activity loss in cortical neurons after TBI and its subsequent transition into hyperactivity over time is not well characterized, however, particularly in models of TBI in vivo. In the current study, changes in neuronal activity in the primary motor cortex after moderate controlled cortical impact (CCI) in mice were studied using a single-unit recording technique in vivo. Recordings were made at different time points after CCI from cortical layer V pyramidal neurons that were within 1-2 mm from the anterior edge of the injured foci. Within 1-4 h after CCI, the frequency of spontaneous single-unit activity depressed significantly, with the mean firing frequency decreasing from 2.59 ± 0.18 Hz in the sham group to 1.05 ± 0.20 Hz of the injured group. The firing frequencies recovered to the normal level at 1 day and 7 days post-CCI, but became significantly higher at 3 days and 14 days post-CCI. The results suggest that TBI caused initial loss of activity in neurons of the perilesional cortical region, which was followed by compensatory recovery and enhancement of activity. These time-dependent changes in neuronal activity may contribute to the development of hyperexcitability through homeostatic activity regulation.

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Section: Journal Of Neurotraumasupporting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Transition from Initial Hypoactivity to Hyperactivity in Cortical Layer V Pyramidal Neurons after Traumatic Brain Injury In Vivo

Ping

Jin

2016

Journal of Neurotrauma

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“…This non-invasive electrophysiological technique is superior to the patch clamp method. MEA can be applied to a wide variety of cells, especially in the study of excitable cells such as neurons (77), cardiomyocytes (78), muscle fibers (79), and pancreatic beta cells (80). Recently, we found MEA is also a powerful tool in study of amino acid sensing.…”

Section: Microelectrode Arraymentioning

confidence: 99%

Intestinal enteroendocrine L cells in amino acid sensing and diseases

Ding

Huang

et al. 2018

Front Biosci

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Enteroendocrine L cells are open-type enteroendocrine cells that play an important role in amino acid sensing. They detect amino acids by a number of membrane receptors such as calcium-sensing receptor and G protein coupled receptor family C group 6 subtype A. The receptors activate signaling pathways and trigger cellular electrical activities, inducing gut hormones secretion (glucagon-like peptide 1, glucagon-like peptide 2 and peptide YY). This review focuses on an array of findings on L cells as models, receptors and signaling pathways, electrical activities and hormones secretion in amino acid sensing. Several diseases that are closely related to L cells are also reviewed.

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“…At stroke onset, the cutoff of blood supply to the brain causes ATP depletion, immediate loss of cerebral ion homeostasis, sudden anoxic depolarization in the ischemic core and spreading depression (SD)-like depolarization in the ischemic penumbra or peri-infarct regions[65,66]. Large amounts of glutamate released from intracellular spaces into extracellular spaces increases intracellular Ca 2+ and Ca 2+ -dependent protease activity[51].…”

Section: Exploration Of the Multifaceted Protective Mechanisms Of Ipostcmentioning

confidence: 99%

Hurdles to Clear Before Clinical Translation of Ischemic Postconditioning Against Stroke

Zhao

2013

Transl. Stroke Res.

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Ischemic postconditioning has been established for its protective effects against stroke in animal models. It is performed after post-stroke reperfusion and refers to a series of induced ischemia or a single brief one. This review article addresses major hurdles in clinical translation of ischemic postconditioning to stroke patients, including potential hazards, the lack of well-defined protective paradigms, and the paucity of deeply-understood protective mechanisms. A hormetic model, often used in toxicology to describe a dose-dependent response to a toxic agent, is suggested to study both beneficial and detrimental effects of ischemic postconditioning. Experimental strategies are discussed, including how to define the hazards of ischemic (homologous) postconditioning and the possibility of employing non-ischemic (heterologous) postconditioning to facilitate clinical translation. This review concludes that a more detailed assessment of ischemic postconditioning and studies of a broad range of heterologous postconditioning models are warranted for future clinical translation.

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Measurement of neuronal activity of individual neurons after stroke in the rat using a microwire electrode array

Cited by 15 publications

References 29 publications

Transition from Initial Hypoactivity to Hyperactivity in Cortical Layer V Pyramidal Neurons after Traumatic Brain Injury In Vivo

Transition from Initial Hypoactivity to Hyperactivity in Cortical Layer V Pyramidal Neurons after Traumatic Brain Injury In Vivo

Intestinal enteroendocrine L cells in amino acid sensing and diseases

Hurdles to Clear Before Clinical Translation of Ischemic Postconditioning Against Stroke

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