Glutamine Protects Neuronal Function Against Hypoxia in vitro

The mechanism of mild traumatic brain injury (mTBI) is directly related to the relationship between the mechanical response of neurons and their biological/chemical functions since the neuron is the main functional component of brain.1 The hypotheses is that the external mechanical load will firstly cause the mechanical deformation of neurons, and then, when the mechanical deformation of neurons reaches to a critical point (the mechanical deformation threshold), it will initiate the chemical/biological response (e.g. neuronal function loss). Therefore, defining and measuring the mechanical deformation threshold for the neuronal cell injury is an important first step to understand the mechanism of mTBI. Typically, the mechanical response of neurons is investigated based on the deformation of in vitro model, in which the neurons are cultured on the elastic substrate (e.g. PDMS membranes). The elastic membrane is deformed by the external load, e.g. equibiaxial stretching. The substrate deformation is considered to be the deformation of neurons since the substrate is several orders stiffer than the neurons and the neurons are perfectly bonded with the substrate. The fluoresce method is typically used to test the cell injury, e.g. the cell vitality and the neuron internal ROS level.1, 2

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Sustained elevation of extracellular adenosine and activation of A1 receptors underlie the post-ischaemic inhibition of neuronal function in rat hippocampus in vitro

Journal of Neurochemistry ◽

10.1111/j.1471-4159.2006.03823.x ◽

2006 ◽

Vol 97 (5) ◽

pp. 1357-1368 ◽

Cited By ~ 51

Author(s):

Tim Pearson ◽

Karen Damian ◽

Rachel E. Lynas ◽

Bruno G. Frenguelli

Keyword(s):

Rat Hippocampus ◽

Neuronal Function ◽

Extracellular Adenosine

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Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Journal of Applied Physiology ◽

10.1152/japplphysiol.00920.2002 ◽

2003 ◽

Vol 95 (3) ◽

pp. 883-909 ◽

Cited By ~ 70

Author(s):

Jay B. Dean ◽

Daniel K. Mulkey ◽

Alfredo J. Garcia ◽

Robert W. Putnam ◽

Richard A. Henderson

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Ambient Pressure ◽

Inert Gases ◽

Neuronal Function ◽

Cellular Mechanisms ◽

Electrophysiological Studies ◽

The Central Nervous System ◽

Electrophysiological Methods

As ambient pressure increases, hydrostatic compression of the central nervous system, combined with increasing levels of inspired Po2, Pco2, and N2partial pressure, has deleterious effects on neuronal function, resulting in O2toxicity, CO2toxicity, N2narcosis, and high-pressure nervous syndrome. The cellular mechanisms responsible for each disorder have been difficult to study by using classic in vitro electrophysiological methods, due to the physical barrier imposed by the sealed pressure chamber and mechanical disturbances during tissue compression. Improved chamber designs and methods have made such experiments feasible in mammalian neurons, especially at ambient pressures <5 atmospheres absolute (ATA). Here we summarize these methods, the physiologically relevant test pressures, potential research applications, and results of previous research, focusing on the significance of electrophysiological studies at <5 ATA. Intracellular recordings and tissue Po2measurements in slices of rat brain demonstrate how to differentiate the neuronal effects of increased gas pressures from pressure per se. Examples also highlight the use of hyperoxia (≤3 ATA O2) as a model for studying the cellular mechanisms of oxidative stress in the mammalian central nervous system.

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Hypoxia and Neuronal Function under in Vitro Conditions

Pharmacology & Therapeutics ◽

10.1016/s0163-7258(98)00061-8 ◽

1999 ◽

Vol 82 (1) ◽

pp. 71-86 ◽

Cited By ~ 41

Author(s):

Karen Nieber

Keyword(s):

Neuronal Function

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Lactic acidosis and recovery of neuronal function following cerebral hypoxia in vitro

Brain Research ◽

10.1016/0006-8993(88)91354-6 ◽

1988 ◽

Vol 438 (1-2) ◽

pp. 311-314 ◽

Cited By ~ 55

Author(s):

Avital Schurr ◽

Wei-Quiang Dong ◽

Kenneth H. Reid ◽

Catherine A. West ◽

Benjamin M. Rigor

Keyword(s):

Lactic Acidosis ◽

Cerebral Hypoxia ◽

Neuronal Function

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Author response: TrpV1 receptor activation rescues neuronal function and network gamma oscillations from Aβ-induced impairment in mouse hippocampus in vitro

10.7554/elife.37703.025 ◽

2018 ◽

Author(s):

Hugo Balleza-Tapia ◽

Sophie Crux ◽

Yuniesky Andrade-Talavera ◽

Pablo Dolz-Gaiton ◽

Daniela Papadia ◽

...

Keyword(s):

Gamma Oscillations ◽

Receptor Activation ◽

Author Response ◽

Neuronal Function ◽

Trpv1 Receptor ◽

Mouse Hippocampus

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Abstract P358: Cardiac Innervation Remodeling And Impaired Brain Derived Neurotrophic Factor (bdnf) Levels In Physiological Aging Vivo Model

Circulation Research ◽

10.1161/res.129.suppl_1.p358 ◽

2021 ◽

Vol 129 (Suppl_1) ◽

Author(s):

Andrea Elia ◽

Alessandro Cannavo ◽

Giuseppina Gambino ◽

Maria Cimini ◽

Nicola Ferrara ◽

...

Keyword(s):

Nervous System ◽

Nerve Fibers ◽

Autonomic Nerve ◽

Cardiac Innervation ◽

Neuronal Function ◽

Rat Serum ◽

Physiological Aging ◽

Protein Levels ◽

Old Rats

Aging is a multifactorial process associated with gradual loss of function and decay involving several neurohormonal systems, such as the autonomic nervous system (ANS). Progressive remodeling of ANS, induces a circulating catecholamines spillover and cardiac autonomic fibers depletion with raising both morbidities and mortality risk. Neurotrophic factors (NF) play a pivotal role in modulating neuronal function and are impaired in cardiovascular disorders. Whether and how physiological aging impacts these neurobiomarkers and cardiac innervation remains still unclear. Therefore, we investigated the impact of aging on neurotrophins (such as BDNF and NGF) production and secretion and its consequences, on cardiac nervous system homeostasis. In vivo, we used young (age: 3 months; n=10) and old (age: 24 months; n=11) male Fisher rats. In vitro, human neuroblastoma cells (SH-SY5Y) were stimulated with serum withdrawn from both experimental groups. Old rats showed a significant reduction in overall ANS fiber density, sympathetic (marked by dopamine β-hydroxylase, dβh) and cholinergic compartment (evidenced by vesicular acetylcholine transporter, VaChT) compared to the young group, assessed by immunohistochemical staining. In addition, we observed a marked downregulation of GAP-43 and BDNF protein levels in left ventricle total lysates via immunoblot analysis, in aged hearts as opposed to young ones. Conversely, no changes were observed in NGF protein expression. To further investigate the autocrine effect of aging on autonomic nerve fibers, we treated SH-SY5Y cells in vitro, with blood serum obtained by young or old rats. Both stimuli induced a remarkable increase in neuronal sprouting, as evidenced via crystal violet assay. Nevertheless, we found a bulky drop in the neuronal function of cells stimulated with old rat serum. Interestingly, this effect was accompanied by a sizeable blunt in GAP-43 and BDNF protein levels, compared to cells treated with young rat serum. Taken together, our data suggest that neuronal function impairment aging-induced associated with significant BDNF impoverishment, might favor maladaptive remodeling of cardiac ANS.

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