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Aluminum alters NMDA receptor 1A and 2A/B expression on neonatal hippocampal neurons in rats
Chia-Yi Yuan, Guoo-Shyng Hsu, Yih-Jing Lee
Journal of Biomedical Science , 2011, DOI: 10.1186/1423-0127-18-81
Abstract: Utilizing a cultured neuron cells in vitro model, we have assessed Al influence on neuronal specific gene expression alteration by immunoblot and immunohistochemistry and neural proliferation rate changes by MTT assay.Microscopic images showed that the neurite outgrowth of hippocampal neurons increased along with the Al dosages (37, 74 μM Al (AlCl3)). MTT results also indicated that Al increased neural cell viability. On the other hand, the immunocytochemistry staining suggested that the protein expressions of NMDAR 1A and NMDAR 2A/B decreased with the Al dosages (p < 0.05).Treated hippocampal neurons with 37 and 74 μM of Al for 14 days increased neural cell viability, but hampered NMDAR 1A and NMDAR 2A/B expressions. It was suggested that Al exposure might alter the development of hippocampal neurons in neonatal rats.Aluminum (Al) is the second most abundant mineral in the soil, and it is also the major component of many legal food additives [1]. Al toxicities have been reported in renal disease patient with dialysis, due to high aluminum content in the dialysate and/or ingestion of Al-containing phosphate binder [2], resulting in microcytic hypochromic anemia, dialysis osteomalacia and dialysis encephalopathy [3]. The Al-content in the brain of person with Alzheimer's disease (AD) was reported to be higher than the age-matched non-AD elderly [4], although there are certain number of other reports disagreed with it [5,6]. Al over-loading has also been demonstrated in premature infants receiving intravenous fluid therapy [7]. These observations may imply that Al toxicity had a higher incidence in the population with kidney malfunction or immature kidney, such as nephropathy patients or in neonates. Although the absorption of Al in the gastrointestinal tract is less than 0.3%, and absorbed Al is mostly excreted through kidney in healthy individuals [8], the toxicity of dietary Al has raised concerns under certain patho-physiological, or even healthy conditions.The ne
Dynamic Characteristics of the Hippocampal Neuron under Conductance’s Changing
Yueping Peng,Nan Zou,Haiying Wu
International Journal of Information Engineering and Electronic Business , 2011,
Abstract: The hippocampal CA1 pyramid neuron has plenty of discharge actions. In the thesis, the dynamic characteristics of the hippocampal neuron model are analyzed and discussed by the neurodynamic theory and methods. Under a certain amplitude current’s stimulation, the change of gNa(the maximum conductance of the transient sodium channel) and gKdr (the maximum conductance of the delay rectification potassium channel) can cause different dynamic characteristics of the neuron model. The transient Na+ current(INa ) caused by gNa is indispensable in the discharge’s formation process of the model. The model can generate the discharge process only when gNa reaches a certain threshold. In the discharge process of the neuron model, gNa’s changing affects little and the ISIs approximate to a straight line. The delay rectification K+ current(Ikdr) caused by gKdr isn’t indispensable in the discharge’s formation process of the model. But gKdr’s changing affects much in the discharge process of the neuron model. With gKdr’s changing, the neuron model undergoes different dynamic bifurcation process, and has plenty of discharge patterns such as the chaos, period, and so on. This investigation is helpful to know and investigate the dynamic characteristics and the bifurcation mechanism of the hippocampal neuron; and it provides a certain theory assist to investigate the neural diseases such as the Alzheimer disease by neurodynamics.
Developmental and Activity-Dependent miRNA Expression Profiling in Primary Hippocampal Neuron Cultures  [PDF]
Myrrhe van Spronsen, Eljo Y. van Battum, Marijn Kuijpers, Vamshidhar R. Vangoor, M. Liset Rietman, Joris Pothof, Laura F. Gumy, Wilfred F. J. van IJcken, Anna Akhmanova, R. Jeroen Pasterkamp, Casper C. Hoogenraad
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0074907
Abstract: MicroRNAs (miRNAs) are evolutionarily conserved non-coding RNAs of ~22 nucleotides that regulate gene expression at the level of translation and play vital roles in hippocampal neuron development, function and plasticity. Here, we performed a systematic and in-depth analysis of miRNA expression profiles in cultured hippocampal neurons during development and after induction of neuronal activity. MiRNA profiling of primary hippocampal cultures was carried out using locked nucleic-acid-based miRNA arrays. The expression of 264 different miRNAs was tested in young neurons, at various developmental stages (stage 2–4) and in mature fully differentiated neurons (stage 5) following the induction of neuronal activity using chemical stimulation protocols. We identified 210 miRNAs in mature hippocampal neurons; the expression of most neuronal miRNAs is low at early stages of development and steadily increases during neuronal differentiation. We found a specific subset of 14 miRNAs with reduced expression at stage 3 and showed that sustained expression of these miRNAs stimulates axonal outgrowth. Expression profiling following induction of neuronal activity demonstrates that 51 miRNAs, including miR-134, miR-146, miR-181, miR-185, miR-191 and miR-200a show altered patterns of expression after NMDA receptor-dependent plasticity, and 31 miRNAs, including miR-107, miR-134, miR-470 and miR-546 were upregulated by homeostatic plasticity protocols. Our results indicate that specific miRNA expression profiles correlate with changes in neuronal development and neuronal activity. Identification and characterization of miRNA targets may further elucidate translational control mechanisms involved in hippocampal development, differentiation and activity-depended processes.
Inhibition of RhoA GTPase and the subsequent activation of PTP1B protects cultured hippocampal neurons against amyloid β toxicity
Pedro J Chacon, Rosa Garcia-Mejias, Alfredo Rodriguez-Tebar
Molecular Neurodegeneration , 2011, DOI: 10.1186/1750-1326-6-14
Abstract: We show here that Aβ activates the RhoA GTPase by binding to p75NTR, thereby preventing the NGF-induced activation of protein tyrosine phosphatase 1B (PTP1B) that is required for neuron survival. We also show that the inactivation of RhoA GTPase and the activation of PTP1B protect cultured hippocampal neurons against the noxious effects of Aβ. Indeed, either pharmacological inhibition of RhoA with C3 ADP ribosyl transferase or the transfection of cultured neurons with a dominant negative form of RhoA protects cultured hippocampal neurons from the effects of Aβ. In addition, over-expression of PTP1B also prevents the deleterious effects of Aβ on cultured hippocampal neurons.Our findings indicate that potentiating the activity of NGF at the level of RhoA inactivation and PTP1B activation may represent a new means to combat the noxious effects of Aβ in Alzheimer's disease.According to the amyloid hypothesis, amyloid beta (Aβ) aggregates form deposits in the brain, the process that precipitates the different manifestations of Alzheimer's disease (AD) [1]. Consequently, most therapeutic approaches to treat AD centre on this peptide: on the one hand attempting to limit the production of Aβ or the formation of fibrils and aggregates [2,3], while on the other hand, favouring its clearance. Therapeutic approaches aimed at clearing Aβ plaques have received special attention, and methods for active or passive immunisation have proven effective in reducing Aβ content in the brain. Nevertheless, these strategies have failed to conclusively ameliorate or retard cognitive deterioration in AD patients [4,5].Another approach that could be considered involves blocking the signals induced by Aβ that provoke neuronal death. However, despite extensive studies into the effects of Aβ on neurons, our understanding of Aβ signalling remains fragmented, and a consistent framework for such processes has yet to be defined. Still, recent publications have reinforced the notion that Aβ interferes
Long-Term Recording of LTP in Cultured Hippocampal Slices  [PDF]
Ken Shimono,Michel Baudry,Lam Ho,Makoto Taketani,Gary Lynch
Neural Plasticity , 2002, DOI: 10.1155/np.2002.249
Abstract: Long-term potentiation (LTP) was elicited by high frequency stimulation in hippocampal slices cultured on multi-electrode arrays. LTP lasting more than 1 h was recorded in 75% of slices, and a significant number of slices exhibited a non-decaying LTP that lasted more than 48 h. LTP induction was completely and reversibly blocked by an antagonist of the NMDA receptor, APV. Our results suggest the possibility of using chronic recording in hippocampal slices cultured on multi-electrode arrays to study the mechanisms underlying LTP maintenance and stabilization.
Long-Term Culture of Rat Hippocampal Neurons at Low Density in Serum-Free Medium: Combination of the Sandwich Culture Technique with the Three-Dimensional Nanofibrous Hydrogel PuraMatrix  [PDF]
Ai Kaneko, Yoshiyuki Sankai
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0102703
Abstract: The primary culture of neuronal cells plays an important role in neuroscience. There has long been a need for methods enabling the long-term culture of primary neurons at low density, in defined serum-free medium. However, the lower the cell density, the more difficult it is to maintain the cells in culture. Therefore, we aimed to develop a method for long-term culture of neurons at low density, in serum-free medium, without the need for a glial feeder layer. Here, we describe the work leading to our determination of a protocol for long-term (>2 months) primary culture of rat hippocampal neurons in serum-free medium at the low density of 3×104 cells/mL (8.9×103 cells/cm2) without a glial feeder layer. Neurons were cultured on a three-dimensional nanofibrous hydrogel, PuraMatrix, and sandwiched under a coverslip to reproduce the in vivo environment, including the three-dimensional extracellular matrix, low-oxygen conditions, and exposure to concentrated paracrine factors. We examined the effects of varying PuraMatrix concentrations, the timing and presence or absence of a coverslip, the timing of neuronal isolation from embryos, cell density at plating, medium components, and changing the medium or not on parameters such as developmental pattern, cell viability, neuronal ratio, and neurite length. Using our method of combining the sandwich culture technique with PuraMatrix in Neurobasal medium/B27/L-glutamine for primary neuron culture, we achieved longer neurites (≥3,000 μm), greater cell viability (≥30%) for 2 months, and uniform culture across the wells. We also achieved an average neuronal ratio of 97%, showing a nearly pure culture of neurons without astrocytes. Our method is considerably better than techniques for the primary culture of neurons, and eliminates the need for a glial feeder layer. It also exhibits continued support for axonal elongation and synaptic activity for long periods (>6 weeks).
Study on the Hippocampal Neuron's Minimal Models' Discharge Patterns  [cached]
Yueping Peng,Haiying Wu,Nan Zou
International Journal of Image, Graphics and Signal Processing , 2011,
Abstract: The hippocampal CA1 pyramid neuron has plenty of discharge actions. The one-compartment model of CA1 pyramid neuron developed by David is a nine-dimension complex dynamic model. In the thesis, the currents related to the nine-dimension complex model are analyzed and classified by the model’s reduction theory and methods based on neurodynamics, and four minimal models are gotten: (I_Na+I_Kdr)-minimal model, (I_Na+I_M)-minimal model, (I_Na+I_Ca+I_y)-minimal model, and (I_Na+I_Ca+I_sAHP)-minimal model. These minimal models have plenty of dynamic actions, and under the current’s stimulation, they can all generate regular discharge and have period discharge pattern, bursting pattern, the chaos discharge pattern, and so on. Compared with the initial nine-dimension complex model, these minimal models’ dimension are much reduced, and are more convenient to numerical simulation, calculating, and analyzing. In addition, these minimal models provide a simpler and flexible method to discuss the specific currents’ dynamic characteristics and functions of the initial nine-dimension complex model by the theory of neurodynamics.
GABA Withdrawal Modifies Network Activity in Cultured Hippocampal Neurons  [PDF]
H. Golan,K. Mikenberg,V. Greenberger,M. Segal
Neural Plasticity , 2000, DOI: 10.1155/np.2000.31
Abstract: Dissociated hippocampal neurons, grown in culture for 2 to 3 weeks, tended to fire bursts of synaptic currents at fairly regular intervals, representing network activity. A brief exposure of cultured neurons to GABA caused a total suppression of the spontaneous network activity. Following a washout of GABA, the activity was no longer clustered in bursts and instead, the cells fired at a high rate tonic manner. The effect of removing GABA could be seen as long as 1 to 2 days after GABA withdrawal and is expressed as an increase in the number of active cells in a network, as well as in their firing rates. Such striking effects of GABA removal may underlie part of the GABA withdrawal syndrome seen elsewhere.
Full Length Bid is sufficient to induce apoptosis of cultured rat hippocampal neurons
Hans-Georg K?nig, Markus Rehm, Daniel Gudorf, Stan Krajewski, Atan Gross, Manus W Ward, Jochen HM Prehn
BMC Cell Biology , 2007, DOI: 10.1186/1471-2121-8-7
Abstract: Western blot experiments confirmed a translocation of FL-Bid to the mitochondria during excitotoxic apoptosis that was associated with the release of cytochrome-C from mitochondria. These results were confirmed by immunofluorescence analysis of Bid translocation during excitotoxic cell death using an antibody raised against the amino acids 1–58 of mouse Bid that is not able to detect tBid. Finally, inducible overexpression of FL-Bid or a Bid mutant that can not be cleaved by caspase-8 was sufficient to induce apoptosis in the hippocampal neuron cultures.Our data suggest that translocation of FL-Bid is sufficient for the activation of mitochondrial cell death pathways in response to glutamate receptor overactivation.Excitotoxic neuron death has been implicated in the pathogenesis of ischemic, traumatic, and seizure-induced brain injury [1]. When glutamate receptor overactivation is intense, cell death is necrotic and characterized by a disturbance of cellular ion and volume homeostasis, leading to mitochondrial membrane potential (ΔΨm) depolarization, free radical production, ATP depletion and early plasma membrane leakage [2-5]. However, when glutamate receptor overactivation is subtle, mitochondria transiently recover their energetics, and a delayed cell death may result [3,6,7]. Under these conditions, excitotoxic neuron death is associated with the release of the pro-apoptotic factors cytochrome-C (cyt-C) and Apoptosis-Inducing Factor (AIF) from mitochondria [6-10].The mechanisms of cyt-C and AIF release during excitotoxic neuron death remain unresolved. In the evolutionary conserved apoptosis pathway, the release of cyt-C requires the pro-apoptotic Bcl-2 family members Bax or Bak [11]. Both proteins are believed to form megachannels in the outer mitochondrial membrane large enough to release intermembrane space proteins [12]. In order to cause this increased permeability, Bax and Bak undergo a conformational change and insert into the outer mitochondrial membran
Formation of Essential Ultrastructural Interface between Cultured Hippocampal Cells and Gold Mushroom-Shaped MEA- Toward “IN-CELL” Recordings from Vertebrate Neurons  [PDF]
Anna Fendyur,Joseph Shappir,Micha E. Spira
Frontiers in Neuroengineering , 2011, DOI: 10.3389/fneng.2011.00014
Abstract: Using cultured Aplysia neurons we recently reported on the development of a novel approach in which an extracellular, non-invasive multi-electrode-array system provides multisite, attenuated, intracellular recordings of subthreshold synaptic potentials, and action potentials (APs), the so called “IN-CELL” recording configuration (to differentiate it from intracellular recordings). Because of its non-invasive nature, the configuration can be used for long term semi intracellular electrophysiological monitoring of APs and synaptic potentials. Three principals converge to generate the IN-CELL configuration: (a) engulfment of approximately 1 μm size gold mushroom-shaped microelectrodes (gMμE) by the neurons, (b) formation of high seal resistance between the cell’s plasma membrane and the engulfed gMμE, and (c), autonomous localized increased conductance of the membrane patch facing the gMμE. Using dissociated rat hippocampal cultures we report here that the necessary morphological and ultrastructural relationships to generate the IN-CELL recording configuration are formed between hippocampal cells and the gMμEs. Interestingly, even <1 μm thin branches expand and engulf the gMμE structures. Recordings of spontaneous electrical activity revealed fast ~2 ms, 0.04–0.75 mV positive monophasic APs (FPMP). We propose that the FPMP are attenuated APs generated by neurons that engulf gMμEs. Computer simulations of analog electrical circuits depicting the cell–gMμE configuration point out the parameters that should be altered to improve the neuron–gMμE electrical coupling.
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