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Статті в журналах з теми "Substrat neuronal"

Автор: Grafiati

Опубліковано: 15 березня 2025

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1

Zarka, D., A. M. Cebolla, and G. Cheron. "Neurones miroirs, substrat neuronal de la compréhension de l’action?" L'Encéphale 48, no. 1 (February 2022): 83–91. http://dx.doi.org/10.1016/j.encep.2021.06.005.

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2

Rutka, Roman, Anne Denis, Laurent Vercueil, and Pascal Hot. "Crises psychogènes non épileptiques : état des connaissances et apports de l’évaluation des traitements émotionnels." Santé mentale au Québec 41, no. 1 (July 5, 2016): 123–39. http://dx.doi.org/10.7202/1036968ar.

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Des crises psychogènes non épileptiques (CPNE) sont des manifestations transitoires d’allure neurologique pouvant évoquer, à tort, le diagnostic de crise épileptique, mais qui n’en présentent en réalité pas l’origine neurologique. Les CPNE ont rencontré ces cinq dernières années un intérêt croissant tant dans la description de la population concernée, que des origines du trouble et du substrat neuronal qui pourraient les sous-tendre. L’existence d’un profil particulier de traitements émotionnels constitue à ce jour une piste prometteuse de caractérisation de cette population qui a reçu une série de confirmations récentes. Nous présentons ici les données issues de différents domaines allant de la psychologie clinique aux neurosciences affectives et examinant les spécificités de traitements émotionnels rapportés dans les CPNE, ainsi que les pistes d’études à développer afin de mieux les caractériser.

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3

Friedlander, D. R., P. Milev, L. Karthikeyan, R. K. Margolis, R. U. Margolis, and M. Grumet. "The neuronal chondroitin sulfate proteoglycan neurocan binds to the neural cell adhesion molecules Ng-CAM/L1/NILE and N-CAM, and inhibits neuronal adhesion and neurite outgrowth." Journal of Cell Biology 125, no. 3 (May 1, 1994): 669–80. http://dx.doi.org/10.1083/jcb.125.3.669.

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We have previously shown that aggregation of microbeads coated with N-CAM and Ng-CAM is inhibited by incubation with soluble neurocan, a chondroitin sulfate proteoglycan of brain, suggesting that neurocan binds to these cell adhesion molecules (Grumet, M., A. Flaccus, and R. U. Margolis. 1993. J. Cell Biol. 120:815). To investigate these interactions more directly, we have tested binding of soluble 125I-neurocan to microwells coated with different glycoproteins. Neurocan bound at high levels to Ng-CAM and N-CAM, but little or no binding was detected to myelin-associated glycoprotein, EGF receptor, fibronectin, laminin, and collagen IV. The binding to Ng-CAM and N-CAM was saturable and in each case Scatchard plots indicated a high affinity binding site with a dissociation constant of approximately 1 nM. Binding was significantly reduced after treatment of neurocan with chondroitinase, and free chondroitin sulfate inhibited binding of neurocan to Ng-CAM and N-CAM. These results indicate a role for chondroitin sulfate in this process, although the core glycoprotein also has binding activity. The COOH-terminal half of neurocan was shown to have binding properties essentially identical to those of the full-length proteoglycan. To study the potential biological functions of neurocan, its effects on neuronal adhesion and neurite growth were analyzed. When neurons were incubated on dishes coated with different combinations of neurocan and Ng-CAM, neuronal adhesion and neurite extension were inhibited. Experiments using anti-Ng-CAM antibodies as a substrate also indicate that neurocan has a direct inhibitory effect on neuronal adhesion and neurite growth. Immunoperoxidase staining of tissue sections showed that neurocan, Ng-CAM, and N-CAM are all present at highest concentration in the molecular layer and fiber tracts of developing cerebellum. The overlapping localization in vivo, the molecular binding studies, and the striking effects on neuronal adhesion and neurite growth support the view that neurocan may modulate neuronal adhesion and neurite growth during development by binding to neural cell adhesion molecules.

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4

Gruenbaum, Lore M., and Thomas J. Carew. "Growth Factor Modulation of Substrate-Specific Morphological Patterns in Aplysia Bag Cell Neurons." Learning & Memory 6, no. 3 (May 1, 1999): 292–306. http://dx.doi.org/10.1101/lm.6.3.292.

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Components of the extracellular matrix (ECM) can act not only as passive substrates for neuronal attachment and outgrowth but also as active sites for signal transduction. Thus, specific ECM components may modulate effects of growth factors (GFs) that play an important role in structural changes in development and adult neuronal plasticity. In this study we examined the interaction of cultured Aplysia bag cell neurons (BCNs) with components of ECM and different GFs. Different ECM substrata induce a substrate-specific BCN morphology: BCNs grown on collagen or poly-l-lysine have larger soma diameter and more extensive neurite outgrowth than BCNs grown on laminin or fibronectin. BCNs also interact in a substrate-dependent way with GFs: BDNF treatment leads to a reduction of outgrowth on poly-l-lysine but an enhancement on fibronectin and laminin. CNTF reduces the soma diameter on collagen IV but enlarges it on laminin or fibronectin. In contrast, NGF induces a reduction of both soma diameter and outgrowth, on all substrata. Plating of BCNs in the presence of anti-β1-integrin reduces adhesion to fibronectin but does not change outgrowth. In contrast, RGD peptides block adhesion to laminin and poly-l-lysine and, additionally, reduce outgrowth on laminin. These data suggest that BCNs use different β1-integrin-dependent as well as RGD-dependent mechanisms for adhesion and outgrowth on different ECM substrata, providing possible sites of modulation by specific GFs.

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5

Vorhold, Verena. "The Neuronal Substrate of Risky Choice." Annals of the New York Academy of Sciences 1128, no. 1 (April 2008): 41–52. http://dx.doi.org/10.1196/annals.1399.006.

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6

TOESCU, E. C., and J. XIONG. "Metabolic Substrates of Neuronal Aging." Annals of the New York Academy of Sciences 1019, no. 1 (June 2004): 19–23. http://dx.doi.org/10.1196/annals.1297.004.

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7

da Cunha, A., L. E. Eiden, and D. M. Rausch. "Neuronal substrates for SIV encephalopathy." Advances in Neuroimmunology 4, no. 3 (January 1994): 265–71. http://dx.doi.org/10.1016/s0960-5428(06)80266-4.

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8

Athamneh, Ahmad I. M., Alexander X. Cartagena-Rivera, Arvind Raman, and Daniel M. Suter. "Substrate Deformation Predicts Neuronal Growth Cone Advance." Biophysical Journal 109, no. 7 (October 2015): 1358–71. http://dx.doi.org/10.1016/j.bpj.2015.08.013.

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9

Calof, A. L., and A. D. Lander. "Relationship between neuronal migration and cell-substratum adhesion: laminin and merosin promote olfactory neuronal migration but are anti-adhesive." Journal of Cell Biology 115, no. 3 (November 1, 1991): 779–94. http://dx.doi.org/10.1083/jcb.115.3.779.

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Regulation by the extracellular matrix (ECM) of migration, motility, and adhesion of olfactory neurons and their precursors was studied in vitro. Neuronal cells of the embryonic olfactory epithelium (OE), which undergo extensive migration in the central nervous system during normal development, were shown to be highly migratory in culture as well. Migration of OE neuronal cells was strongly dependent on substratum-bound ECM molecules, being specifically stimulated and guided by laminin (or the laminin-related molecule merosin) in preference to fibronectin, type I collagen, or type IV collagen. Motility of OE neuronal cells, examined by time-lapse video microscopy, was high on laminin-containing substrata, but negligible on fibronectin substrata. Quantitative assays of adhesion of OE neuronal cells to substrata treated with different ECM molecules demonstrated no correlation, either positive or negative, between the migratory preferences of cells and the strength of cell-substratum adhesion. Moreover, measurements of cell adhesion to substrata containing combinations of ECM proteins revealed that laminin and merosin are anti-adhesive for OE neuronal cells, i.e., cause these cells to adhere poorly to substrata that would otherwise be strongly adhesive. The evidence suggests that the anti-adhesive effect of laminin is not the result of interactions between laminin and other ECM molecules, but rather an effect of laminin on cells, which alters the way in which cells adhere. Consistent with this view, laminin was found to interfere strongly with the formation of focal contacts by OE neuronal cells.

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10

Lai, James C. K. "Oxidative metabolism in neuronal and non-neuronal mitochondria." Canadian Journal of Physiology and Pharmacology 70, S1 (May 15, 1992): S130—S137. http://dx.doi.org/10.1139/y92-254.

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Methodological advances have allowed the isolation of two populations of synaptic (SM and SM2) and two populations of nonsynaptic (A and B) mitochondria from rat forebrain. All four populations of brain mitochondria are metabolically active and essentially free from nonmitochondrial contaminants. They (SM, SM2, A, and B) can oxidize a variety of substrates; the best substrate is pyruvate. With pyruvate as the substrate, the respiratory control ratios (i.e., state 3/state 4) in all four populations are routinely >6. Results from numerous enzyme activity measurements provide strong support for the hypothesis that brain mitochondria are very heterogeneous with respect to their enzyme contents and that the enzymatic activities in a particular population of mitochondria, be they synaptic or nonsynaptic, differ from those in another population of mitochondria derived from either the same or another brain region. The major methodological advances in brain mitochondrial isolation greatly facilitate metabolic studies. For example, we have demonstrated that the K+ stimulation of brain mitochondrial pyruvate oxidation is mediated through a K+-induced elevation of the activation state of the pyruvate dehydrogenase complex and the K+ stimulation of the flux through the pyruvate dehydrogenase complex. Our previous and ongoing studies using primary cultures of hypothalamic neurons and astrocytes are consistent with the proposal that brain cells are heterogeneous with respect to their capabilities in energy metabolism. I can envisage that in the not-so-distant future, one could adapt these preparations of cells as the starting material for the isolation of mitochondria of known cellular origin for metabolic studies.Key words: heterogeneity of brain mitochondria, regulation of intermediary metabolism.

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11

Orr, D. J., and R. A. Smith. "Neuronal maintenance and neurite extension of adult mouse neurones in non-neuronal cell-reduced cultures is dependent on substratum coating." Journal of Cell Science 91, no. 4 (December 1, 1988): 555–61. http://dx.doi.org/10.1242/jcs.91.4.555.

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Adult mouse DRG neurones have been maintained for 14 days in cultures where non-neuronal cell proliferation was inhibited by the inclusion of 5 × 10(−6) microM-cytosine arabinoside (AraC) in the medium from the onset of culture. On uncoated plastic neurone numbers significantly declined in the absence of non-neuronal cell outgrowth compared with uninhibited co-cultures. However, when neurones were maintained in the presence of AraC on certain coated surfaces this decrease in neurone numbers was not observed. Combinations of fibronectin (FN) and laminin (LAM) proved most effective for 7 and 14 days in vitro, although either was beneficial if used separately. Microexudates produced by the fibroblast line, 3T6, also significantly improved neuronal counts for 14 days in vitro. However, a microexudate derived from primary cultures of mouse hepatocytes, although advantageous for 7 days in vitro, was not effective in maintaining neurones over the 14-day culture period, reminiscent of previous observations when synthetic cationic agents were used. Electrophoretic analysis of the fibroblast exudate indicated that fibronectin was present in the substrate-attached material generated by this cell line. The reduction in non-neuronal cell growth facilitated the monitoring of neuronal structural detail by scanning electron microscopy. Examination of neurite extension, indicative of neurone differentiation, was particularly improved. FN/LAM and the fibroblast-derived exudate increased nerve fibre growth, whilst the hepatocyte exudate had little effect on neurite regeneration, and polylysine had a detrimental effect. The data demonstrate that substrata can have a significant effect on maintenance and differentiation of adult neurones in primary culture.(ABSTRACT TRUNCATED AT 250 WORDS)

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12

Labiner, David M. "Neuronal Substrates of Sleep and Epilepsy." Sleep 27, no. 2 (March 2004): 344. http://dx.doi.org/10.1093/sleep/27.2.344.

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13

Tononi, G. "Neuronal substrates of sleep and epilepsy." Neuroscience 132, no. 4 (January 2005): 1199. http://dx.doi.org/10.1016/j.neuroscience.2005.02.001.

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14

Verkhratsky, A., and E. C. Toescu. "Neuronal-glial networks as substrate for CNS integration." Journal of Cellular and Molecular Medicine 10, no. 4 (October 2006): 1–11. http://dx.doi.org/10.1111/j.1582-4934.2006.tb00445.x.

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15

Verkhratsky, A., and E. C. Toescu. "Neuronal-glial networks as substrate for CNS integration." Journal of Cellular and Molecular Medicine 10, no. 4 (October 2006): 826–36. http://dx.doi.org/10.1111/j.1582-4934.2006.tb00527.x.

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16

Eraser, P. E., L. Lévesque та D. R. McLachlan. "Alzheimer Aβ Amyloid Forms an Inhibitory Neuronal Substrate". Journal of Neurochemistry 62, № 3 (28 червня 2008): 1227–30. http://dx.doi.org/10.1046/j.1471-4159.1994.62031227.x.

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17

Verkhratsky, A., and E. C. Toescu. "Neuronal-glial networks as substrate for CNS integration." Journal of Cellular and Molecular Medicine 10, no. 4 (October 2006): 869–79. http://dx.doi.org/10.2755/jcmm010.004.07.

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18

Huang, Kun, Shaun Sanders, Roshni Singaraja, Paul Orban, Tony Cijsouw, Pamela Arstikaitis, Anat Yanai, Michael R. Hayden, and Alaa El‐Husseini. "Neuronal palmitoyl acyl transferases exhibit distinct substrate specificity." FASEB Journal 23, no. 8 (March 19, 2009): 2605–15. http://dx.doi.org/10.1096/fj.08-127399.

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19

Rodriguez Sala, Martina, Swetha Chandrasekaran, Omar Skalli, Marcus Worsley, and Firouzeh Sabri. "Enhanced neurite outgrowth on electrically conductive carbon aerogel substrates in the presence of an external electric field." Soft Matter 17, no. 17 (2021): 4489–95. http://dx.doi.org/10.1039/d1sm00183c.

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It has been established that aerogels are a suitable substrate for neuronal scaffold. In this study, the cell behavior of neuronal cells cultured on aerogels with an electrical stimulation is evaluated.

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20

Bono, Mario de, and Andres Villu Maricq. "NEURONAL SUBSTRATES OF COMPLEX BEHAVIORS INC. ELEGANS." Annual Review of Neuroscience 28, no. 1 (July 21, 2005): 451–501. http://dx.doi.org/10.1146/annurev.neuro.27.070203.144259.

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21

Takahashi-Fujigasaki, J., K. Arai, N. Funata, and H. Fujigasaki. "SUMOylation substrates in neuronal intranuclear inclusion disease." Neuropathology and Applied Neurobiology 32, no. 1 (February 2006): 92–100. http://dx.doi.org/10.1111/j.1365-2990.2005.00705.x.

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22

Rudolph, Uwe, and Bernd Antkowiak. "Molecular and neuronal substrates for general anaesthetics." Nature Reviews Neuroscience 5, no. 9 (September 2004): 709–20. http://dx.doi.org/10.1038/nrn1496.

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23

Kamphuis, Simone, Peter W. Dicke, and Peter Thier. "Neuronal substrates of gaze following in monkeys." European Journal of Neuroscience 29, no. 8 (April 2009): 1732–38. http://dx.doi.org/10.1111/j.1460-9568.2009.06730.x.

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24

Lovat, Viviana, Davide Pantarotto, Laura Lagostena, Barbara Cacciari, Micaela Grandolfo, Massimo Righi, Giampiero Spalluto, Maurizio Prato, and Laura Ballerini. "Carbon Nanotube Substrates Boost Neuronal Electrical Signaling." Nano Letters 5, no. 6 (June 2005): 1107–10. http://dx.doi.org/10.1021/nl050637m.

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25

Gründemann, Dirk, Gernot Liebich, Nicholas Kiefer, Sandra Köster, and Edgar Schömig. "Selective Substrates for Non-Neuronal Monoamine Transporters." Molecular Pharmacology 56, no. 1 (July 1, 1999): 1–10. http://dx.doi.org/10.1124/mol.56.1.1.

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26

Gründemann, Dirk, Gernot Liebich, Nicholas Kiefer, Sandra Köster, and Edgar Schömig. "Selective Substrates for Non-Neuronal Monoamine Transporters." Molecular Pharmacology 56, no. 1 (July 1999): 1–10. https://doi.org/10.1016/s0026-895x(24)26377-x.

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27

Deramecourt, Vincent, and Florence Pasquier. "Neuronal substrate of cognitive impairment in post-stroke dementia." Brain 137, no. 9 (August 12, 2014): 2404–5. http://dx.doi.org/10.1093/brain/awu188.

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28

Micholt, Liesbeth, Annette Gärtner, Dimiter Prodanov, Dries Braeken, Carlos G. Dotti, and Carmen Bartic. "Substrate Topography Determines Neuronal Polarization and Growth In Vitro." PLoS ONE 8, no. 6 (June 13, 2013): e66170. http://dx.doi.org/10.1371/journal.pone.0066170.

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29

Stiess, Michael, and Frank Bradke. "Controlled Demolition: Smurf1 Regulates Neuronal Polarity by Substrate Switching." Neuron 69, no. 2 (January 2011): 183–85. http://dx.doi.org/10.1016/j.neuron.2011.01.007.

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30

Fukushima, Kikuro, Chris R. S. Kaneko, and Albert F. Fuchs. "The neuronal substrate of integration in the oculomotor system." Progress in Neurobiology 39, no. 6 (December 1992): 609–39. http://dx.doi.org/10.1016/0301-0082(92)90016-8.

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31

Migliorini, Elisa, Gianluca Grenci, Jelena Ban, Alessandro Pozzato, Massimo Tormen, Marco Lazzarino, Vincent Torre, and Maria Elisabetta Ruaro. "Acceleration of neuronal precursors differentiation induced by substrate nanotopography." Biotechnology and Bioengineering 108, no. 11 (June 21, 2011): 2736–46. http://dx.doi.org/10.1002/bit.23232.

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32

Sumi, Takuma, Hideaki Yamamoto, and Ayumi Hirano-Iwata. "Suppression of hypersynchronous network activity in cultured cortical neurons using an ultrasoft silicone scaffold." Soft Matter 16, no. 13 (2020): 3195–202. http://dx.doi.org/10.1039/c9sm02432h.

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33

MAHER, Fran, Theresa M. DAVIES-HILL, and Ian A. SIMPSON. "Substrate specificity and kinetic parameters of GLUT3 in rat cerebellar granule neurons." Biochemical Journal 315, no. 3 (May 1, 1996): 827–31. http://dx.doi.org/10.1042/bj3150827.

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This study examines the apparent affinity, catalytic-centre activity (‘turnover number’) and stereospecificity of the neuronal glucose transporter GLUT3 in primary cultured cerebellar granule neurons. Using a novel variation of the 3-O-[14C]methylglucose transport assay, by measuring zero-trans kinetics at 25 °C, GLUT3 was determined to be a high-apparent-affinity, high-activity, glucose transporter with a Km of 2.87±0.23 mM (mean±S.E.M.) for 3-O-methylglucose, a Vmax of 18.7± 0.48 nmol/min per 106 cells, and a corresponding catalytic-centre activity of 853 s-1. Transport of 3-O-methylglucose was competed by glucose, mannose, 2-deoxyglucose and galactose, but not by fructose. This methodology is compared with the more common 2-[3H]deoxyglucose methodology and the [U-14C]glucose transport method. The high affinity and transport activity of the neuronal glucose transporter GLUT3 appears to be an appropriate adaptation to meet the demands of neuronal metabolism at prevailing interstitial brain glucose concentrations (1–2 mM).

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34

Smith, Marie L., P. Fries, F. Gosselin, R. Goebel, and P. G. Schyns. "Inverse Mapping the Neuronal Substrates of Face Categorizations." Cerebral Cortex 19, no. 10 (January 23, 2009): 2428–38. http://dx.doi.org/10.1093/cercor/bhn257.

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35

Jones, Barbara E. "From waking to sleeping: neuronal and chemical substrates." Trends in Pharmacological Sciences 26, no. 11 (November 2005): 578–86. http://dx.doi.org/10.1016/j.tips.2005.09.009.

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36

Teixeira, Ana I., Shirin Ilkhanizadeh, Jens A. Wigenius, Joshua K. Duckworth, Olle Inganäs, and Ola Hermanson. "The promotion of neuronal maturation on soft substrates." Biomaterials 30, no. 27 (September 2009): 4567–72. http://dx.doi.org/10.1016/j.biomaterials.2009.05.013.

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37

Staii, Cristian. "Biased Random Walk Model of Neuronal Dynamics on Substrates with Periodic Geometrical Patterns." Biomimetics 8, no. 2 (June 20, 2023): 267. http://dx.doi.org/10.3390/biomimetics8020267.

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Neuronal networks are complex systems of interconnected neurons responsible for transmitting and processing information throughout the nervous system. The building blocks of neuronal networks consist of individual neurons, specialized cells that receive, process, and transmit electrical and chemical signals throughout the body. The formation of neuronal networks in the developing nervous system is a process of fundamental importance for understanding brain activity, including perception, memory, and cognition. To form networks, neuronal cells extend long processes called axons, which navigate toward other target neurons guided by both intrinsic and extrinsic factors, including genetic programming, chemical signaling, intercellular interactions, and mechanical and geometrical cues. Despite important recent advances, the basic mechanisms underlying collective neuron behavior and the formation of functional neuronal networks are not entirely understood. In this paper, we present a combined experimental and theoretical analysis of neuronal growth on surfaces with micropatterned periodic geometrical features. We demonstrate that the extension of axons on these surfaces is described by a biased random walk model, in which the surface geometry imparts a constant drift term to the axon, and the stochastic cues produce a random walk around the average growth direction. We show that the model predicts key parameters that describe axonal dynamics: diffusion (cell motility) coefficient, average growth velocity, and axonal mean squared length, and we compare these parameters with the results of experimental measurements. Our findings indicate that neuronal growth is governed by a contact-guidance mechanism, in which the axons respond to external geometrical cues by aligning their motion along the surface micropatterns. These results have a significant impact on developing novel neural network models, as well as biomimetic substrates, to stimulate nerve regeneration and repair after injury.

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38

Kung, Frank H., and Ellen Townes-Anderson. "Creating Custom Neural Circuits on Multiple Electrode Arrays Utilizing Optical Tweezers for Precise Nerve Cell Placement." Methods and Protocols 3, no. 2 (June 20, 2020): 44. http://dx.doi.org/10.3390/mps3020044.

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Precise creation, maintenance, and monitoring of neuronal circuits would facilitate the investigation of subjects such as neuronal development or synaptic plasticity, or assist in the development of neuronal prosthetics. Here we present a method to precisely control the placement of multiple types of neuronal retinal cells onto a commercially available multiple electrode array (MEA), using custom-built optical tweezers. We prepared the MEAs by coating a portion of the MEA with a non-adhesive substrate (Poly (2-hydroxyethyl methacrylate)), and the electrodes with an adhesive cell growth substrate. We then dissociated the retina of adult tiger salamanders, plated them onto prepared MEAs, and utilized the optical tweezers to create retinal circuitry mimicking in vivo connections. In our hands, the optical tweezers moved ~75% of photoreceptors, bipolar cells, and multipolar cells, an average of ~2000 micrometers, at a speed of ~16 micrometers/second. These retinal circuits were maintained in vitro for seven days. We confirmed electrophysiological activity by stimulating the photoreceptors with the MEA and measuring their response with calcium imaging. In conclusion, we have developed a method of utilizing optical tweezers in conjunction with MEAs that allows for the design and maintenance of custom neural circuits for functional analysis.

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39

Panov, Alexander, Zulfiya Orynbayeva, Valentin Vavilin, and Vyacheslav Lyakhovich. "Fatty Acids in Energy Metabolism of the Central Nervous System." BioMed Research International 2014 (2014): 1–22. http://dx.doi.org/10.1155/2014/472459.

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In this review, we analyze the current hypotheses regarding energy metabolism in the neurons and astroglia. Recently, it was shown that up to 20% of the total brain’s energy is provided by mitochondrial oxidation of fatty acids. However, the existing hypotheses consider glucose, or its derivative lactate, as the only main energy substrate for the brain. Astroglia metabolically supports the neurons by providing lactate as a substrate for neuronal mitochondria. In addition, a significant amount of neuromediators, glutamate and GABA, is transported into neurons and also serves as substrates for mitochondria. Thus, neuronal mitochondria may simultaneously oxidize several substrates. Astrocytes have to replenish the pool of neuromediators by synthesis de novo, which requires large amounts of energy. In this review, we made an attempt to reconcileβ-oxidation of fatty acids by astrocytic mitochondria with the existing hypothesis on regulation of aerobic glycolysis. We suggest that, under condition of neuronal excitation, both metabolic pathways may exist simultaneously. We provide experimental evidence that isolated neuronal mitochondria may oxidize palmitoyl carnitine in the presence of other mitochondrial substrates. We also suggest that variations in the brain mitochondrial metabolic phenotype may be associated with different mtDNA haplogroups.

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Chen, Chun-Yen, Chao-Nan Lin, Rey-Shyong Chern, Yu-Chuan Tsai, Yung-Hsien Chang, and Chi-Hsien Chien. "Neuronal Activity Stimulated by Liquid Substrates Injection at Zusanli (ST36) Acupoint: The Possible Mechanism ofAquapuncture." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/627342.

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Aquapunctureis a modified acupuncture technique and it is generally accepted that it has a greater therapeutic effect than acupuncture because of the combination of the acupoint stimulation and the pharmacological effect of the drugs. However, to date, the mechanisms underlying the effects ofaquapunctureremain unclear. We hypothesized that both the change in the local spatial configuration and the substrate stimulation ofaquapuncturewould activate neuronal signaling. Thus, bee venom, normal saline, and vitamins B1 and B12 were injected into a Zusanli (ST36) acupoint as substrate ofaquapuncture, whereas a dry needle was inserted into ST36 as a control. Afteraquapuncture, activated neurons expressing Fos protein were mainly observed in the dorsal horn of the spinal cord in lumbar segments L3–5, with the distribution nearly identical among all groups. However, the bee venom injection induced significantly more Fos-expressing neurons than the other substrates. Based on these data, we suggest that changes in the spatial configuration of the acupoint activate neuronal signaling and that bee venom may further strengthen this neuronal activity. In conclusion, the mechanisms for the effects ofaquapunctureappear to be the spatial configuration changes occurring within the acupoint and the ability of injected substrates to stimulate neuronal activity.

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Friedman, Gabriel N., Mohsen Jamali, Firas Bounni, and Ziv Williams. "344 Studying the Single-cellular Substrates of Autism in a Mouse Model." Neurosurgery 64, CN_suppl_1 (August 24, 2017): 277–78. http://dx.doi.org/10.1093/neuros/nyx417.344.

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Abstract INTRODUCTION Social dysfunction is among the most prominent features of autism spectrum disorder (ASD) as well as many other developmental and neuropsychiatric conditions. What precise neuronal mechanisms are disrupted in ASD, however, are unknown. The goal of this study is to provide a basic cellular-level understanding and treatment model for ASD. METHODS We developed an alternating appetitive/aversive paradigm in which socially-paired mice experienced both acute stress and food reward while we simultaneously recorded neuronal activity from medial prefrontal cortex. We compared WT to SHANK3 -/+ mice as a model of ASD, to explore the neuronal correlates socially relevant information and its dysfunction. RESULTS >Individual medial prefrontal neurons in SHANK3 -/+ mice displayed markedly different response profiles compared to that of WT. Specifically, neurons in SHANK3 -/+ mice demonstrated little differential response when presented with another unfamiliar mouse or nonsocial totem undergoing the same condition. However, in trials where the recorded mouse and a familiar mouse both receive a negative (painful) stimulus, SHANK3 -/+ mice demonstrated a significantly attenuated firing rate in response to the conspecific mouse, while the WT mice did not show any such differences. This attenuation was not observed when the other mice received positive (rewarding) stimuli. CONCLUSION Our study reveals some of the basic neuronal coding mechanisms that are disrupted in ASD. In particular, they demonstrate that, at the cellular level, autistic mice lack the neuronal-equivalent of an “empathic” response compared to wild-type. This neuronal response may provide a foundational mechanism for egocentric behavioral often found in ASD and suggests a basic model for testing neurobiologically plausible treatments for individuals with autism.

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Low, K. "Molecular and Neuronal Substrate for the Selective Attenuation of Anxiety." Science 290, no. 5489 (October 6, 2000): 131–34. http://dx.doi.org/10.1126/science.290.5489.131.

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Hopp, J. Johanna, and Albert F. Fuchs. "The characteristics and neuronal substrate of saccadic eye movement plasticity." Progress in Neurobiology 72, no. 1 (January 2004): 27–53. http://dx.doi.org/10.1016/j.pneurobio.2003.12.002.

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Morillon, Benjamin, and Charles E. Schroeder. "Neuronal oscillations as a mechanistic substrate of auditory temporal prediction." Annals of the New York Academy of Sciences 1337, no. 1 (March 2015): 26–31. http://dx.doi.org/10.1111/nyas.12629.

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Woerly, S., G. Maghami, R. Duncan, V. Subr, and K. Ulbrich. "Synthetic polymer derivatives as substrata for neuronal adhesion and growth." Brain Research Bulletin 30, no. 3-4 (January 1993): 423–32. http://dx.doi.org/10.1016/0361-9230(93)90274-f.

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Kim, Eunhee, Seung-Jun Yoo, Cheil Moon, Bradley J. Nelson, and Hongsoo Choi. "SU-8-based nanoporous substrate for migration of neuronal cells." Microelectronic Engineering 141 (June 2015): 173–77. http://dx.doi.org/10.1016/j.mee.2015.03.016.

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Harmey, Dympna, Anthony Smith, Scott Simanski, Carole Zaki Moussa, and Nagi G. Ayad. "The Anaphase Promoting Complex Induces Substrate Degradation during Neuronal Differentiation." Journal of Biological Chemistry 284, no. 7 (December 1, 2008): 4317–23. http://dx.doi.org/10.1074/jbc.m804944200.

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Simon, Alexandra, Susanne Karbach, Alice Habermeier, and Ellen I. Closs. "Decoding the Substrate Supply to Human Neuronal Nitric Oxide Synthase." PLoS ONE 8, no. 7 (July 9, 2013): e67707. http://dx.doi.org/10.1371/journal.pone.0067707.

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Hämmerle, H., U. Egert, A. Mohr, and W. Nisch. "Extracellular recording in neuronal networks with substrate integrated microelectrode arrays." Biosensors and Bioelectronics 9, no. 9-10 (1994): 691–96. http://dx.doi.org/10.1016/0956-5663(94)80067-7.

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Carman, Zachary, Isabella Phillips, Arsha Moorthy, Abdulraheem Kaimari, Alireza Sarvestani, and Chamaree de Silva. "BPS2025 - Neuronal growth is independent of substrate rigidity in 2D." Biophysical Journal 124, no. 3 (February 2025): 308a. https://doi.org/10.1016/j.bpj.2024.11.1713.

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