Journal articles on the topic 'Molecular neuroscience'

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1

Seeburg, Peter H. "Molecular neuroscience: challenges ahead." Frontiers in Neuroscience 2, no. 1 (July 15, 2008): 2–3. http://dx.doi.org/10.3389/neuro.01.015.2008.

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2

Bradke, Frank, and Yukiko Goda. "Editorial overview: Molecular neuroscience." Current Opinion in Neurobiology 69 (August 2021): iii—v. http://dx.doi.org/10.1016/j.conb.2021.07.013.

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3

Ryan, Timothy A., and Yishi Jin. "Editorial overview: Molecular neuroscience." Current Opinion in Neurobiology 57 (August 2019): iii—vi. http://dx.doi.org/10.1016/j.conb.2019.06.002.

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4

Kiberstis, P. A. "MOLECULAR NEUROSCIENCE: Promoting Diversity." Science 297, no. 5583 (August 9, 2002): 901a—901. http://dx.doi.org/10.1126/science.297.5583.901a.

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5

Tuszynski,, Jack, Roman Poznanski, and Lleuvelyn Cacha. "Journal of Multiscale Neuroscience." Journal of Multiscale Neuroscience 1, no. 1 (May 28, 2022): 41–53. http://dx.doi.org/10.56280/1531676736.

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We define quantum analogs as vibrational excitations of quasi-particles coupled to electromagnetically-mediated resonance energy transfer in water (a crystal lattice). This paper addresses how neural magnetic resonance spectra of the brain’s magnetic field influence dipolar oscillation waves in crystal lattices of interfacial water molecules to produce correlates of phenomenal consciousness. We explore dipolar oscillation waves in hydrophobic protein cavities of aromatic amino acids as a conduit for coherent propagation of vibrational excitation and hydrogen bond distortion associated with phase coherence present in the magnetic field intensity oscillations at a frequency at which the energy switches from its trapped form as excited phonon states to free, cavity-mode magnetic field energy states. A quasi-polaritons that reflect “hydro-ionic waves” is a macroscopic quantum effect of crystal lattice vibrations, consisting of vibron polaritons coupled to ions across the neocortex, except the cerebellum, due to the absence of protein-protein interactions. They are quantum-like at the core and hence can exhibit quantum-like signaling properties when resonant energy is transferred as dipolar waves in hydrophobic protein cavities of aromatic amino acids. This is due to aromatic residue flexibility in molecular electromagnetic resonances. Finally, the archetypal molecular patterning of conscious experiences, which carries an inherent ambiguity necessary for non-contextually applying ‘meaning’ that encompasses cognitive signatures of conscious experience, satisfies the nature of quantum analogs and their transmutative properties.
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6

Schaller, Bernhard, Jan F. Cornelius, and Nora Sandu. "Molecular Medicine Successes in Neuroscience." Molecular Medicine 14, no. 7-8 (May 9, 2008): 361–64. http://dx.doi.org/10.2119/2008-00055.schaller.

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7

Tomita, Susumu, and Brenda L. Bloodgood. "Editorial overview: Molecular neuroscience 2017." Current Opinion in Neurobiology 45 (August 2017): A1—A4. http://dx.doi.org/10.1016/j.conb.2017.07.002.

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8

Chakraborty, Ashok, and Anil Diwan. "Biomarkers and molecular mechanisms of Amyotrophic Lateral Sclerosis." AIMS Neuroscience 9, no. 4 (2022): 423–43. http://dx.doi.org/10.3934/neuroscience.2022023.

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<abstract> <p>Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease in adults involving non-demyelinating motor disorders. About 90% of ALS cases are sporadic, while 10–12% of cases are due to some genetic reasons. Mutations in superoxide dismutase 1 (<italic>SOD1</italic>), <italic>TAR</italic>, <italic>c9orf72</italic> (chromosome 9 open reading frame 72) and <italic>VAPB</italic> genes are commonly found in ALS patients. Therefore, the mechanism of ALS development involves oxidative stress, endoplasmic reticulum stress, glutamate excitotoxicity and aggregation of proteins, neuro-inflammation and defective RNA function. Cholesterol and LDL/HDL levels are also associated with ALS development. As a result, sterols could be a suitable biomarker for this ailment. The main mechanisms of ALS development are reticulum stress, neuroinflammation and RNA metabolism. The multi-nature development of ALS makes it more challenging to pinpoint a treatment.</p> </abstract>
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9

D Potdar, Pravin, and Aashutosh U Shetti. "Molecular Biomarkers for Diagnosis & Therapies of Alzheimer’s Disease." AIMS Neuroscience 3, no. 4 (2016): 433–53. http://dx.doi.org/10.3934/neuroscience.2016.4.433.

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10

Pavlov, Valentin A., Sangeeta S. Chavan, and Kevin J. Tracey. "Molecular and Functional Neuroscience in Immunity." Annual Review of Immunology 36, no. 1 (April 26, 2018): 783–812. http://dx.doi.org/10.1146/annurev-immunol-042617-053158.

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11

Stein, D. J. "S.26.04 Molecular neuroscience of PTSD." European Neuropsychopharmacology 20 (August 2010): S204. http://dx.doi.org/10.1016/s0924-977x(10)70230-3.

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12

Jacobs, A. H., H. Li, A. Winkeler, R. Hilker, C. Knoess, A. R�ger, N. Galldiks, et al. "PET-based molecular imaging in neuroscience." European Journal of Nuclear Medicine and Molecular Imaging 30, no. 7 (July 1, 2003): 1051–65. http://dx.doi.org/10.1007/s00259-003-1202-5.

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13

Diamond, I., and A. S. Gordon. "Cellular and molecular neuroscience of alcoholism." Physiological Reviews 77, no. 1 (January 1, 1997): 1–20. http://dx.doi.org/10.1152/physrev.1997.77.1.1.

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Recent advances in neuroscience have made it possible to investigate the pathophysiology of alcoholism at a cellular and molecular level. Evidence indicates that ethanol affects hormone- and neurotransmitter-activated signal transduction, leading to short-term changes in regulation of cellular functions and long-term changes in gene expression. Such changes in the brain probably underlie many of the acute and chronic neurological events in alcoholism. In addition, genetic vulnerability also plays a role in alcoholism and, perhaps, in alcoholic medical disorders.
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14

Papageorgiou, Ismini E. "Neuroscience Scaffolded by Informatics: A Raging Interdisciplinary Field." Symmetry 15, no. 1 (January 4, 2023): 153. http://dx.doi.org/10.3390/sym15010153.

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Following breakthrough achievements in molecular neurosciences, the current decade witnesses a trend toward interdisciplinary and multimodal development. Supplementation of neurosciences with tools from computer science solidifies previous knowledge and sets the ground for new research on “big data” and new hypothesis-free experimental models. In this Special Issue, we set the focus on informatics-supported interdisciplinary neuroscience accomplishments symmetrically combining wet-lab and clinical routines. Video-tracking and automated mitosis detection in vitro, the macromolecular modeling of kinesin motion, and the unsupervised classification of the brain’s macrophage activation status share a common denominator: they are energized by machine and deep learning. Essential clinical neuroscience questions such as the estimated risk of brain aneurysm rupture and the surgical outcome of facial nerve transplantation are addressed in this issue as well. Precise and rapid evaluation of complex clinical data by deep learning and data mining dives deep to reveal symmetrical and asymmetrical features beyond the abilities of human perception or the limits of linear algebraic modeling. This editorial opts to motivate researchers from the wet lab, computer science, and clinical environments to join forces in reshaping scientific platforms, share and converge high-quality data on public platforms, and use informatics to facilitate interdisciplinary information exchange.
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15

Harrison, Paul J. "Neuroscience." British Journal of Psychiatry 159, no. 6 (December 1991): 891–93. http://dx.doi.org/10.1192/bjp.159.6.891.

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Neuroscience, encouraged by the advent of approaches at the molecular level, is finally beginning to play an important part in the theoretical basis of psychiatry. Although its immediate effect on clinical practice remains limited, this too is likely to change within the near future. Psychiatrists, and Membership candidates in particular, are now expected to be au fait with everything from conduction of the nerve impulse to second messengers and linkage analysis. Unfortunately, the complexity and breadth of the underlying science is expanding at an ever-increasing rate, making it difficult to keep up to date with advances. The following are offered as readable overviews of the neuroscientific areas especially relevant to psychiatry, with an emphasis on publications or editions produced within the past three years, since the rate of progress renders most texts rapidly redundant. The broader question of how all this neuroscience is going to alter psychiatry – for better or worse – has also attracted considerable debate, if few conclusions (e.g. Pardes, 1986; Detre, 1987).
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16

Frost, J. James. "Molecular Imaging to Biomarker Development in Neuroscience." Annals of the New York Academy of Sciences 1144, no. 1 (November 2008): 251–55. http://dx.doi.org/10.1196/annals.1418.027.

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17

Mills, Carolyn Virginia. "Library Materials in Molecular and Cellular Neuroscience." Science & Technology Libraries 13, no. 3-4 (September 7, 1993): 57–70. http://dx.doi.org/10.1300/j122v13n03_04.

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18

Pfaff, Samuel L., and Frank S. Walsh. "The molecular and cellular neuroscience editorial board." Molecular and Cellular Neuroscience 33, no. 1 (September 2006): 1. http://dx.doi.org/10.1016/j.mcn.2006.07.002.

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19

Brunso-Bechtold, Judy K. "Principles of Cellular, Molecular, and Developmental Neuroscience." Trends in Neurosciences 13, no. 9 (September 1990): 386–87. http://dx.doi.org/10.1016/0166-2236(90)90026-7.

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20

Moonat, Sachin, Bela G. Starkman, Amul Sakharkar, and Subhash C. Pandey. "Neuroscience of alcoholism: molecular and cellular mechanisms." Cellular and Molecular Life Sciences 67, no. 1 (September 10, 2009): 73–88. http://dx.doi.org/10.1007/s00018-009-0135-y.

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21

JANICAK, PHILIP G. "Molecular Neuropharmacology: A Foundation for Clinical Neuroscience." American Journal of Psychiatry 159, no. 7 (July 2002): 1251. http://dx.doi.org/10.1176/appi.ajp.159.7.1251.

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22

Crick, Francis. "The impact of molecular biology on neuroscience." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1392 (December 29, 1999): 2021–25. http://dx.doi.org/10.1098/rstb.1999.0541.

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How our brains work is one of the major unsolved problems of biology. This paper describes some of the techniques of molecular biology that are already being used to study the brains of animals. Mainly as a result of the human genome project many new techniques will soon become available which could decisively influence the progress of neuroscience. I suggest that neuroscientists should tell molecular biologists what their difficulties are, in the hope that this will stimulate the production of useful new biological tools.
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23

Marangos, Paul J. "Dedication for the Journal of Molecular Neuroscience." Journal of Molecular Neuroscience 1, no. 1 (March 1989): 1–2. http://dx.doi.org/10.1007/bf02896849.

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24

Bloom, Floyd E. "Molecular Neuropharmacology: A Foundation for Clinical Neuroscience." Archives of Neurology 60, no. 9 (September 1, 2003): 1339. http://dx.doi.org/10.1001/archneur.60.9.1339-c.

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25

Gozes, Illana. "Journal of Molecular Neuroscience: Impacting Our Brains." Journal of Molecular Neuroscience 54, no. 3 (October 21, 2014): 291–92. http://dx.doi.org/10.1007/s12031-014-0444-y.

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26

Siddappaji, Kiran Kumar, and Shubha Gopal. "Molecular mechanisms in Alzheimer's disease and the impact of physical exercise with advancements in therapeutic approaches." AIMS Neuroscience 8, no. 3 (2021): 357–89. http://dx.doi.org/10.3934/neuroscience.2021020.

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27

Cunningham, J. Thomas, Ronald H. Freeman, and Michael C. Hosokawa. "INTEGRATION OF NEUROSCIENCE AND ENDOCRINOLOGY IN HYBRID PBL CURRICULUM." Advances in Physiology Education 25, no. 4 (December 2001): 233–40. http://dx.doi.org/10.1152/advances.2001.25.4.233.

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At the University of Missouri-Columbia, the medical school employs a problem-based learning curriculum that began in 1993. Since the curriculum was changed, student performance on step 1 of the United States Medical Licensing Examination has significantly increased from slightly below the national average to almost one-half a standard deviation above the national mean. In the first and second years, classes for students are organized in classes or blocks that are 8 wk long, followed by 1 wk for evaluation. Initially, basic science endocrinology was taught in the fourth block of the first year with immunology and molecular biology. Student and faculty evaluations of the curriculum indicated that endocrinology did not integrate well with the rest of the material taught in that block. To address these issues, basic science endocrinology was moved into another block with neurosciences. We integrate endocrinology with neurosciences by using the hypothalamus and its role in neuroendocrinology as a springboard for endocrinology. This is accomplished by using clinical cases with clear neuroscience and endocrinology aspects such as Cushing’s disease and multiple endocrine neoplastic syndrome type 1.
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28

Rao, SathyanarayanaT S., B. Praveena, and JagannathaK S. Rao. "Geriatric mental health: Recent trends in molecular neuroscience." Indian Journal of Psychiatry 52, no. 1 (2010): 3. http://dx.doi.org/10.4103/0019-5545.58886.

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29

Inubushi, Toshiro. "Molecular Imaging for Neuroscience Research(Progress in Neuroimaging)." Japanese Journal of Neurosurgery 19, no. 6 (2010): 440–46. http://dx.doi.org/10.7887/jcns.19.440.

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30

Smith, P., and C. Hall. "Molecular Biology in Basic and Clinical Neuroscience Research." Journal of Neurology, Neurosurgery & Psychiatry 51, no. 2 (February 1, 1988): 322. http://dx.doi.org/10.1136/jnnp.51.2.322.

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31

Young, Anne B. "Huntington's Disease: Lessons from and for Molecular Neuroscience." Neuroscientist 1, no. 1 (January 1995): 51–58. http://dx.doi.org/10.1177/107385849500100108.

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32

Callaway, Edward M. "A molecular and genetic arsenal for systems neuroscience." Trends in Neurosciences 28, no. 4 (April 2005): 196–201. http://dx.doi.org/10.1016/j.tins.2005.01.007.

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33

Hall, Christine. "Molecular biology in basic and clinical neuroscience research." FEBS Letters 226, no. 1 (December 21, 1987): 193–94. http://dx.doi.org/10.1016/0014-5793(87)80579-3.

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34

Jain, Kewal K. "Neuropharmacology: Molecular Neuropharmacology: A Foundation for Clinical Neuroscience." Trends in Pharmacological Sciences 23, no. 2 (February 2002): 99. http://dx.doi.org/10.1016/s0165-6147(02)01903-x.

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35

Selzer, Michael E. "Book ReviewPrinciples of Cellular, Molecular, and Developmental Neuroscience." New England Journal of Medicine 321, no. 11 (September 14, 1989): 770. http://dx.doi.org/10.1056/nejm198909143211122.

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36

Campbell, I. C., M. K. Balasubramanian, and V. Palaniappun. "What has Molecular Neuroscience to offer to Clinicians." Indian Journal of Psychological Medicine 14, no. 2 (July 1991): 7–16. http://dx.doi.org/10.1177/0975156419910203.

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37

A. Mirisis, Anastasios, Anamaria Alexandrescu, Thomas J. Carew, and Ashley M. Kopec. "The Contribution of Spatial and Temporal Molecular Networks in the Induction of Long-term Memory and Its Underlying Synaptic Plasticity." AIMS Neuroscience 3, no. 3 (2016): 356–84. http://dx.doi.org/10.3934/neuroscience.2016.3.356.

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38

Ragan, C. Ian. "Metal Ions in Neuroscience." Metal-Based Drugs 4, no. 3 (January 1, 1997): 125–32. http://dx.doi.org/10.1155/mbd.1997.125.

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Metal ions are believed to participate in many neurodegenerative conditions. In excitotoxic cell death there is convincing evidence for the participation of Ca2+ and Zn2+ ions although the exact molecular mechanisms by which these metals exert their effects are unclear. Only in one instance has the metal binding site of metalloenzymes been exploited for therapeutic purposes and this is the use of Li+ in the treatment of bipolar affective disorder. Again the exact molecular target is not clear but is likely to involve a Mg2+-dependent enzyme of an intracellular signalling pathway. In Parkinson's disease, the selective loss of dopaminergic neurones in the substantia nigra may be caused by radical-mediated damage and there is good evidence to suggest that Fe2+ or 3+ is important in promoting formation of radical species. The evidence that free radicals are important in mediating other neurodegenerative conditions is less strong but still substantial enough to suggest that removal of reactive oxygen species or preventing their formation may be a valid approach to therapy.
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39

Kandel, Eric R., and Larry R. Squire. "Neuroscience." Annals of the New York Academy of Sciences 935, no. 1 (January 25, 2006): 118–35. http://dx.doi.org/10.1111/j.1749-6632.2001.tb03477.x.

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40

Vogt, Nina. "Collaborative neuroscience." Nature Methods 17, no. 1 (January 2020): 22. http://dx.doi.org/10.1038/s41592-019-0706-2.

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41

Nguyen, Khue Vu. "Potential molecular link between the β-amyloid precursor protein (APP) and hypoxanthine-guanine phosphoribosyltransferase (HGprt) enzyme in Lesch-Nyhan disease and cancer." AIMS Neuroscience 8, no. 4 (2021): 548–57. http://dx.doi.org/10.3934/neuroscience.2021030.

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<abstract> <p>Lesch-Nyhan disease (LND) is a rare X-linked inherited neurogenetic disorders of purine metabolic in which the cytoplasmic enzyme, hypoxanthine-guanine phosphoribosyltransferase (HGprt) is defective. Despite having been characterized over 60 years ago, however, up to now, there is no satisfactory explanation of how deficits in enzyme HGprt can lead to LND with the development of the persistent and severe self-injurious behavior. Recently, a role for epistasis between the mutated hypoxanthine phosphoribosyltransferase 1 (<italic>HPRT1</italic>) and the β-amyloid precursor protein (APP) genes affecting the regulation of alternative APP pre-mRNA splicing in LND has been demonstrated. Furthermore, there were also some reported cases of LND developing thrombosis while APP is an important regulator of vein thrombosis and controls coagulation. Otherwise, the surface expression of HGprt enzyme was also observed in several somatic tissue cancers while APP and the APP-like protein-2 (APLP2) are deregulated in cancer cells and linked to increased tumor cell proliferation, migration, and invasion. The present review provides a discussion about these findings and suggests a potential molecular link between APP and HGprt via epistasis between <italic>HPRT1</italic> and <italic>APP</italic> genes affecting the regulation of alternative APP pre-mRNA splicing. As a perspective, expression vectors for HGprt enzyme and APP are constructed as described in Ref. # 24 (Nguyen KV, Naviaux RK, Nyhan WL (2020) Lesch-Nyhan disease: I. Construction of expression vectors for hypoxanthine-guanine phosphoribosyltransferase (HGprt) enzyme and amyloid precursor protein (APP). <italic>Nucleosides Nucleotides Nucleic Acids</italic> 39: 905–922), and they could be used as tools for clarification of these issues. In addition, these expression vectors, especially the one with the glycosyl-phosphatidylinositol (GPI) anchor can be used as a model for the construction of expression vectors for any protein targeting to the cell plasma membrane for studying intermolecular interactions and could be therefore useful in the vaccines as well as antiviral drugs development (studying intermolecular interactions between the spike glycoprotein of the severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, as well as its variants and the angiotensin-converting enzyme 2, ACE2, in coronavirus disease 2019 (COVID-19) <xref ref-type="bibr" rid="b43">[43]</xref>,<xref ref-type="bibr" rid="b44">[44]</xref>, for example).</p> </abstract>
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42

Miranda Feitosa, Leonardo, Camila Ferreira Alves, Natália Ramalho Figueiredo, Wilker Leite Nascimento, Amanda Beatriz Adriano da Silva, Saulo Rivera Ikeda, Nadia Shigaeff, Caio Maximino, and Monica Lima‐Maximino. "Open Practical Laboratories in the Neurosciences: An outreach program for neuroscience communication in middle schools." Journal of Neuroscience Research 99, no. 6 (March 2, 2021): 1504–14. http://dx.doi.org/10.1002/jnr.24800.

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43

McCandless, David W. "Fundamental neuroscience." Metabolic Brain Disease 12, no. 1 (March 1997): 93. http://dx.doi.org/10.1007/bf02676357.

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44

French, L., and P. Pavlidis. "Informatics in neuroscience." Briefings in Bioinformatics 8, no. 6 (May 4, 2007): 446–56. http://dx.doi.org/10.1093/bib/bbm047.

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45

Genc, Sermin, Tolga F. Koroglu, and Kursad Genc. "RNA interference in neuroscience." Molecular Brain Research 132, no. 2 (December 2004): 260–70. http://dx.doi.org/10.1016/j.molbrainres.2004.02.004.

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46

Struth, Christiane. "In-Between Proust and Neuroscience." Mnemosyne, no. 6 (October 15, 2018): 11. http://dx.doi.org/10.14428/mnemosyne.v0i6.14193.

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In his autobiography allusive of Marcel Proust’s literary autobiography À la recherche du temps perdu, Kandel describes and explores his own development as a molecular scientist who started out as a student of history and psychoanalysis with more than just a penchant for literature. Despite his conversion to neuroscience, which is told in great detail, Kandel’s motives in studying the brain are informed mainly by humanist ideals and episodes from his personal past. The author creates an image of himself as a scientist who is guided in his molecular research by both his good intuitions and received theories from the humanities. Hence, the aim of the present paper is to show how the author succeeds in modelling his scientific ethos at the interface of the humanities and the natural sciences and in what ways he generates a public image of himself as a ‘self-made man’ or, rather, scientist.
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47

Wouterlood, Floris G. "Neuroscience protocols." Brain Research 665, no. 2 (December 1994): 327–30. http://dx.doi.org/10.1016/0006-8993(94)91357-9.

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48

Davis, Ronald L. "OLFACTORY MEMORY FORMATION INDROSOPHILA: From Molecular to Systems Neuroscience." Annual Review of Neuroscience 28, no. 1 (July 21, 2005): 275–302. http://dx.doi.org/10.1146/annurev.neuro.28.061604.135651.

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49

Heumann, Rolf. "Highlight: Perspectives of molecular neuroscience in health and disease." Biological Chemistry 397, no. 3 (March 1, 2016): 175. http://dx.doi.org/10.1515/hsz-2016-0110.

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50

Nemenman, Ilya. "Gain control in molecular information processing: lessons from neuroscience." Physical Biology 9, no. 2 (April 1, 2012): 026003. http://dx.doi.org/10.1088/1478-3975/9/2/026003.

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