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Journal articles on the topic 'D-aspartate'

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Published: 4 June 2021

Last updated: 20 February 2023

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1

Yamada, Ryohei, Hisae Nagasaki, Yoko Nagata, Yasuo Wakabayashi, and Akio Iwashima. "Administration of D-aspartate increases D-aspartate oxidase activity in mouse liver." Biochimica et Biophysica Acta (BBA) - General Subjects 990, no. 3 (March 1989): 325–28. http://dx.doi.org/10.1016/s0304-4165(89)80053-4.

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2

Kim, P. M., X. Duan, A. S. Huang, C. Y. Liu, G. l. Ming, H. Song, and S. H. Snyder. "Aspartate racemase, generating neuronal D-aspartate, regulates adult neurogenesis." Proceedings of the National Academy of Sciences 107, no. 7 (January 26, 2010): 3175–79. http://dx.doi.org/10.1073/pnas.0914706107.

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3

Man, Eugene H., George H. Fisher, Iris L. Payan, Rodolfo Cadilla-Perezrios, Nancy M. Garcia, Radhika Chemburkar, Georgine Arends, and William H. Frey. "d-Aspartate in Human Brain." Journal of Neurochemistry 48, no. 2 (February 1987): 510–15. http://dx.doi.org/10.1111/j.1471-4159.1987.tb04122.x.

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4

Furuchi, Takemitsu, and Hiroshi Homma. "Free D-Aspartate in Mammals." Biological & Pharmaceutical Bulletin 28, no. 9 (2005): 1566–70. http://dx.doi.org/10.1248/bpb.28.1566.

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5

Katane, Masumi, and Hiroshi Homma. "D-Aspartate Oxidase: The Sole Catabolic Enzyme Acting on Free D-Aspartate in Mammals." Chemistry & Biodiversity 7, no. 6 (June 16, 2010): 1435–49. http://dx.doi.org/10.1002/cbdv.200900250.

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6

Kera, Yoshio, Hideaki Aoyama, Nobuyoshi Watanabe, and Ryo-hei Yamada. "Distribution of d-aspartate oxidase and free d-glutamate and d-aspartate in chicken and pigeon tissues." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 115, no. 1 (September 1996): 121–26. http://dx.doi.org/10.1016/0305-0491(96)00089-2.

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7

Huang, Yanhua H., Sukumaran Muralidharan, Saurabh R. Sinha, Joseph P. Y. Kao, and Dwight E. Bergles. "Ncm-d-aspartate: A novel caged d-aspartate suitable for activation of glutamate transporters and N-methyl-d-aspartate (NMDA) receptors in brain tissue." Neuropharmacology 49, no. 6 (November 2005): 831–42. http://dx.doi.org/10.1016/j.neuropharm.2005.07.018.

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8

Nagasaki, H., R. Yamada, R. Konno, Y. Yasumura, and A. Iwashima. "D-Aspartate oxidase activity and D-aspartate content in a mutant mouse strain lacking D-amino acid oxidase." Experientia 46, no. 5 (May 1990): 468–70. http://dx.doi.org/10.1007/bf01954233.

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9

Huang, Alex S., Dan A. Lee, and Seth Blackshaw. "d-Aspartate and d-aspartate oxidase show selective and developmentally dynamic localization in mouse retina." Experimental Eye Research 86, no. 4 (April 2008): 704–9. http://dx.doi.org/10.1016/j.exer.2008.01.015.

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10

Huang, A. S. "D-Aspartate Regulates Melanocortin Formation and Function: Behavioral Alterations in D-Aspartate Oxidase-Deficient Mice." Journal of Neuroscience 26, no. 10 (March 8, 2006): 2814–19. http://dx.doi.org/10.1523/jneurosci.5060-05.2006.

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11

Topo, Enza, George Fisher, Andrea Sorricelli, Francesco Errico, Alessandro Usiello, and Antimo D'Aniello. "Thyroid Hormones and D-Aspartic Acid, D-Aspartate Oxidase, D-Aspartate Racemase, H2O2, and ROS in Rats and Mice." Chemistry & Biodiversity 7, no. 6 (June 16, 2010): 1467–78. http://dx.doi.org/10.1002/cbdv.200900360.

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12

Homma, H., Z. Xong, and K. Imai. "D-Aspartate in the rat testis." Biochemical Society Transactions 28, no. 5 (October 1, 2000): A342. http://dx.doi.org/10.1042/bst028a342.

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13

Falvo, Sara, Alessandra Santillo, Gabriella Chieffi Baccari, Federica Cioffi, and Maria Maddalena Di Fiore. "d-aspartate and N-methyl-d-aspartate promote proliferative activity in mouse spermatocyte GC-2 cells." Reproductive Biology 22, no. 1 (March 2022): 100601. http://dx.doi.org/10.1016/j.repbio.2021.100601.

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14

Storer, R. J., and P. J. Goadsby. "Trigeminovascular nociceptive transmission involves N-methyl-d-aspartate and non-N-methyl-d-aspartate glutamate receptors." Neuroscience 90, no. 4 (June 1999): 1371–76. http://dx.doi.org/10.1016/s0306-4522(98)00536-3.

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15

Katane, Masumi, and Hiroshi Homma. "ChemInform Abstract: D-Aspartate Oxidase: The Sole Catabolic Enzyme Acting on Free D-Aspartate in Mammals." ChemInform 41, no. 36 (August 12, 2010): no. http://dx.doi.org/10.1002/chin.201036260.

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16

Beard, M. E. "D-aspartate oxidation by rat and bovine renal peroxisomes: an electron microscopic cytochemical study." Journal of Histochemistry & Cytochemistry 38, no. 9 (September 1990): 1377–81. http://dx.doi.org/10.1177/38.9.1974901.

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D-amino acid oxidase, a peroxisomal enzyme, and D-aspartate oxidase, a potential peroxisomal enzyme, share biochemical attributes. Both produce hydrogen peroxide in flavin-requiring oxidative reactions. Such similarities suggest that D-aspartate oxidase may also be localized to peroxisomes. Definitive identification of D-aspartate oxidase as a peroxisomal enzyme depends, however, on visualization at the electron microscopic level. Using incubation conditions shown to be specific for the enzyme in biochemical studies, this report extends the cytochemical localization of D-amino acid oxidase to bovine renal peroxisomes, and shows that D-aspartate can be oxidized by rat and bovine renal peroxisomes. An unexpected finding was the sensitivity of both D-amino acid oxidase activity (proline specific) and D-aspartate oxidase activity to inhibition by agents used in biochemical studies to discriminate between the two enzyme activities. Therefore, it is possible that, in the cytochemical system used in this study, (a) either D-proline and D-aspartate are substrates for only one enzyme or (b) the two enzymes have additional overlapping biochemical properties.

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17

Deng, Meichun, Shao-Rui Chen, Hong Chen, and Hui-Lin Pan. "α2δ-1–Bound N-Methyl-d-aspartate Receptors Mediate Morphine-induced Hyperalgesia and Analgesic Tolerance by Potentiating Glutamatergic Input in Rodents." Anesthesiology 130, no. 5 (May 1, 2019): 804–19. http://dx.doi.org/10.1097/aln.0000000000002648.

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Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Chronic use of μ-opioid receptor agonists paradoxically causes both hyperalgesia and the loss of analgesic efficacy. Opioid treatment increases presynaptic N-methyl-d-aspartate receptor activity to potentiate nociceptive input to spinal dorsal horn neurons. However, the mechanism responsible for this opioid-induced activation of presynaptic N-methyl-d-aspartate receptors remains unclear. α2δ-1, formerly known as a calcium channel subunit, interacts with N-methyl-d-aspartate receptors and is primarily expressed at presynaptic terminals. This study tested the hypothesis that α2δ-1–bound N-methyl-d-aspartate receptors contribute to presynaptic N-methyl-d-aspartate receptor hyperactivity associated with opioid-induced hyperalgesia and analgesic tolerance. Methods Rats (5 mg/kg) and wild-type and α2δ-1–knockout mice (10 mg/kg) were treated intraperitoneally with morphine twice/day for 8 consecutive days, and nociceptive thresholds were examined. Presynaptic N-methyl-d-aspartate receptor activity was recorded in spinal cord slices. Coimmunoprecipitation was performed to examine protein–protein interactions. Results Chronic morphine treatment in rats increased α2δ-1 protein amounts in the dorsal root ganglion and spinal cord. Chronic morphine exposure also increased the physical interaction between α2δ-1 and N-methyl-d-aspartate receptors by 1.5 ± 0.3 fold (means ± SD, P = 0.009, n = 6) and the prevalence of α2δ-1–bound N-methyl-d-aspartate receptors at spinal cord synapses. Inhibiting α2δ-1 with gabapentin or genetic knockout of α2δ-1 abolished the increase in presynaptic N-methyl-d-aspartate receptor activity in the spinal dorsal horn induced by morphine treatment. Furthermore, uncoupling the α2δ-1–N-methyl-d-aspartate receptor interaction with an α2δ-1 C terminus–interfering peptide fully reversed morphine-induced tonic activation of N-methyl-d-aspartate receptors at the central terminal of primary afferents. Finally, intraperitoneal injection of gabapentin or intrathecal injection of an α2δ-1 C terminus–interfering peptide or α2δ-1 genetic knockout abolished the mechanical and thermal hyperalgesia induced by chronic morphine exposure and largely preserved morphine’s analgesic effect during 8 days of morphine treatment. Conclusions α2δ-1–Bound N-methyl-d-aspartate receptors contribute to opioid-induced hyperalgesia and tolerance by augmenting presynaptic N-methyl-d-aspartate receptor expression and activity at the spinal cord level.

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18

Shibata, Kimihiko, Noriko Sugaya, Yuko Kuboki, Hiroko Matsuda, Katsumasa Abe, Shouji Takahashi, and Yoshio Kera. "Aspartate racemase and D-aspartate in starfish; possible involvement in testicular maturation." Bioscience, Biotechnology, and Biochemistry 84, no. 1 (September 3, 2019): 95–102. http://dx.doi.org/10.1080/09168451.2019.1660614.

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19

Fleck, Mark W., German Barrionuevo, and Alan M. Palmer. "Synaptosomal and vesicular accumulation of l-glutamate, l-aspartate and d-aspartate." Neurochemistry International 39, no. 3 (September 2001): 217–25. http://dx.doi.org/10.1016/s0197-0186(01)00018-3.

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20

Molla, Gianluca, Antonio Chaves‐Sanjuan, Antonio Savinelli, Marco Nardini, and Loredano Pollegioni. "Structure and kinetic properties of human d ‐aspartate oxidase, the enzyme‐controlling d ‐aspartate levels in brain." FASEB Journal 34, no. 1 (November 29, 2019): 1182–97. http://dx.doi.org/10.1096/fj.201901703r.

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21

Roginski, Raymond S., Farida Goubaeva, Maya Mikami, Emma Fried-Cassorla, Mohan R. Nair, and Jay Yang. "GRINL1A colocalizes with N-methyl D-aspartate receptor NR1 subunit and reduces N-methyl D-aspartate toxicity." NeuroReport 19, no. 17 (November 2008): 1721–26. http://dx.doi.org/10.1097/wnr.0b013e328317f05f.

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22

Shibata, Kimihiko, Atsuko Tarui, Natsumi Todoroki, Shinjiro Kawamoto, Shouji Takahashi, Yoshio Kera, and Ryo-hei Yamada. "Occurrence of N-methyl-l-aspartate in bivalves and its distribution compared with that of N-methyl-d-aspartate and d,l-aspartate." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 130, no. 4 (December 2001): 493–500. http://dx.doi.org/10.1016/s1096-4959(01)00455-9.

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23

D'ANIELLO, Salvatore, Patrizia SPINELLI, Gabriele FERRANDINO, Kevin PETERSON, Mara TSESARSKIA, George FISHER, and Antimo D'ANIELLO. "Cephalopod vision involves dicarboxylic amino acids: D-aspartate, L-aspartate and L-glutamate." Biochemical Journal 386, no. 2 (February 22, 2005): 331–40. http://dx.doi.org/10.1042/bj20041070.

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In the present study, we report the finding of high concentrations of D-Asp (D-aspartate) in the retina of the cephalopods Sepia officinalis, Loligo vulgaris and Octopus vulgaris. D-Asp increases in concentration in the retina and optic lobes as the animal develops. In neonatal S. officinalis, the concentration of D-Asp in the retina is 1.8±0.2 μmol/g of tissue, and in the optic lobes it is 5.5±0.4 μmol/g of tissue. In adult animals, D-Asp is found at a concentration of 3.5±0.4 μmol/g in retina and 16.2±1.5 μmol/g in optic lobes (1.9-fold increased in the retina, and 2.9-fold increased in the optic lobes). In the retina and optic lobes of S. officinalis, the concentration of D-Asp, L-Asp (L-aspartate) and L-Glu (L-glutamate) is significantly influenced by the light/dark environment. In adult animals left in the dark, these three amino acids fall significantly in concentration in both retina (approx. 25% less) and optic lobes (approx. 20% less) compared with the control animals (animals left in a diurnal/nocturnal physiological cycle). The reduction in concentration is in all cases statistically significant (P=0.01–0.05). Experiments conducted in S. officinalis by using D-[2,3-3H]Asp have shown that D-Asp is synthesized in the optic lobes and is then transported actively into the retina. D-aspartate racemase, an enzyme which converts L-Asp into D-Asp, is also present in these tissues, and it is significantly decreased in concentration in animals left for 5 days in the dark compared with control animals. Our hypothesis is that the dicarboxylic amino acids, D-Asp, L-Asp and L-Glu, play important roles in vision.

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24

Hsu, Chin, Jau-Nan Lee, Mei-Ling Ho, Bi-Hwa Cheng, Pi-Hseuh Shirley Li, and John Yuh-Lin Yu. "The facilitatory effect of N-methyl-D-aspartate on sexual receptivity in female rats through GnRH release." Acta Endocrinologica 128, no. 4 (April 1993): 385–88. http://dx.doi.org/10.1530/acta.0.1280385.

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The purpose of this study was to examine whether N-methyl-D-aspartate affects the sexual receptivity of female rats. Monosodium L-glutamate was used as a neurotoxin to induce hypogonadal status. Matured normal and monosodium L-glutamate-treated rats were ovariectomized and implanted subcutaneously with estradiol capsules. One week later, lordosis responsiveness was observed before and 10 min after N-methyl-D-aspartate (40 mg/kg of BW, ip) administration. The results showed that N-methyl-D-aspartate caused a remarkable increase of lordosis quotient in control rats but not in monosodium L-glutamate-treated rats. Moreover, the possible action site of N-methyl-D-aspartate in the enhancement of receptivity was evaluated by the post-castrational LH rise, pituitary LH release in response to GnRH, and N-methyl-D-aspartate-evoked GnRH releasability. The results revealed that: (a) serum levels of LH in monosodium L-glutamate-treated rats were lower (p <0.01) than those of control rats after ovariectomy; (b) there was no significant difference of pituitary LH release responsiveness to GnRH test between two groups; and (c) N-methyl-D-aspartate-evoked LH release in monosodium L-glutamate-treated rats was similar to that in the control rats. In conclusion, N-methyl-D-aspartate may facilitate the sexual receptivity through stimulating GnRH release. The failure of N-methyl-D-aspartate in enhancing receptivity in monosodium L-glutamate-treated rats is probably due to the cellular damage by monosodium L-glutamate on specific areas responsible for lordosis.

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25

Matsuda, Satsuki, Masumi Katane, Kazuhiro Maeda, Yuusuke Kaneko, Yasuaki Saitoh, Tetsuya Miyamoto, Masae Sekine, and Hiroshi Homma. "Biosynthesis of d-aspartate in mammals: the rat and human homologs of mouse aspartate racemase are not responsible for the biosynthesis of d-aspartate." Amino Acids 47, no. 5 (February 3, 2015): 975–85. http://dx.doi.org/10.1007/s00726-015-1926-0.

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26

Millichap, J. Gordon. "Anti-N-Methyl-D-Aspartate Receptor Encephalitis." Pediatric Neurology Briefs 27, no. 5 (May 1, 2013): 39. http://dx.doi.org/10.15844/pedneurbriefs-27-5-9.

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27

Williams, Michael, Patricia A. Loo, Deborah E. Murphy, Albert F. Braunwalder, Michael F. Jarvis, and Matthew A. Sills. "The N-Methyl-D-Aspartate Receptor Complex." Journal of Receptor Research 8, no. 1-4 (January 1988): 195–203. http://dx.doi.org/10.3109/10799898809048987.

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28

Libá, Zuzana, Jitka Hanzalová, Věra Sebroňová, and Vladimír Komárek. "Anti‑N‑ Methyl‑ D‑ Aspartate Receptor Encephalitis." Česká a slovenská neurologie a neurochirurgie 77/110, no. 5 (September 29, 2014): 624–30. http://dx.doi.org/10.14735/amcsnn2014624.

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29

Sukiennik, Andrew W., and Richard M. Kream. "N-methyl-d-aspartate receptors and pain." Current Opinion in Anaesthesiology 8, no. 5 (October 1995): 445–49. http://dx.doi.org/10.1097/00001503-199510000-00015.

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30

Li, Hua, Yan-ke Guo, Ying-lin Cui, and Tao Peng. "Anti-N-methyl-D-aspartate receptor encephalitis." Medicine 97, no. 50 (December 2018): e13625. http://dx.doi.org/10.1097/md.0000000000013625.

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31

Lim, Sian Y., Ragesh Panikkath, Charoen Mankongpaisarnrung, Ebtesam Islam, Zachary Mulkey, and Kenneth Nugent. "Anti-N-Methyl-d-Aspartate Receptor Encephalitis." American Journal of the Medical Sciences 345, no. 6 (June 2013): 491–93. http://dx.doi.org/10.1097/maj.0b013e3182760e3b.

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32

Boni, R., R. Santillo, G. Macchia, P. Spinelli, G. Ferrandino, and A. D’Aniello. "d-Aspartate and reproductive activity in sheep." Theriogenology 65, no. 7 (April 2006): 1265–78. http://dx.doi.org/10.1016/j.theriogenology.2005.07.019.

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33

Zhao, Bailey, and David G. Nelson. "Anti–N-Methyl-D-Aspartate Receptor Encephalitis." Pediatric Emergency Care 35, no. 9 (September 2019): e159-e161. http://dx.doi.org/10.1097/pec.0000000000001853.

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34

Chenard, B. L., T. W. Butler, I. A. Shalaby, M. A. Prochniak, B. K. Koe, and C. B. Fox. "Oxindole N-Methyl-D-Aspartate (NMDA) antagonists." Bioorganic & Medicinal Chemistry Letters 3, no. 1 (January 1993): 91–94. http://dx.doi.org/10.1016/s0960-894x(00)80098-0.

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35

Hung, Te-Yu, Ning-Hui Foo, and Ming-Chi Lai. "Anti-N-Methyl-d-Aspartate Receptor Encephalitis." Pediatrics & Neonatology 52, no. 6 (December 2011): 361–64. http://dx.doi.org/10.1016/j.pedneo.2011.08.012.

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36

Fisher, George H., Iris L. Payan, Shou-Jian Chou, Eugene H. Man, Stan Cerwinski, Theresa Martin, Carolyn Emory, and William H. Frey. "Racemized D-aspartate in Alzheimer neurofibrillary tangles." Brain Research Bulletin 28, no. 1 (January 1992): 127–31. http://dx.doi.org/10.1016/0361-9230(92)90239-t.

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37

Homma, H. "Biochemistry of D-aspartate in mammalian cells." Amino Acids 32, no. 1 (June 7, 2006): 3–11. http://dx.doi.org/10.1007/s00726-006-0354-6.

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38

Puggioni, Vincenzo, Antonio Savinelli, Matteo Miceli, Gianluca Molla, Loredano Pollegioni, and Silvia Sacchi. "Biochemical characterization of mouse d-aspartate oxidase." Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1868, no. 10 (October 2020): 140472. http://dx.doi.org/10.1016/j.bbapap.2020.140472.

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39

Halbert, Roger Kelsey. "Anti-N-Methyl-D-Aspartate Receptor Encephalitis." Journal of Neuroscience Nursing 48, no. 5 (October 2016): 270–73. http://dx.doi.org/10.1097/jnn.0000000000000232.

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40

Dietrich, W. D., O. Alonso, M. Halley, R. Busto, and M. Y. T. Globus. "Intraventricular infusion of N-methyl-d-aspartate." Acta Neuropathologica 84, no. 6 (November 1992): 621–29. http://dx.doi.org/10.1007/bf00227739.

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41

Dietrich, W. D., M. Halley, O. Alonso, M. Y. T. Globus, and R. Busto. "Intraventricular infusion of N-methyl-D-aspartate." Acta Neuropathologica 84, no. 6 (November 1992): 630–37. http://dx.doi.org/10.1007/bf00227740.

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42

Olney, John W. "Excitotoxicity and N-methyl-D-Aspartate receptors." Drug Development Research 17, no. 4 (1989): 299–319. http://dx.doi.org/10.1002/ddr.430170406.

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43

Korinek, M., M. Sedlacek, O. Cais, I. Dittert, and L. Vyklicky. "Temperature dependence of N-methyl-d-aspartate receptor channels and N-methyl-d-aspartate receptor excitatory postsynaptic currents." Neuroscience 165, no. 3 (February 2010): 736–48. http://dx.doi.org/10.1016/j.neuroscience.2009.10.058.

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44

Nicoletti, Carolina G., Fabrizia Monteleone, Girolama A. Marfia, Alessandro Usiello, Fabio Buttari, Diego Centonze, and Francesco Mori. "Oral D-Aspartate enhances synaptic plasticity reserve in progressive multiple sclerosis." Multiple Sclerosis Journal 26, no. 3 (February 7, 2019): 304–11. http://dx.doi.org/10.1177/1352458519828294.

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Background: Synaptic plasticity reserve correlates with clinical recovery after a relapse in relapsing–remitting forms of multiple sclerosis (MS) and is significantly compromised in patients with progressive forms of MS. These findings suggest that progression of disability in MS is linked to reduced synaptic plasticity reserve. D-Aspartate, an endogenous aminoacid approved for the use in humans as a dietary supplement, enhances synaptic plasticity in mice. Objective: To test whether D-Aspartate oral intake increases synaptic plasticity reserve in progressive MS patients. Methods: A total of 31 patients affected by a progressive form of MS received either single oral daily doses of D-Aspartate 2660 mg or placebo for 4 weeks. Synaptic plasticity reserve and trans-synaptic cortical excitability were measured through transcranial magnetic stimulation (TMS) protocols before and after D-Aspartate. Results: Both TMS-induced long-term potentiation (LTP), intracortical facilitation (ICF) and short-interval ICF increased after 2 and 4 weeks of D-Aspartate but not after placebo, suggesting an enhancement of synaptic plasticity reserve and increased trans-synaptic glutamatergic transmission. Conclusion: Daily oral D-Aspartate 2660 mg for 4 weeks enhances synaptic plasticity reserve in patients with progressive MS, opening the path to further studies assessing its clinical effects on disability progression.

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45

ffrench-Mullen, J. M., N. Hori, and D. O. Carpenter. "Receptors for excitatory amino acids on neurons in rat pyriform cortex." Journal of Neurophysiology 55, no. 6 (June 1, 1986): 1283–94. http://dx.doi.org/10.1152/jn.1986.55.6.1283.

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The actions of a variety of agonists and antagonists of the excitatory amino acids on rat pyriform cortex pyramidal neurons were studied in a submerged, perfused brain slice. The order of potency for the agonists, applied by ionophoresis, was kainate greater than quisqualate greater than N-methyl-D-aspartate greater than aspartate = glutamate. The endogenous monosynaptic excitation of pyramidal neurons upon stimulation of the lateral olfactory tract was blocked post-synaptically by DL-2-amino-4-phosphonobutyric acid, although this drug did not consistently block any of the exogenous responses. The synaptic excitation was not blocked, however, by antagonists presumed specific for the quisqualate (glutamate diethyl ester), kainate, (gamma-D-glutamylglycine), or N-methyl-D-aspartate (DL-2-amino-5-phosphonovaleric acid, DL-2-amino-7-phosphonohetaonic acid) receptors. Several antagonists blocked N-methyl-D-aspartate responses at lower concentrations than those to aspartate, and other antagonists distinguished between kainate and quisqualate responses. These results suggest that 1) pyriform neurons have a variety of receptors that have properties somewhat different from those found in other preparations and 2) the endogenous transmitter activates a receptor distinct from those activated by kainate, quisqualate, and N-methyl-D-aspartate.

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46

Benická, Alžběta, Radovan Pilka, and Patrik Flodr. "Autoimmune anti-N-methyl-D-aspartate receptor encephalitis – paraneoplastic syndrome of ovarian teratoma." Česká gynekologie 86, no. 6 (December 21, 2021): 397–99. http://dx.doi.org/10.48095/cccg2021397.

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Objective: Case presentation and subsequent diagnostic and therapeutic procedure of autoimmune encephalitis caused by the presence of ovarian teratoma. Case report: We describe the case of a young woman with symptoms of an acute psychotic attack unresponsive to antipsychotic treatment. Anti-N-methyl-D-aspartate receptor encephalitis was diagnosed within the interdisciplinary cooperation at the University Hospital in Olomouc. Conclusion: This type of rare and potentially fatal paraneoplastic limbic encephalitis occurs predominantly in young women. Due to the high variability of neuropsychiatric symptoms, the diagnosis of the disease is very difficult, and therefore patients are often primarily incorrectly treated for other neurological or psychiatric diseases. The most prognostically important part is early diagnosis and adequate therapy. Key words: ovarian teratoma – anti-N-methyl-D-aspartate receptor encephalitis (anti-NMDAR encephalitis) – paraneoplastic syndrome

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Kiriyama, Yoshimitsu, and Hiromi Nochi. "D-Amino Acids in the Nervous and Endocrine Systems." Scientifica 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/6494621.

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Abstract:

Amino acids are important components for peptides and proteins and act as signal transmitters. Only L-amino acids have been considered necessary in mammals, including humans. However, diverse D-amino acids, such as D-serine, D-aspartate, D-alanine, and D-cysteine, are found in mammals. Physiological roles of these D-amino acids not only in the nervous system but also in the endocrine system are being gradually revealed. N-Methyl-D-aspartate (NMDA) receptors are associated with learning and memory. D-Serine, D-aspartate, and D-alanine can all bind to NMDA receptors. H2S generated from D-cysteine reduces disulfide bonds in receptors and potentiates their activity. Aberrant receptor activity is related to diseases of the central nervous system (CNS), such as Alzheimer’s disease, amyotrophic lateral sclerosis, and schizophrenia. Furthermore, D-amino acids are detected in parts of the endocrine system, such as the pineal gland, hypothalamus, pituitary gland, pancreas, adrenal gland, and testis. D-Aspartate is being investigated for the regulation of hormone release from various endocrine organs. Here we focused on recent findings regarding the synthesis and physiological functions of D-amino acids in the nervous and endocrine systems.

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Zaar, K., A. Völkl, and H. D. Fahimi. "d-aspartate oxidase in rat, bovine and sheep kidney cortex is localized in peroxisomes." Biochemical Journal 261, no. 1 (July 1, 1989): 233–38. http://dx.doi.org/10.1042/bj2610233.

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Abstract:

D-Aspartate oxidase (EC 1.4.3.1) was assayed in subcellular fractions and in highly purified peroxisomes from rat, bovine and sheep kidney cortex as well as from rat liver. During all steps of subcellular-fractionation procedures, D-aspartate oxidase co-fractionated with peroxisomal marker enzymes. In highly purified preparations of peroxisomes, the enrichment of D-aspartate oxidase activity over the homogenate is about 32-fold, being comparable with that of the peroxisomal marker enzymes catalase and D-amino acid oxidase. Disruption of the peroxisomes by freezing and thawing released more than 90% of the enzyme activity, which is typical for soluble peroxisomal-matrix proteins. Our findings provide strong evidence that in these tissues D-aspartate oxidase is a peroxisomal-matrix protein and should be added as an additional flavoprotein oxidase to the known set of peroxisomal oxidases.

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Moore, L. E., J. T. Buchanan, and C. R. Murphey. "Localization and interaction of N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors of lamprey spinal neurons." Biophysical Journal 68, no. 1 (January 1995): 96–103. http://dx.doi.org/10.1016/s0006-3495(95)80163-3.

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Errico, Francesco, Alessandra Bonito-Oliva, Vincenza Bagetta, Daniela Vitucci, Rosaria Romano, Elisa Zianni, Francesco Napolitano, et al. "Higher free d-aspartate and N-methyl-d-aspartate levels prevent striatal depotentiation and anticipate l-DOPA-induced dyskinesia." Experimental Neurology 232, no. 2 (December 2011): 240–50. http://dx.doi.org/10.1016/j.expneurol.2011.09.013.

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