Phospholipids (PLs) of neuronal membranes are active universal neuromodulators. They regulate many functions of the neurons, including receptors signaling, which during a hemorrhagic shock (HS) get damaged, leading to encephalopathy. An analysis of the data, presented in this review, suggests that the dysregulation of PL metabolism in synaptic membranes is a key mechanism of encephalopathy during HS. Stabilizing the PL composition of the neuronal membranes may become one of the most important treatment methods for shock-induced disorders of brain functions.
| Published in | American Journal of BioScience (Volume 3, Issue 4) |
| DOI | 10.11648/j.ajbio.20150304.13 |
| Page(s) | 133-140 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2024. Published by Science Publishing Group |
Phospholipids, Synaptic Membranes, Hemorrhagic Shock
| [1] | V. L. Kozhura, Zh.V. Solov'eva, I.S. Novoderzhkina, N.V. Nosova. “The neurochemical, molecular and ultrastructural mechanisms of the formation of latent postresuscitation encephalopathy”. Anesteziol. Reanimatol. [in Russian]. nn. 5, pp. 52-56, May 1996 |
| [2] | V.V. Moroz. “Postreanimatological illness as dysregulation pathology.” Dysregulation Pathology [in Russian], Moskow. 2002, pp. 233-259 |
| [3] | H.Y Kim., B.X Huang. A.A. Spector. “Phosphatidylserine in the brain: metabolism and function”. Prog Lipid Res. vol. 56, pp. 1-18, November 2014 |
| [4] | M.C. Waugh. PIPs in neurological diseases. Biochem. Biophys. Acta, in press. |
| [5] | J. Klein. “Membrane breakdown in acute and chronic neurodegeneration: focus on choline-containing phospholipids”. J. Neural. Transm. vol.107, pp. 1027 1063, February 2000 |
| [6] | V.A. Tsirlin. “Bulbar vasomotor center – morpho functional and neurochemical Organization”. Arterial Hypertension [in Russian]. nn. 8, pp. 77- 81, August 2003 |
| [7] | G.F. Leskova. “Role of synaptic membranes phospholipids in regulation of neurotransmission mechanisms in Medula Oblangata during hemorrhagic shock in cats”. Pathogenesis [in Russian]. nn. 4, pp. 57-65, April 2006 |
| [8] | G.F. Leskova. “Changes in phospholipid composition of synaptic membranes in frontal lobes of cerebral hemispheres in cats at various stages of hemorrhagic shock”. Bull. Exp. Biol. Med. vol.146, pp. 401-404, April 2008 |
| [9] | H. Kubista, K. Kosenburger, P. Mahlknecht, H. Drobny, S. Boehm. “Inhibition of transmitter release from rat sympathetic neurons via presynaptic M1 muscarinic acetylcholine receptors”. Br. J. Pharmacol. vol. 156, pp.1342–1352, April 2009 |
| [10] | T.G. Borda, G. Cremaschi, L. Sterin-Borda. “Haloperidol-mediated phosphoinositide hydrolysis via direct activation of alpha1-adrenoceptors in frontal cerebral rat cortex”. Can. J. Physiol. Pharmacol. vol. 77, pp. 22-28, January 1999 |
| [11] | M.J. Berridge, M.D. Bootman, P. Lipp. “Calcium – a life and death signal”. Nature. vol. 395, pp. 645-648, October1998 |
| [12] | S. Koizumi, P. Rosa, G.B. Willars. “Mechanisms underlying the neuronal calcium sensor-1-evoked enhancement of exocytosis in PC12 cell”. J. Biol. Chem. vol. 277, pp. 30315-30324, May 2002 |
| [13] | Q. Zheng, J.A. Bobich, J. Vidugiriene. “Neuronal calcium sensor-1facilitates neuronal exocytosis through phosphatidylinositol 4-kinase”. J. Neurochim. vol. 92, pp. 442-451, February 2005 |
| [14] | C.U.M. Smith Elements of molecular neurology. Atrium. Chister. Wiley & Sons. LTD. 2002. |
| [15] | R.,Masgrau, J.M. Servitja, K.W.Yong, R. Pardo, E. Sarri, S.R. Nahorski, F. Picatoste. “Characterization of the metabotropic glutamate receptors mediating phospholipase C activation and calcium release in cerebellar granule cells: calcium-dependence of the phospholipase C response”. Eur. J. Neurosci. vol. 13, pp. 248-256, January 2001 |
| [16] | A.A. Boldyrev. “Functional interaction between various glutamate receptors”. Bull. Exp. Biol. Med. [in Russian]. vol. 130, pp. 244-251, September 2000 |
| [17] | I.I. Abramez, I.B. Komissarova. “Glutamatergic mechanisms of brain Ischemic damages”. J. AMN Ukraina [in Russian]. nn. 7, pp. 613-633, July 2001 |
| [18] | P.V. Avdonin. “The structura and signal properties of G-protein-coupled receptors complexes”. Biol. Membr. [in Russian]. vol. 22, pp. 3-26, January 2005 |
| [19] | V.A.Tkachuk. “Molecular mechanisms of neuroendocrine regulation”. Soros. Educational J. [in Russian]. nn. 6, pp. 16-20, June 1998 |
| [20] | C.P. Morgan, A. Skippen, B. Segui, A. Ball, V. Allen-Baume, B. Larijani, J., Murray-Rust, N. McDonald, G. Sapkota, N. Morrice, S. Cockcroft. “Phosphorylation of a distinct structural form of phosphatidylinositol transfer protein alpha at Ser16 by protein kinase C disrupts receptor-mediated phospholipase C signaling by inhibiting deliver of phosphatidylinositol to membranes”. J. Biol. Chem. vol. 279, pp. 47159-47171, November 2004 |
| [21] | S.M. Baijalieh, R.H. Scheller. “The biochemistry of neurotransmitter secretion”. J. Biol. Chem. vol. 270, pp. 1971-1974, February 1995 |
| [22] | S.K. DebBurman, J. Ptasienski, E. E. Boetticher, J.W. Lomasney, J.L.Benovic, M.M. Hosey. “Lipid-mediated regulation of G protein-coupled receptor kinases 2 and 3. J. Biol. Chem. vol. 270, pp. 5742-5747, March 1995 |
| [23] | K.W. Young, D. Billups, C.P. Nelson, N. Johnston, J.M. Willets, M.J. Schell, R.A. Challiss, S.R. Nahorski. “Muscarinic acetylcholine receptor activation enhances hippocampal neuron excitability and potentiates synaptically evoked Ca(2+) signals via phosphatidylinositol 4,5-bisphosphate depletion”. Mol. Cell. Neurosci. vol, 30, pp. 48-57, September 2005 |
| [24] | S.J. Veerasingham, M.,Yamazato, K.H. Berecek, J.M. Wyss, M.K. Raizada. “Increased PI3-kinase in presympathetic brain areas of the spontaneously hypertensive rat”. Circ. Res. vol. 96, pp. 277-279, January 2005 |
| [25] | T.T. Ching, D.S. Wang, A.L. Hsu, P.J. Lu, C.S. Chen. “Identification of multiple phosphoinositide-specific phospholipases D as new regulatory enzymes for phosphatidylinositol 3,4, 5-trisphosphate”. J. Biol. Chem. vol. 274, pp. 8611-8617, March 1999 |
| [26] | Y. Sang, D. Cui, X. Wang. “Phospholipase D and phosphatidic acid-mediated generation of superoxide in Arabidopsis”. Plant Physiol. vol.126, pp. 449-458, August 2001 |
| [27] | S.T. Kim, Y.H. Chung, H.S. Lee, S.J. Chung, J.H. Lee, U.D. Sohn, Y.K. Shin, E.S. Park, H.C. Kim, J.H. Jeong. “Protective effects of phosphatidylcholine on oxaliplatin-induced neuropathy in rats. Life Sci., in press. |
| [28] | T. Hirabayashi, T. Murayama, T. Shimiza. “Regulatory mechanism and physiological role of cytosolic phospholipase A2.” Biol. Pharmacol. Bull. vol. 27, pp. 1168-1173, August 2004 |
| [29] | G. Massicotte. “Modification of glutamate receptors by phospholipase A2: its role in adaptive neural plasticity.” Cell. Mol. Life Sci. vol. 57, pp. 1542-1550, October 2000 |
| [30] | F. St-Gelas, C. Menard, P. Congar, L.E. Trudeau, G. Massicotte. Postsynaptic injection of calcium-independent phospholipase A2 inhibitors selectively increases AMPA receptor-mediated synaptic transmission. Hippocampus. vol.14, pp. 319-325, January 2004 |
| [31] | H. Nishio, T. Takeuchi, F. Hata, O. Yagasaki. “Ca(2+)-independent fusion of synaptic vesicles with phospholipase A2-treated presynaptic membranes in vitro”. Biochem. J. vol. 318 (3), pp. 981-987, September 1996 |
| [32] | M.A. DeCoster, G. Lambeau, M. Lazdunski, N.G. Bazan. “Secreted phospholipase A2 potentiates glutamate-induced calcium increase and cell death in primary neuronal cultures”. J. Neurosci. Res. vol. 67, pp. 634-645, March 2002 |
| [33] | A.L. Taylor, S.J. Hewett. “Potassium-evoked glutamate release liberates arachidonic acid from cortical neurons”. J. Biol. Chem. vol. 277, pp. 43881-43887, November 1992 |
| [34] | Q. Chen, D.P. Li, H.L. Pan. “Presynaptic alpha1 adrenergic receptors differentially regulate synaptic glutamate and GABA release to hypothalamic presympathetic neurons”. J. Pharmacol. Exp. Ther. vol. 316, pp. 733-742, 2006 |
| [35] | J.D., Navarro-Lopez, J.M. Delgado-Garcia, J. Yajeya. “Cooperative glutamatergic and cholinergic mechanisms generate short-term modifications of synaptic effectiveness in prepositus hypoglossi neurons”. J. Neurosci. vol. 25, pp. 9902-9906, February 2005 |
| [36] | F. Facchinetti, N.J. Hack, R. Balázs. “Calcium influx via ionotropic glutamate receptors causes long lasting inhibition of metabotropic glutamate receptor-coupled phosphoinositide hydrolysis”. Neurochem. Int. vol. 33, pp. 263-270, September 1998 |
| [37] | F.E. Sieber, R.J. Traystman, L.J. Martin. “Delayed neuronal death after global incomplete ischemia in dogs is accompanied by changes in phospholipase C protein expression”. J. Cereb. Blood Flow. Metab. vol.17, 527- 533, May 1997 |
| [38] | M.M. http://www.ncbi.nlm.nih.gov/pubmed/2201284Billah, J.C. Anthes. “The regulation and cellular functions of phosphatidylcholine hydrolysis”. Biochem J. vol. 269, pp. 281-291, July 1990 |
| [39] | S. Llahi, J.N. Fain. “Alpha 1-adrenergic receptor mediated activation of phospholipase D in rat cerebral cortex”. J. Biol. Chem. vol.. 267, pp. 3679-3685, February 1992 |
| [40] | N.G. Bazan, B. Tu, E.B. Rodriguez de Turco. “What synaptic lipid signaling tells us about seizure-induced damage and epileptogenesis”. Prog. Brain Res. vol. 135, pp. 175-185, 2002 |
| [41] | W.B. Bollag, X. Zhong, M.E. Dodd, D.M. Hardy, X. Zheng, W.T. Allred. “Phospholipased signaling and extracellular signal-regulated kinase-1and –2 phosphorylation (activation) are required for maximal phorbol ester-induced transglutaminase activity, a marker of keratinocyte differentiation”. J. Pharmacol. Exp. Ther. vol. 312, pp.1223-1231, March 2005 |
| [42] | Min D.S., Park S.K., Exton J.H. “Characterization of a rat brain phospholipase D isozyme”. J. Biol. Chem. vol. 273, pp. 7044-7051, March 1998 |
| [43] | M.R Castillo, J.R. Babson. “Ca(2+)-dependent mechanisms of cell injury in cultured cortical neurons”. Neurosci. vol. 86, pp. 1133-1144, October 1998 |
| [44] | M. McDermontti, M.J. Wakelam, A.J. Morris. “Phospholipase D”. Biochem. Cell. Biol. vol. 82, pp. 225-253, February 2004 |
| [45] | M. Liscovitch, V., Chalifa, P. Pertile, C.S. Chen, L.C Cantley.”Novel function of phosphatidylinositol 4, 5-bisphosphate as a cofactor for brain membrane phospholipase D”. J. Biol. Chem. vol. 269, pp. 21403-21406, August 1994 |
| [46] | T. Gasull, E. Sarri., N. Degregorio-Rocasolano, R. Trullas. “NMDA receptor overactivation inhibits phospholipid synthesis by decreasing choline ethanolamine phosphotransferase activity”. J. Neurosci. vol. 23, pp. 4100-4107, May 2003 |
| [47] | R.M. Adibhatla, J.F. Hatcher, R.J. Dempsey. “Cytidine-5'-diphosphocholine affects CTP phosphocholine cytidylyltransferase and lyso phosphatidylcholine after transient brain ischemia”. J. Neurosci. Res. vol. 76, pp. 390-396, May 2004 |
| [48] | V. L. Kozhura. “Neurobiological mechanisms of massive blood loss”. Anaestheziol. Reanimatol. [in Russian]. nn. 6, pp. 51-53javascript:babSpeakIt('английский',170574);, June 2001 |
| [49] | S. Persard, V. Panagia. “Abnormal synthesis of N-methylated phospholipids during calcium paradox of the heart”. J. Mol. Cell. Cardiol. vol. 27, pp. 579-587, 1995 |
| [50] | A.A. Vartanyan, G.V. Apikyan, V.F Vanyushin. “Methylation of phospholipids and synaptic capture of mediator amino acids”. Izv. AN USSR [in Russian], ser. Biol., nn. 5, pp. 786-789, May November 1990 |
| [51] | O.S. Belokoneva, O.V. Zaycev. “Role of membrane lipids in regulation of neuromediators receptors functioning”. Biochemistry [in Russian]. vol. 58, pp. 1685-1708, November 1993 |
| [52] | [52] V.P. Fisenko. “Neurochemical laws of opioid analgesics action on cortex. Bull. Exp. Biol. Med. [in Russian]. vol. 132, pp. 4-11, July 2001 |
| [53] | W. Zhu Z.Z. Pan. “Mu-opioid-mediated inhibition of glutamate synaptic transmission in rat central amygdala neurons”. Neuroscience. vol.133, pp. 97-103, 2005 |
| [54] | V. L. Kozhura, N.V. Nosova. “Apoptosis as the mechanism of delayed posthypoxic encephalopathy”. Bull. Exp. Biol. Med. [in Russian]. appendix 2, pp. 30-32, 2000 |
| [55] | D.M. Faller, D.M. Schilde. “Molecular Вiology of Сell”. [in Russian]. Moskow. 2003. |
| [56] | M.A. McDaniel, S.F. Maier, G.O. Einstein. "Brain-specific" nutrients: a memory cure?” Nutrition. vol. 19, pp. 957-975, November – December 2003 |
| [57] | M. Kingsley. “Effects of phosphatidylserine supplementation on exercising Humans”. Sports Med. vol. 36, pp. 657-669, 2006 |
| [58] | J.T. Wong, K. Tran, G.N. Pierce, A.C. Chan, K. O, P.C. Choy. “Lysophosphatidylcholine stimulates the release of arachidonic acid in human endothelial cells”. J. Biol Chem. vol. 273, pp. 6830-6836, March 1998 |
| [59] | H. Ozaka, K. Ishii, H. Arai, N. Kume, T. Kita. “Lysophosphatidylcholine activates mitogen-activated protein kinases by a tyrosine kinase-dependent pathway in bovine aortic endothelial cells”. Atherosclerosis. vol. 143, pp. 261-266, April 1999 |
| [60] | B.V., Bassa, D.D. Roh, N.D. Varzirl, M.A. Kirschenbaum, V.S. Kamanna. “Lysophosphatidylcholine activates mesangial cell PKC and MAP kinase by PLCgamma-1 and tyrosine kinase-Ras pathways”. Am. J. Physiol. Renal. Physiol. vol. 277 (2), pp. F328-F337, September 1999 |
| [61] | S.Y. Liu, C.H. Yu, J.A. Hays, V. Panagia, N.S. Dhalla. “Modification of heart sarcolemmal phosphoinositide pathway by lysophosphatidylcholine”. Biochim. Biophys. Acta. vol.1349, pp. 264-274, November 1997 |
| [62] | D.A. Cox, M.L. Cohen. “Lysophosphatidylcholine stimulates phospholipase D in human coronary endothelial cells: role of PKC”. Am. J. Phisiol. vol. 271 (2), pp. H1706-H1710, October 1996 |
| [63] | L.S. Golfman, N.J. Haughey, J.T. Wong, J.Y. Jiang, D. Lee, J.D. Geiger, P.C. Choy. “Lysophosphatidylcholine induces arachidonic acid release and calcium overload in cardiac myoblastic H9c2 cells”. J. Lipid. Res. vol. 40, pp. 1818-1826, October 1999. |
APA Style
Galina Fedorovna Leskova. (2015). Dysregulation of Phospholipid Metabolism in Synaptic Membranes and Their Role in Encephalopathy Forming After a Hemorrhagic Shock. American Journal of BioScience, 3(4), 133-140. https://doi.org/10.11648/j.ajbio.20150304.13
ACS Style
Galina Fedorovna Leskova. Dysregulation of Phospholipid Metabolism in Synaptic Membranes and Their Role in Encephalopathy Forming After a Hemorrhagic Shock. Am. J. BioScience 2015, 3(4), 133-140. doi: 10.11648/j.ajbio.20150304.13
AMA Style
Galina Fedorovna Leskova. Dysregulation of Phospholipid Metabolism in Synaptic Membranes and Their Role in Encephalopathy Forming After a Hemorrhagic Shock. Am J BioScience. 2015;3(4):133-140. doi: 10.11648/j.ajbio.20150304.13
Share This Article
Twitter
Linked In
Facebook
Copy
Download@article{10.11648/j.ajbio.20150304.13,
author = {Galina Fedorovna Leskova},
title = {Dysregulation of Phospholipid Metabolism in Synaptic Membranes and Their Role in Encephalopathy Forming After a Hemorrhagic Shock},
journal = {American Journal of BioScience},
volume = {3},
number = {4},
pages = {133-140},
doi = {10.11648/j.ajbio.20150304.13},
url = {https://doi.org/10.11648/j.ajbio.20150304.13},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajbio.20150304.13},
abstract = {Phospholipids (PLs) of neuronal membranes are active universal neuromodulators. They regulate many functions of the neurons, including receptors signaling, which during a hemorrhagic shock (HS) get damaged, leading to encephalopathy. An analysis of the data, presented in this review, suggests that the dysregulation of PL metabolism in synaptic membranes is a key mechanism of encephalopathy during HS. Stabilizing the PL composition of the neuronal membranes may become one of the most important treatment methods for shock-induced disorders of brain functions.},
year = {2015}
}
TY - JOUR T1 - Dysregulation of Phospholipid Metabolism in Synaptic Membranes and Their Role in Encephalopathy Forming After a Hemorrhagic Shock AU - Galina Fedorovna Leskova Y1 - 2015/07/01 PY - 2015 N1 - https://doi.org/10.11648/j.ajbio.20150304.13 DO - 10.11648/j.ajbio.20150304.13 T2 - American Journal of BioScience JF - American Journal of BioScience JO - American Journal of BioScience SP - 133 EP - 140 PB - Science Publishing Group SN - 2330-0167 UR - https://doi.org/10.11648/j.ajbio.20150304.13 AB - Phospholipids (PLs) of neuronal membranes are active universal neuromodulators. They regulate many functions of the neurons, including receptors signaling, which during a hemorrhagic shock (HS) get damaged, leading to encephalopathy. An analysis of the data, presented in this review, suggests that the dysregulation of PL metabolism in synaptic membranes is a key mechanism of encephalopathy during HS. Stabilizing the PL composition of the neuronal membranes may become one of the most important treatment methods for shock-induced disorders of brain functions. VL - 3 IS - 4 ER -
Information
Email: