Relationships between cholinergic phenotype and acetyl-CoA level in hybrid murine neuroblastoma cells of septal origin
High susceptibility of cholinergic neurons to neurotoxic signals may result from their utilization of acetyl‐CoA for both energy production and acetylcholine synthesis. SN56 cholinergic cells were transfected stably with cDNA for choline acetyltransferase. Transfected cells (SN56ChAT2) expressed cho...
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Published in | Journal of neuroscience research Vol. 73; no. 5; pp. 717 - 721 |
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Abstract | High susceptibility of cholinergic neurons to neurotoxic signals may result from their utilization of acetyl‐CoA for both energy production and acetylcholine synthesis. SN56 cholinergic cells were transfected stably with cDNA for choline acetyltransferase. Transfected cells (SN56ChAT2) expressed choline acetyltransferase activity and acetylcholine content, 17 times and 2 times higher, respectively, than did nontransfected cells. Transfection did not change pyruvate dehydrogenase but decreased the acetyl‐CoA level by 62%. Differentiation by cAMP and retinoic acid caused an increase of choline acetyltransferase activity and decrease of acetyl‐CoA levels in both cell lines. Negative correlation was found between choline acetyltransferase activity and acetyl‐CoA level in these cells. SN56ChAT2 cells were more susceptible to excess NO than were native SN56 cells, as evidenced by the thiazolyl blue reduction assay. Thus, the sensitivity of cholinergic neurons to pathologic conditions may depend on the cholinergic phenotype‐dependent availability of acetyl‐CoA. © 2003 Wiley‐Liss, Inc. |
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AbstractList | High susceptibility of cholinergic neurons to neurotoxic signals may result from their utilization of acetyl‐CoA for both energy production and acetylcholine synthesis. SN56 cholinergic cells were transfected stably with cDNA for choline acetyltransferase. Transfected cells (SN56ChAT2) expressed choline acetyltransferase activity and acetylcholine content, 17 times and 2 times higher, respectively, than did nontransfected cells. Transfection did not change pyruvate dehydrogenase but decreased the acetyl‐CoA level by 62%. Differentiation by cAMP and retinoic acid caused an increase of choline acetyltransferase activity and decrease of acetyl‐CoA levels in both cell lines. Negative correlation was found between choline acetyltransferase activity and acetyl‐CoA level in these cells. SN56ChAT2 cells were more susceptible to excess NO than were native SN56 cells, as evidenced by the thiazolyl blue reduction assay. Thus, the sensitivity of cholinergic neurons to pathologic conditions may depend on the cholinergic phenotype‐dependent availability of acetyl‐CoA. © 2003 Wiley‐Liss, Inc. Abstract High susceptibility of cholinergic neurons to neurotoxic signals may result from their utilization of acetyl‐CoA for both energy production and acetylcholine synthesis. SN56 cholinergic cells were transfected stably with cDNA for choline acetyltransferase. Transfected cells (SN56ChAT2) expressed choline acetyltransferase activity and acetylcholine content, 17 times and 2 times higher, respectively, than did nontransfected cells. Transfection did not change pyruvate dehydrogenase but decreased the acetyl‐CoA level by 62%. Differentiation by cAMP and retinoic acid caused an increase of choline acetyltransferase activity and decrease of acetyl‐CoA levels in both cell lines. Negative correlation was found between choline acetyltransferase activity and acetyl‐CoA level in these cells. SN56ChAT2 cells were more susceptible to excess NO than were native SN56 cells, as evidenced by the thiazolyl blue reduction assay. Thus, the sensitivity of cholinergic neurons to pathologic conditions may depend on the cholinergic phenotype‐dependent availability of acetyl‐CoA. © 2003 Wiley‐Liss, Inc. High susceptibility of cholinergic neurons to neurotoxic signals may result from their utilization of acetyl-CoA for both energy production and acetylcholine synthesis. SN56 cholinergic cells were transfected stably with cDNA for choline acetyltransferase. Transfected cells (SN56ChAT2) expressed choline acetyltransferase activity and acetylcholine content, 17 times and 2 times higher, respectively, than did nontransfected cells. Transfection did not change pyruvate dehydrogenase but decreased the acetyl-CoA level by 62%. Differentiation by cAMP and retinoic acid caused an increase of choline acetyltransferase activity and decrease of acetyl-CoA levels in both cell lines. Negative correlation was found between choline acetyltransferase activity and acetyl-CoA level in these cells. SN56ChAT2 cells were more susceptible to excess NO than were native SN56 cells, as evidenced by the thiazolyl blue reduction assay. Thus, the sensitivity of cholinergic neurons to pathologic conditions may depend on the cholinergic phenotype-dependent availability of acetyl-CoA. |
Author | Tomaszewicz, Maria Madziar, Beata Ćwikowska, Justyna Pawełczyk, Tadeusz Szutowicz, Andrzej Bielarczyk, Hanna |
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Cites_doi | 10.55782/ane-1996-1137 10.1016/S0021-9258(18)69735-2 10.1111/j.1471-4159.1981.tb05319.x 10.1016/S0928-4257(99)80009-6 10.1002/jnr.10040 10.1046/j.1471-4159.2001.00271.x 10.1046/j.1460-9568.1999.00571.x 10.1016/S0014-5793(97)00568-1 10.1111/j.1471-4159.1983.tb08140.x 10.1002/ana.410170505 10.1007/BF02680012 10.1016/0006-8993(90)90626-M 10.1007/BF00965673 10.1016/0003-2697(81)90527-3 10.1111/j.1749-6632.1982.tb31213.x 10.1046/j.1471-4159.1997.69041374.x 10.1097/00001756-200004070-00007 10.1111/j.1471-4159.1975.tb11895.x 10.1016/0003-2697(87)90495-7 10.1016/0003-2697(76)90527-3 10.1016/0006-2952(61)90145-9 |
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References_xml | – volume: 387 start-page: 382 year: 1982 end-page: 403 article-title: The role of the cholinergic system in thiamin deficiency publication-title: Ann N Y Acad Sci – volume: 7 start-page: 88 year: 1961 end-page: 95 article-title: A new and rapid colorimetric determination of acetylcholinesterase activity publication-title: Biochem Pharmacol – volume: 115 start-page: 81 year: 1981 end-page: 87 article-title: Determination of pyruvate dehydrogenase and acetyl‐CoA synthetase using citrate synthase publication-title: Anal Biochem – volume: 69 start-page: 1374 year: 1997 end-page: 1381 article-title: Cellular acetylcholine content and neuronal differentiation publication-title: J Neurochem – volume: 78 start-page: 248 year: 1976 end-page: 254 article-title: A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein‐dye binding publication-title: Anal Biochem – volume: 234 start-page: 2544 year: 1959 end-page: 2547 article-title: Citrate cleavage enzyme. 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Distribution and purification publication-title: J Biol Chem – volume: 66 start-page: 1009 year: 2001 end-page: 1018 article-title: Aluminum, NO and nerve growth factor neurotoxicity in cholinergic neurons publication-title: J Neurosci Res – volume: 24 start-page: 407 year: 1975 end-page: 409 article-title: A rapid radiochemical method for the determination of choline acetyltransferase publication-title: J Neurochem – volume: 11 start-page: 931 year: 2000 end-page: 936 article-title: Differential vulnerability of primary cultured cholinergic neurons to nitric oxide excess publication-title: Neuroreport – volume: 77 start-page: 804 year: 2001 end-page: 811 article-title: Estradiol protects against ATP depletion, mitochondrial membrane potential decline and generation of reactive oxygen species induced by 3‐nitropropionic acid in SK‐N‐SH human neuroblastoma cells publication-title: J Neurochem – volume: 410 start-page: 175 year: 1997 end-page: 179 article-title: Modulation of cholinergic locus expression by glucocorticoids and retinoic acid is cell‐type specific publication-title: FEBS Lett – volume: 7 start-page: 799 year: 1982 end-page: 810 article-title: ATP citrate lyase in cholinergic nerve endings publication-title: Neurochem Res – volume: 15 start-page: 29 year: 2000 end-page: 44 article-title: Acetyl‐CoA metabolism in cholinergic neurons and their susceptibility to neurotoxic inputs publication-title: Metab Brain Dis – volume: 512 start-page: 190 year: 1990 end-page: 200 article-title: Development and characterization of clonal cell lines derived from septal cholinergic neurons publication-title: Brain Res – volume: 40 start-page: 1664 year: 1983 end-page: 1670 article-title: The enzymes of acetyl‐CoA metabolism in differentiating cholinergic (S‐20) and noncholinergic (NIE‐115) neuroblastoma cells publication-title: J Neurochem – volume: 53 start-page: 1083 year: 1995 end-page: 1088 article-title: Altered cholinergic metabolism in rat CNS following aluminum exposure: implications on learning performance publication-title: J Neurochem – volume: 11 start-page: 1523 year: 1999 end-page: 1534 article-title: Acetylcholine synthesis and quantal release reconstituted by transfection of mediatophore and choline acetyltransferase cDNAs publication-title: Eur J Neurosci – volume: 56 start-page: 323 year: 1996 end-page: 339 article-title: Disturbances of acetyl‐CoA, energy and acetylcholine metabolism in some encephalopathies publication-title: Acta Neurobiol Exp – volume: 17 start-page: 444 year: 1985 end-page: 449 article-title: An immunological study of the pyruvate dehydrogenase deficit in Alzheimer's disease publication-title: Ann Neurol – volume: 164 start-page: 292 year: 1987 end-page: 296 article-title: Elimination of CoASH interference from acetyl‐CoA cycling assay by maleic anhydride publication-title: Anal Biochem – volume: 37 start-page: 258 year: 1981 end-page: 260 article-title: Quantitation of cholinergic synaptosomes from guinea pig brain publication-title: J Neurochem – volume: 92 start-page: 379 year: 1998 end-page: 384 article-title: Influence of retinoic acid and of cyclic AMP on the expression of choline acetyltransferase and of vesicular acetylcholine transporter in NG108‐15 cells publication-title: J Physiol (Paris) – volume: 56 start-page: 323 year: 1996 ident: e_1_2_6_21_1 article-title: Disturbances of acetyl‐CoA, energy and acetylcholine metabolism in some encephalopathies publication-title: Acta Neurobiol Exp doi: 10.55782/ane-1996-1137 contributor: fullname: Szutowicz A – volume: 234 start-page: 2544 year: 1959 ident: e_1_2_6_15_1 article-title: Citrate cleavage enzyme. 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Snippet | High susceptibility of cholinergic neurons to neurotoxic signals may result from their utilization of acetyl‐CoA for both energy production and acetylcholine... High susceptibility of cholinergic neurons to neurotoxic signals may result from their utilization of acetyl-CoA for both energy production and acetylcholine... Abstract High susceptibility of cholinergic neurons to neurotoxic signals may result from their utilization of acetyl‐CoA for both energy production and... |
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SubjectTerms | Acetyl Coenzyme A - genetics Acetyl Coenzyme A - metabolism acetyl-CoA acetylcholine Acetylcholine - genetics Acetylcholine - metabolism Animals ATP Citrate (pro-S)-Lyase - metabolism cDNA transfection Cell Differentiation Cell Survival choline acetyltransferase Choline O-Acetyltransferase - genetics Choline O-Acetyltransferase - metabolism Cyclic AMP - metabolism Hybrid Cells Mice Neuroblastoma - genetics Neuroblastoma - metabolism Neurons - physiology Nitric Oxide - metabolism Oxidative Stress Phenotype Pyruvate Dehydrogenase Complex - metabolism Rats Septum Pellucidum - physiology SN56 Transfection Tretinoin - metabolism Tumor Cells, Cultured |
Title | Relationships between cholinergic phenotype and acetyl-CoA level in hybrid murine neuroblastoma cells of septal origin |
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