| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| M Koga, H Miyata, N Tsuno, K Nakayama, S Ushijima, Y Tanaka, Y Hiraga, N Kobayash. [Relationship between cholinergic symptoms caused by distigmine and the activities of serum AChE and BChE]. Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology. vol 17. issue 3. 1997-11-19. PMID:9278940. |
this study suggests that the values of serum ache and bche may be useful markers for the manifestation of adverse cholinergic effects caused by distigmine. |
1997-11-19 |
2023-08-12 |
Not clear |
| A Alvarez, C Opazo, R Alarcón, J Garrido, N C Inestros. Acetylcholinesterase promotes the aggregation of amyloid-beta-peptide fragments by forming a complex with the growing fibrils. Journal of molecular biology. vol 272. issue 3. 1997-10-28. PMID:9325095. |
in order to identify the structural domains of the amyloid-beta-peptide (abeta) involved in the aggregation induced by ache, we have studied the effect of this cholinergic enzyme on abeta peptide fragments of different sizes. |
1997-10-28 |
2023-08-12 |
Not clear |
| C Erb, J Klein, A Köppen, K Löffelholz, H Jeltsch, J C Casse. Modulation of hippocampal acetylcholine release after fimbria-fornix lesions and septal transplantation in rats. Neuroscience letters. vol 231. issue 1. 1997-10-23. PMID:9280154. |
the extent of cholinergic (re)innervation was determined by acetylcholinesterase (ache) staining and densitometry. |
1997-10-23 |
2023-08-12 |
rat |
| X Cousin, C Bo. [Acetylcholinesterase from snake venoms]. Comptes rendus des seances de la Societe de biologie et de ses filiales. vol 191. issue 3. 1997-10-02. PMID:9295965. |
acetylcholinesterase (ache) plays a key role in cholinergic transmission. |
1997-10-02 |
2023-08-12 |
Not clear |
| X Cousin, C Bo. [Acetylcholinesterase from snake venoms]. Comptes rendus des seances de la Societe de biologie et de ses filiales. vol 191. issue 3. 1997-10-02. PMID:9295965. |
the presence of ache in tissues devoid of cholinergic function is also well known and raises the question of its role. |
1997-10-02 |
2023-08-12 |
Not clear |
| G Sberna, J Sáez-Valero, K Beyreuther, C L Masters, D H Smal. The amyloid beta-protein of Alzheimer's disease increases acetylcholinesterase expression by increasing intracellular calcium in embryonal carcinoma P19 cells. Journal of neurochemistry. vol 69. issue 3. 1997-09-25. PMID:9282941. |
one of the characteristic changes that occurs in alzheimer's disease is the loss of acetylcholinesterase (ache) from both cholinergic and noncholinergic neurons of the brain. |
1997-09-25 |
2023-08-12 |
Not clear |
| W Yao, D A Godfre. Densitometric evaluation of markers for cholinergic transmission in rat superior olivary complex. Neuroscience letters. vol 229. issue 1. 1997-09-12. PMID:9224792. |
cholinergic transmission in the rat superior olivary complex (soc) was assessed by densitometric measurements of labeling with several markers: acetylcholinesterase (ache) histochemistry, choline acetyltransferase (chat) immunohistochemistry, and muscarinic acetylcholine receptor (m35) immunohistochemistry and n-methylscopolamine (nms) binding autoradiography, as well as its subtype 2 (m2) immunohistochemistry. |
1997-09-12 |
2023-08-12 |
rat |
| W Yao, D A Godfre. Densitometric evaluation of markers for cholinergic transmission in rat superior olivary complex. Neuroscience letters. vol 229. issue 1. 1997-09-12. PMID:9224792. |
the markers which may occur in cholinergic neurons (chat, m2 receptor and ache) showed dense labeling in the ventral nucleus of the trapezoid body (vntb), in line with other evidence that it contains cholinergic neuron somata. |
1997-09-12 |
2023-08-12 |
rat |
| T Naumann, T Deller, R Bender, M Frotsche. 192 IgG-saporin-induced loss of cholinergic neurons in the septum abolishes cholinergic sprouting after unilateral entorhinal lesion in the rat. The European journal of neuroscience. vol 9. issue 6. 1997-09-03. PMID:9215714. |
this cholinergic sprouting has been demonstrated by acetylcholinesterase (ache) histochemistry, a method said selectively to label cholinergic septohippocampal fibres in the hippocampus. |
1997-09-03 |
2023-08-12 |
rat |
| T Naumann, T Deller, R Bender, M Frotsche. 192 IgG-saporin-induced loss of cholinergic neurons in the septum abolishes cholinergic sprouting after unilateral entorhinal lesion in the rat. The European journal of neuroscience. vol 9. issue 6. 1997-09-03. PMID:9215714. |
however, a recent report has questioned this concept, suggesting that ache may not be an adequate marker to monitor cholinergic sprouting and that other, non-cholinergic axons sprouting after entorhinal cortex lesion cause the dense ache-positive band in the denervated outer molecular layer. |
1997-09-03 |
2023-08-12 |
rat |
| T Naumann, T Deller, R Bender, M Frotsche. 192 IgG-saporin-induced loss of cholinergic neurons in the septum abolishes cholinergic sprouting after unilateral entorhinal lesion in the rat. The European journal of neuroscience. vol 9. issue 6. 1997-09-03. PMID:9215714. |
in order to determine the contribution of cholinergic septohippocampal fibres to the dense ache band appearing after entorhinal cortex lesion, the neurotoxin 192 igg-saporin, known to destroy cholinergic neurons in the basal forebrain selectively, was used. |
1997-09-03 |
2023-08-12 |
rat |
| T Naumann, T Deller, R Bender, M Frotsche. 192 IgG-saporin-induced loss of cholinergic neurons in the septum abolishes cholinergic sprouting after unilateral entorhinal lesion in the rat. The European journal of neuroscience. vol 9. issue 6. 1997-09-03. PMID:9215714. |
the cholinergic sprouting response in the molecular layer, as visualized with ache histochemistry, was abolished in all animals treated with immunotoxin. |
1997-09-03 |
2023-08-12 |
rat |
| T Naumann, T Deller, R Bender, M Frotsche. 192 IgG-saporin-induced loss of cholinergic neurons in the septum abolishes cholinergic sprouting after unilateral entorhinal lesion in the rat. The European journal of neuroscience. vol 9. issue 6. 1997-09-03. PMID:9215714. |
these data indicate that the dense ache band forming after entorhinal cortex lesion represents the sprouting of cholinergic septohippocampal fibres. |
1997-09-03 |
2023-08-12 |
rat |
| B Nehru, R Du. The effect of dietary selenium on lead neurotoxicity. Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer. vol 16. issue 1. 1997-09-03. PMID:9256932. |
along with these, a decrease in acetylcholine esterase (ache) and monoamine oxidase (mao) was seen, thus affecting both cholinergic and adrenergic neurotransmitters. |
1997-09-03 |
2023-08-12 |
rat |
| C Andres, R Beeri, A Friedman, E Lev-Lehman, S Henis, R Timberg, M Shani, H Sore. Acetylcholinesterase-transgenic mice display embryonic modulations in spinal cord choline acetyltransferase and neurexin Ibeta gene expression followed by late-onset neuromotor deterioration. Proceedings of the National Academy of Sciences of the United States of America. vol 94. issue 15. 1997-08-27. PMID:9223334. |
to explore the possibility that overproduction of neuronal acetylcholinesterase (ache) confers changes in both cholinergic and morphogenic intercellular interactions, we studied developmental responses to neuronal ache overexpression in motoneurons and neuromuscular junctions of ache-transgenic mice. |
1997-08-27 |
2023-08-12 |
mouse |
| C Andres, R Beeri, A Friedman, E Lev-Lehman, S Henis, R Timberg, M Shani, H Sore. Acetylcholinesterase-transgenic mice display embryonic modulations in spinal cord choline acetyltransferase and neurexin Ibeta gene expression followed by late-onset neuromotor deterioration. Proceedings of the National Academy of Sciences of the United States of America. vol 94. issue 15. 1997-08-27. PMID:9223334. |
these findings demonstrate embryonic feedback mechanisms to neuronal ache overexpression that are attributable to both cholinergic and cell-cell interaction pathways, suggesting that embryonic neurexin ibeta expression is concerted in vivo with ache levels and indicating that postnatal changes in neuronal ache-associated proteins may be involved in late-onset neuromotor pathologies. |
1997-08-27 |
2023-08-12 |
mouse |
| A Lucić, B Radić, M Peraica, M Mesić, I Primozic, Z Binenfel. Antidotal efficacy of quinuclidinium oximes against soman poisoning. Archives of toxicology. vol 71. issue 7. 1997-08-21. PMID:9209694. |
the results indicate that the in vivo effectiveness of quinuclidinium oximes against soman poisoning may not be related to reactivation or protection of ache but rather to some other mechanism of the cholinergic system. |
1997-08-21 |
2023-08-12 |
mouse |
| P G Layer, J Berger, N Kink. Cholinesterases precede "ON-OFF" channel dichotomy in the embryonic chick retina before onset of synaptogenesis. Cell and tissue research. vol 288. issue 3. 1997-08-15. PMID:9134854. |
both levels can be detected easily in the mature retina by choline acetyltransferase (chat) or by acetylcholinesterase (ache); however, the usefulness of these enzymes as developmental markers is restricted, since chat is detected too late, while ache labels not only cholinergic neuropil. |
1997-08-15 |
2023-08-12 |
chicken |
| T Fujii, Y Mori, T Tominaga, I Hayasaka, K Kawashim. Maintenance of constant blood acetylcholine content before and after feeding in young chimpanzees. Neuroscience letters. vol 227. issue 1. 1997-07-30. PMID:9178849. |
the results of the present study indicate that the blood ach of chimpanzees is distributed mainly in the blood cell fraction, and that the blood ach content is not regulated directly by cholinergic nerve activity or by plasma ache activity. |
1997-07-30 |
2023-08-12 |
chimpanzee |
| S Yamada, T Fujii, K Kawashim. Oral administration of KW-5092, a novel gastroprokinetic agent with acetylcholinesterase inhibitory and acetylcholine release enhancing activities, causes a dose-dependent increase in the blood acetylcholine content of beagle dogs. Neuroscience letters. vol 225. issue 1. 1997-07-24. PMID:9143009. |
oral administration of kw-5092 (10-30 mg/kg), a gastroprokinetic agent with acetylcholinesterase (ache) inhibitory and ach release enhancing activities, caused a dose-dependent increase in the ach content of both the blood and plasma, as well as several behavioral side effects due to peripheral cholinergic stimulation. |
1997-07-24 |
2023-08-12 |
Not clear |