Enhancement of acetylcholine release by homoanatoxin-a from Oscillatoria formosa
The strain NIVA-CYA 92 of Oscillatoria formosa Bory ex Gormont produces phycotoxins with neurotoxic properties. Chemical analysis by gas chromatography/mass spectrometry of a water extract of lyophilized material of the organism showed the presence of only homoanatoxin-a. The mechanism of action of...
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| Veröffentlicht in: | Environmental toxicology and pharmacology 1996-10, Vol.2 (2), p.223-232 |
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| creator | Aas, Pl Eriksen, Stig Kolderup, Jørgen Lundy, Paul Haugen, John E. Skulberg, Olav M. Fonnum, Frode |
| description | The strain NIVA-CYA 92 of
Oscillatoria formosa Bory ex Gormont produces phycotoxins with neurotoxic properties. Chemical analysis by gas chromatography/mass spectrometry of a water extract of lyophilized material of the organism showed the presence of only homoanatoxin-a. The mechanism of action of homoanatoxin-a on peripheral cholinergic nerves is so far not known. The neurotoxicity of
O. formosa containing homoanatoxin-a was investigated in rat bronchi, rat brain synaptosomes and in GH
4C
1 cells. The water extract of lyophilized material of the organism produced a concentration-dependent reversible increase in the release of [
3H]acetylcholine from both K
+ (51 mM) depolarised and non-depolarised cholinergic nerves of the rat bronchial smooth muscle. The K
+-evoked release of [
3H]acetylcholine was enhanced by about 75% by a water extract from 15–20 mg/ml of lyophilized algal material. The enhanced release of [
3H]acetylcholine was substantially reduced by the L-type Ca
2+-channel blocker verapamil (100
μM) and not by the N-type Ca
2+-channel blocker
ω-conotoxin GVIA (1.0
μM) or the P-type Ca
2+-channel blocker
ω-agatoxin IV-A (0.2
μM). Chelation of intra-cellular Ca
2+ by 1,2-bis-(aminofenoxi)etan-
N,N,N′,N′-tetraacidic acid/acetoxymethyl (BAPTA/AM) (30
μM) had no effect on the phycotoxin-induced release of [
3H]acetylcholine, indicating that an extracellular pool of Ca
2+ was important for the action of the phycotoxin on the release of [
3H]acetylcholine from peripheral cholinergic nerves. In rat brain synaptosomes the algal extract enhanced the influx of
45Ca
2+ in a tetrodotoxin (1.0
μM) and
ω-conotoxin MVIIC (blocker of N-, P- and Q-type Ca
2+ channels) (1.0
μM) insensitive manner. Patch-clamp studies showed that the phycotoxin opened endogenous voltage dependent L-type Ca
2+ channels in neuronal GH
4C
1 cells. These Ca
2+ channels and the effect of the toxin on the channels were blocked by the L-type Ca
2+-channel antagonist gallopamil (200
μM). The present results suggest, therefore, that the investigated strain of
O. formosa contains homoanatoxin-a, which enhances the release of acetylcholine from peripheral cholinergic nerves through opening of endogenous voltage dependent neuronal L-type Ca
2− channels. |
| doi_str_mv | 10.1016/S1382-6689(96)00059-2 |
| format | Article |
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Oscillatoria formosa Bory ex Gormont produces phycotoxins with neurotoxic properties. Chemical analysis by gas chromatography/mass spectrometry of a water extract of lyophilized material of the organism showed the presence of only homoanatoxin-a. The mechanism of action of homoanatoxin-a on peripheral cholinergic nerves is so far not known. The neurotoxicity of
O. formosa containing homoanatoxin-a was investigated in rat bronchi, rat brain synaptosomes and in GH
4C
1 cells. The water extract of lyophilized material of the organism produced a concentration-dependent reversible increase in the release of [
3H]acetylcholine from both K
+ (51 mM) depolarised and non-depolarised cholinergic nerves of the rat bronchial smooth muscle. The K
+-evoked release of [
3H]acetylcholine was enhanced by about 75% by a water extract from 15–20 mg/ml of lyophilized algal material. The enhanced release of [
3H]acetylcholine was substantially reduced by the L-type Ca
2+-channel blocker verapamil (100
μM) and not by the N-type Ca
2+-channel blocker
ω-conotoxin GVIA (1.0
μM) or the P-type Ca
2+-channel blocker
ω-agatoxin IV-A (0.2
μM). Chelation of intra-cellular Ca
2+ by 1,2-bis-(aminofenoxi)etan-
N,N,N′,N′-tetraacidic acid/acetoxymethyl (BAPTA/AM) (30
μM) had no effect on the phycotoxin-induced release of [
3H]acetylcholine, indicating that an extracellular pool of Ca
2+ was important for the action of the phycotoxin on the release of [
3H]acetylcholine from peripheral cholinergic nerves. In rat brain synaptosomes the algal extract enhanced the influx of
45Ca
2+ in a tetrodotoxin (1.0
μM) and
ω-conotoxin MVIIC (blocker of N-, P- and Q-type Ca
2+ channels) (1.0
μM) insensitive manner. Patch-clamp studies showed that the phycotoxin opened endogenous voltage dependent L-type Ca
2+ channels in neuronal GH
4C
1 cells. These Ca
2+ channels and the effect of the toxin on the channels were blocked by the L-type Ca
2+-channel antagonist gallopamil (200
μM). The present results suggest, therefore, that the investigated strain of
O. formosa contains homoanatoxin-a, which enhances the release of acetylcholine from peripheral cholinergic nerves through opening of endogenous voltage dependent neuronal L-type Ca
2− channels.</description><identifier>ISSN: 1382-6689</identifier><identifier>EISSN: 1872-7077</identifier><identifier>DOI: 10.1016/S1382-6689(96)00059-2</identifier><identifier>PMID: 21781731</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Acetylcholine ; Ca 2+ channel ; Cyanobacterium ; Oscillatoria formosa ; Patch clamp ; Peripheral nervous system ; Phycotoxin ; Vesicle</subject><ispartof>Environmental toxicology and pharmacology, 1996-10, Vol.2 (2), p.223-232</ispartof><rights>1996 Elsevier Science B.V. All rights reserved</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c393t-8cfcbfceb35b7d6514a42ea7735a56a7d818b7fc938fcfc625002edd705d75283</citedby><cites>FETCH-LOGICAL-c393t-8cfcbfceb35b7d6514a42ea7735a56a7d818b7fc938fcfc625002edd705d75283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S1382-6689(96)00059-2$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>309,310,314,780,784,789,790,3550,23930,23931,25140,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21781731$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Renwick, AG</contributor><creatorcontrib>Aas, Pl</creatorcontrib><creatorcontrib>Eriksen, Stig</creatorcontrib><creatorcontrib>Kolderup, Jørgen</creatorcontrib><creatorcontrib>Lundy, Paul</creatorcontrib><creatorcontrib>Haugen, John E.</creatorcontrib><creatorcontrib>Skulberg, Olav M.</creatorcontrib><creatorcontrib>Fonnum, Frode</creatorcontrib><title>Enhancement of acetylcholine release by homoanatoxin-a from Oscillatoria formosa</title><title>Environmental toxicology and pharmacology</title><addtitle>Environ Toxicol Pharmacol</addtitle><description>The strain NIVA-CYA 92 of
Oscillatoria formosa Bory ex Gormont produces phycotoxins with neurotoxic properties. Chemical analysis by gas chromatography/mass spectrometry of a water extract of lyophilized material of the organism showed the presence of only homoanatoxin-a. The mechanism of action of homoanatoxin-a on peripheral cholinergic nerves is so far not known. The neurotoxicity of
O. formosa containing homoanatoxin-a was investigated in rat bronchi, rat brain synaptosomes and in GH
4C
1 cells. The water extract of lyophilized material of the organism produced a concentration-dependent reversible increase in the release of [
3H]acetylcholine from both K
+ (51 mM) depolarised and non-depolarised cholinergic nerves of the rat bronchial smooth muscle. The K
+-evoked release of [
3H]acetylcholine was enhanced by about 75% by a water extract from 15–20 mg/ml of lyophilized algal material. The enhanced release of [
3H]acetylcholine was substantially reduced by the L-type Ca
2+-channel blocker verapamil (100
μM) and not by the N-type Ca
2+-channel blocker
ω-conotoxin GVIA (1.0
μM) or the P-type Ca
2+-channel blocker
ω-agatoxin IV-A (0.2
μM). Chelation of intra-cellular Ca
2+ by 1,2-bis-(aminofenoxi)etan-
N,N,N′,N′-tetraacidic acid/acetoxymethyl (BAPTA/AM) (30
μM) had no effect on the phycotoxin-induced release of [
3H]acetylcholine, indicating that an extracellular pool of Ca
2+ was important for the action of the phycotoxin on the release of [
3H]acetylcholine from peripheral cholinergic nerves. In rat brain synaptosomes the algal extract enhanced the influx of
45Ca
2+ in a tetrodotoxin (1.0
μM) and
ω-conotoxin MVIIC (blocker of N-, P- and Q-type Ca
2+ channels) (1.0
μM) insensitive manner. Patch-clamp studies showed that the phycotoxin opened endogenous voltage dependent L-type Ca
2+ channels in neuronal GH
4C
1 cells. These Ca
2+ channels and the effect of the toxin on the channels were blocked by the L-type Ca
2+-channel antagonist gallopamil (200
μM). The present results suggest, therefore, that the investigated strain of
O. formosa contains homoanatoxin-a, which enhances the release of acetylcholine from peripheral cholinergic nerves through opening of endogenous voltage dependent neuronal L-type Ca
2− channels.</description><subject>Acetylcholine</subject><subject>Ca 2+ channel</subject><subject>Cyanobacterium</subject><subject>Oscillatoria formosa</subject><subject>Patch clamp</subject><subject>Peripheral nervous system</subject><subject>Phycotoxin</subject><subject>Vesicle</subject><issn>1382-6689</issn><issn>1872-7077</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><recordid>eNqFkMlOwzAQhi0EolB4BFBOLIeAl3rJCaGqLFKlIgFny3EmqlESg50i-va4CxzhNKPR98-MPoROCL4imIjrZ8IUzYVQxUUhLjHGvMjpDjogStJcYil3U_-DDNBhjG8YE86Y2kcDSqQikpED9DTp5qaz0ELXZ77OjIV-2di5b1wHWYAGTISsXGZz33rTmd5_uS43WR18m82idU2TZsGliQ-tj-YI7dWmiXC8rUP0ejd5GT_k09n94_h2mltWsD5XtrZlbaFkvJSV4GRkRhSMlIwbLoysFFGlrG3BVJ1QQTnGFKpKYl5JThUbovPN3vfgPxYQe926aCG904FfRK1kQfAIixV59idJeEEUGckE8g1og48xQK3fg2tNWGqC9Uq6XkvXK6O6EHotXdOUO90eWJQtVL-pH8sJuNkAkIR8Ogg6iYNkvXIBbK8r7_458Q3FkpJe</recordid><startdate>19961015</startdate><enddate>19961015</enddate><creator>Aas, Pl</creator><creator>Eriksen, Stig</creator><creator>Kolderup, Jørgen</creator><creator>Lundy, Paul</creator><creator>Haugen, John E.</creator><creator>Skulberg, Olav M.</creator><creator>Fonnum, Frode</creator><general>Elsevier B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>F1W</scope><scope>FR3</scope><scope>H99</scope><scope>L.F</scope><scope>L.G</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19961015</creationdate><title>Enhancement of acetylcholine release by homoanatoxin-a from Oscillatoria formosa</title><author>Aas, Pl ; Eriksen, Stig ; Kolderup, Jørgen ; Lundy, Paul ; Haugen, John E. ; Skulberg, Olav M. ; Fonnum, Frode</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c393t-8cfcbfceb35b7d6514a42ea7735a56a7d818b7fc938fcfc625002edd705d75283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Acetylcholine</topic><topic>Ca 2+ channel</topic><topic>Cyanobacterium</topic><topic>Oscillatoria formosa</topic><topic>Patch clamp</topic><topic>Peripheral nervous system</topic><topic>Phycotoxin</topic><topic>Vesicle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aas, Pl</creatorcontrib><creatorcontrib>Eriksen, Stig</creatorcontrib><creatorcontrib>Kolderup, Jørgen</creatorcontrib><creatorcontrib>Lundy, Paul</creatorcontrib><creatorcontrib>Haugen, John E.</creatorcontrib><creatorcontrib>Skulberg, Olav M.</creatorcontrib><creatorcontrib>Fonnum, Frode</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Engineering Research Database</collection><collection>ASFA: Marine Biotechnology Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Marine Biotechnology Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Environmental toxicology and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aas, Pl</au><au>Eriksen, Stig</au><au>Kolderup, Jørgen</au><au>Lundy, Paul</au><au>Haugen, John E.</au><au>Skulberg, Olav M.</au><au>Fonnum, Frode</au><au>Renwick, AG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhancement of acetylcholine release by homoanatoxin-a from Oscillatoria formosa</atitle><jtitle>Environmental toxicology and pharmacology</jtitle><addtitle>Environ Toxicol Pharmacol</addtitle><date>1996-10-15</date><risdate>1996</risdate><volume>2</volume><issue>2</issue><spage>223</spage><epage>232</epage><pages>223-232</pages><issn>1382-6689</issn><eissn>1872-7077</eissn><abstract>The strain NIVA-CYA 92 of
Oscillatoria formosa Bory ex Gormont produces phycotoxins with neurotoxic properties. Chemical analysis by gas chromatography/mass spectrometry of a water extract of lyophilized material of the organism showed the presence of only homoanatoxin-a. The mechanism of action of homoanatoxin-a on peripheral cholinergic nerves is so far not known. The neurotoxicity of
O. formosa containing homoanatoxin-a was investigated in rat bronchi, rat brain synaptosomes and in GH
4C
1 cells. The water extract of lyophilized material of the organism produced a concentration-dependent reversible increase in the release of [
3H]acetylcholine from both K
+ (51 mM) depolarised and non-depolarised cholinergic nerves of the rat bronchial smooth muscle. The K
+-evoked release of [
3H]acetylcholine was enhanced by about 75% by a water extract from 15–20 mg/ml of lyophilized algal material. The enhanced release of [
3H]acetylcholine was substantially reduced by the L-type Ca
2+-channel blocker verapamil (100
μM) and not by the N-type Ca
2+-channel blocker
ω-conotoxin GVIA (1.0
μM) or the P-type Ca
2+-channel blocker
ω-agatoxin IV-A (0.2
μM). Chelation of intra-cellular Ca
2+ by 1,2-bis-(aminofenoxi)etan-
N,N,N′,N′-tetraacidic acid/acetoxymethyl (BAPTA/AM) (30
μM) had no effect on the phycotoxin-induced release of [
3H]acetylcholine, indicating that an extracellular pool of Ca
2+ was important for the action of the phycotoxin on the release of [
3H]acetylcholine from peripheral cholinergic nerves. In rat brain synaptosomes the algal extract enhanced the influx of
45Ca
2+ in a tetrodotoxin (1.0
μM) and
ω-conotoxin MVIIC (blocker of N-, P- and Q-type Ca
2+ channels) (1.0
μM) insensitive manner. Patch-clamp studies showed that the phycotoxin opened endogenous voltage dependent L-type Ca
2+ channels in neuronal GH
4C
1 cells. These Ca
2+ channels and the effect of the toxin on the channels were blocked by the L-type Ca
2+-channel antagonist gallopamil (200
μM). The present results suggest, therefore, that the investigated strain of
O. formosa contains homoanatoxin-a, which enhances the release of acetylcholine from peripheral cholinergic nerves through opening of endogenous voltage dependent neuronal L-type Ca
2− channels.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>21781731</pmid><doi>10.1016/S1382-6689(96)00059-2</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Environmental toxicology and pharmacology, 1996-10, Vol.2 (2), p.223-232 |
| issn | 1382-6689 1872-7077 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_879104068 |
| source | Elsevier ScienceDirect Journals Complete |
| subjects | Acetylcholine Ca 2+ channel Cyanobacterium Oscillatoria formosa Patch clamp Peripheral nervous system Phycotoxin Vesicle |
| title | Enhancement of acetylcholine release by homoanatoxin-a from Oscillatoria formosa |
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