Actions of ginsenoside Rb1 on choline uptake in central cholinergic nerve endings
The ginsenoside Rb1 has previously been reported to improve memory deficits induced by anticholinergic drug treatment, and to facilitate acetylcholine (Ach) release from rat brain hippocampal slices. The increase in ACh release was not associated with an increase in calcium uptake into nerve termina...
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| Veröffentlicht in: | Neurochemistry international 1992-07, Vol.21 (1), p.1-5 |
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| description | The ginsenoside Rb1 has previously been reported to improve memory deficits induced by anticholinergic drug treatment, and to facilitate acetylcholine (Ach) release from rat brain hippocampal slices. The increase in ACh release was not associated with an increase in calcium uptake into nerve terminals, but was associated with an increase in uptake of the precursor choline. In the present studies, analysis of choline uptake kinetics indicated that Rb1 increased the maximum velocity of choline uptake, while the affinity of the choline uptake carrier for choline (Km) was not significantly altered. Acute treatment with Rb1 did not alter the number of [3H]hemicholinium-3 (HC-3) binding sites in any of three cholinergic brain regions examined, suggesting that the increase in the maximum velocity of choline uptake was not associated with an increase in the number of choline carriers. However, chronic (3 day) administration of Rb1 did increase the number of choline uptake sites in the hippocampus, and to a lesser extent in the cortex. |
| doi_str_mv | 10.1016/0197-0186(92)90061-u |
| format | Article |
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G</creator><creatorcontrib>BENISHIN, C. G</creatorcontrib><description>The ginsenoside Rb1 has previously been reported to improve memory deficits induced by anticholinergic drug treatment, and to facilitate acetylcholine (Ach) release from rat brain hippocampal slices. The increase in ACh release was not associated with an increase in calcium uptake into nerve terminals, but was associated with an increase in uptake of the precursor choline. In the present studies, analysis of choline uptake kinetics indicated that Rb1 increased the maximum velocity of choline uptake, while the affinity of the choline uptake carrier for choline (Km) was not significantly altered. Acute treatment with Rb1 did not alter the number of [3H]hemicholinium-3 (HC-3) binding sites in any of three cholinergic brain regions examined, suggesting that the increase in the maximum velocity of choline uptake was not associated with an increase in the number of choline carriers. However, chronic (3 day) administration of Rb1 did increase the number of choline uptake sites in the hippocampus, and to a lesser extent in the cortex.</description><identifier>ISSN: 0197-0186</identifier><identifier>EISSN: 1872-9754</identifier><identifier>DOI: 10.1016/0197-0186(92)90061-u</identifier><identifier>PMID: 1338897</identifier><identifier>CODEN: NEUIDS</identifier><language>eng</language><publisher>Oxford: Elsevier</publisher><subject>Acetylcholine - metabolism ; Animals ; Binding Sites ; Biological and medical sciences ; Biological Transport - drug effects ; Brain - metabolism ; Carrier Proteins ; Cerebral Cortex - drug effects ; Cerebral Cortex - metabolism ; Choline - metabolism ; Corpus Striatum - drug effects ; Corpus Striatum - metabolism ; Ginsenosides ; Hemicholinium 3 - metabolism ; Hippocampus - drug effects ; Hippocampus - metabolism ; Kinetics ; Medical sciences ; Miscellaneous ; Nerve Endings - drug effects ; Nerve Endings - metabolism ; Neuropharmacology ; Organ Specificity ; Panax ; Pharmacology. 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G</creatorcontrib><title>Actions of ginsenoside Rb1 on choline uptake in central cholinergic nerve endings</title><title>Neurochemistry international</title><addtitle>Neurochem Int</addtitle><description>The ginsenoside Rb1 has previously been reported to improve memory deficits induced by anticholinergic drug treatment, and to facilitate acetylcholine (Ach) release from rat brain hippocampal slices. The increase in ACh release was not associated with an increase in calcium uptake into nerve terminals, but was associated with an increase in uptake of the precursor choline. In the present studies, analysis of choline uptake kinetics indicated that Rb1 increased the maximum velocity of choline uptake, while the affinity of the choline uptake carrier for choline (Km) was not significantly altered. Acute treatment with Rb1 did not alter the number of [3H]hemicholinium-3 (HC-3) binding sites in any of three cholinergic brain regions examined, suggesting that the increase in the maximum velocity of choline uptake was not associated with an increase in the number of choline carriers. However, chronic (3 day) administration of Rb1 did increase the number of choline uptake sites in the hippocampus, and to a lesser extent in the cortex.</description><subject>Acetylcholine - metabolism</subject><subject>Animals</subject><subject>Binding Sites</subject><subject>Biological and medical sciences</subject><subject>Biological Transport - drug effects</subject><subject>Brain - metabolism</subject><subject>Carrier Proteins</subject><subject>Cerebral Cortex - drug effects</subject><subject>Cerebral Cortex - metabolism</subject><subject>Choline - metabolism</subject><subject>Corpus Striatum - drug effects</subject><subject>Corpus Striatum - metabolism</subject><subject>Ginsenosides</subject><subject>Hemicholinium 3 - metabolism</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Kinetics</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>Nerve Endings - drug effects</subject><subject>Nerve Endings - metabolism</subject><subject>Neuropharmacology</subject><subject>Organ Specificity</subject><subject>Panax</subject><subject>Pharmacology. Drug treatments</subject><subject>Plants, Medicinal</subject><subject>Rats</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Saponins - pharmacology</subject><subject>Synaptosomes - drug effects</subject><subject>Synaptosomes - metabolism</subject><issn>0197-0186</issn><issn>1872-9754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkFtLAzEQhYMotVb_gUIeRPRhNZfdnc1jKd6gIIp9DmmSrdFtUje7gv_e1NY6DAzMOXMYPoROKbmmhJY3hArICK3KS8GuBCElzfo9NKQVsExAke-j4c5yiI5ifCeEgCDFAA0o51UlYIiex7pzwUccarxwPlofojMWv8wpDh7rt9A4b3G_6tSHxS5trO9a1fwp7cJpnMaXxdYb5xfxGB3Uqon2ZDtHaHZ3-zp5yKZP94-T8TTTXECXMZKDpTUFK1IZzY0pIecwT20KA8oUeUFqMKSmLL1aKKFAESHqnHGmSj5CF5vcVRs-exs7uXRR26ZR3oY-SuAFAwoiGfONUbchxtbWctW6pWq_JSVyTVKuMck1JimY_CUpZ-nsbJvfz5fW_B9t0CX9fKurqFVTt8prF3e2gpc5Bcp_AKvRewQ</recordid><startdate>19920701</startdate><enddate>19920701</enddate><creator>BENISHIN, C. 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G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c397t-2047e1f17e9999dc3dd67437b37bd5d7ad5450f7d0f128975a9a7a099f4232a63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Acetylcholine - metabolism</topic><topic>Animals</topic><topic>Binding Sites</topic><topic>Biological and medical sciences</topic><topic>Biological Transport - drug effects</topic><topic>Brain - metabolism</topic><topic>Carrier Proteins</topic><topic>Cerebral Cortex - drug effects</topic><topic>Cerebral Cortex - metabolism</topic><topic>Choline - metabolism</topic><topic>Corpus Striatum - drug effects</topic><topic>Corpus Striatum - metabolism</topic><topic>Ginsenosides</topic><topic>Hemicholinium 3 - metabolism</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Kinetics</topic><topic>Medical sciences</topic><topic>Miscellaneous</topic><topic>Nerve Endings - drug effects</topic><topic>Nerve Endings - metabolism</topic><topic>Neuropharmacology</topic><topic>Organ Specificity</topic><topic>Panax</topic><topic>Pharmacology. Drug treatments</topic><topic>Plants, Medicinal</topic><topic>Rats</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Saponins - pharmacology</topic><topic>Synaptosomes - drug effects</topic><topic>Synaptosomes - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BENISHIN, C. G</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemistry international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BENISHIN, C. G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Actions of ginsenoside Rb1 on choline uptake in central cholinergic nerve endings</atitle><jtitle>Neurochemistry international</jtitle><addtitle>Neurochem Int</addtitle><date>1992-07-01</date><risdate>1992</risdate><volume>21</volume><issue>1</issue><spage>1</spage><epage>5</epage><pages>1-5</pages><issn>0197-0186</issn><eissn>1872-9754</eissn><coden>NEUIDS</coden><abstract>The ginsenoside Rb1 has previously been reported to improve memory deficits induced by anticholinergic drug treatment, and to facilitate acetylcholine (Ach) release from rat brain hippocampal slices. The increase in ACh release was not associated with an increase in calcium uptake into nerve terminals, but was associated with an increase in uptake of the precursor choline. In the present studies, analysis of choline uptake kinetics indicated that Rb1 increased the maximum velocity of choline uptake, while the affinity of the choline uptake carrier for choline (Km) was not significantly altered. Acute treatment with Rb1 did not alter the number of [3H]hemicholinium-3 (HC-3) binding sites in any of three cholinergic brain regions examined, suggesting that the increase in the maximum velocity of choline uptake was not associated with an increase in the number of choline carriers. However, chronic (3 day) administration of Rb1 did increase the number of choline uptake sites in the hippocampus, and to a lesser extent in the cortex.</abstract><cop>Oxford</cop><pub>Elsevier</pub><pmid>1338897</pmid><doi>10.1016/0197-0186(92)90061-u</doi><tpages>5</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Neurochemistry international, 1992-07, Vol.21 (1), p.1-5 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Acetylcholine - metabolism Animals Binding Sites Biological and medical sciences Biological Transport - drug effects Brain - metabolism Carrier Proteins Cerebral Cortex - drug effects Cerebral Cortex - metabolism Choline - metabolism Corpus Striatum - drug effects Corpus Striatum - metabolism Ginsenosides Hemicholinium 3 - metabolism Hippocampus - drug effects Hippocampus - metabolism Kinetics Medical sciences Miscellaneous Nerve Endings - drug effects Nerve Endings - metabolism Neuropharmacology Organ Specificity Panax Pharmacology. Drug treatments Plants, Medicinal Rats Receptors, Cell Surface - metabolism Saponins - pharmacology Synaptosomes - drug effects Synaptosomes - metabolism |
| title | Actions of ginsenoside Rb1 on choline uptake in central cholinergic nerve endings |
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