Traumatic brain injury reduces hippocampal high-affinity [ 3H]choline uptake but not extracellular choline levels in rats
Hippocampal cholinergic hypofunction may contribute to memory deficits following experimental traumatic brain injury. These studies examined two important factors in acetylcholine synthesis: choline availability and neuronal uptake. No reductions in basal extracellular choline levels, using microdia...
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Veröffentlicht in: | Neuroscience letters 1994-10, Vol.180 (2), p.127-130 |
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creator | Dixon, C.Edward Bao, Juliang Bergmann, John S Johnson, Kenneth M |
description | Hippocampal cholinergic hypofunction may contribute to memory deficits following experimental traumatic brain injury. These studies examined two important factors in acetylcholine synthesis: choline availability and neuronal uptake. No reductions in basal extracellular choline levels, using microdialysis, were observed 2 weeks after cortical impact injury. However, studies of high affinity [
3H]choline uptake in the hippocampus, measured in a synaptosomal preparation, found a reduction in the maximum velocity of choline uptake (
V
max), while no differences in affinity constants (
K
m) were found. The results suggest that post-traumatic cholinergic deficits are not attributable to decreased availability of choline, but may be associated with either a decreased ability of cholinergic neurons to take up choline and/or a loss of cholinergic neurons. |
doi_str_mv | 10.1016/0304-3940(94)90503-7 |
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3H]choline uptake in the hippocampus, measured in a synaptosomal preparation, found a reduction in the maximum velocity of choline uptake (
V
max), while no differences in affinity constants (
K
m) were found. The results suggest that post-traumatic cholinergic deficits are not attributable to decreased availability of choline, but may be associated with either a decreased ability of cholinergic neurons to take up choline and/or a loss of cholinergic neurons.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/0304-3940(94)90503-7</identifier><identifier>PMID: 7700564</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Acetylcholine - biosynthesis ; Animals ; Biological and medical sciences ; Biological Transport ; Brain Injuries - metabolism ; Brain Injuries - psychology ; Brain injury ; Choline ; Choline - pharmacokinetics ; Craniotomy ; Extracellular Space - metabolism ; High affinity choline uptake ; Hippocampus ; Hippocampus - metabolism ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Medical sciences ; Memory Disorders - etiology ; Memory Disorders - physiopathology ; Microdialysis ; Neurons - metabolism ; Rats ; Traumas. Diseases due to physical agents ; Wounds, Nonpenetrating - metabolism ; Wounds, Nonpenetrating - psychology</subject><ispartof>Neuroscience letters, 1994-10, Vol.180 (2), p.127-130</ispartof><rights>1994</rights><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-df5fa5821a414d0a5b3878bb2e8273e6fe43205bb1c4d65c564cbbb455ad0ee83</citedby><cites>FETCH-LOGICAL-c417t-df5fa5821a414d0a5b3878bb2e8273e6fe43205bb1c4d65c564cbbb455ad0ee83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/0304394094905037$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3297037$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7700564$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dixon, C.Edward</creatorcontrib><creatorcontrib>Bao, Juliang</creatorcontrib><creatorcontrib>Bergmann, John S</creatorcontrib><creatorcontrib>Johnson, Kenneth M</creatorcontrib><title>Traumatic brain injury reduces hippocampal high-affinity [ 3H]choline uptake but not extracellular choline levels in rats</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Hippocampal cholinergic hypofunction may contribute to memory deficits following experimental traumatic brain injury. These studies examined two important factors in acetylcholine synthesis: choline availability and neuronal uptake. No reductions in basal extracellular choline levels, using microdialysis, were observed 2 weeks after cortical impact injury. However, studies of high affinity [
3H]choline uptake in the hippocampus, measured in a synaptosomal preparation, found a reduction in the maximum velocity of choline uptake (
V
max), while no differences in affinity constants (
K
m) were found. The results suggest that post-traumatic cholinergic deficits are not attributable to decreased availability of choline, but may be associated with either a decreased ability of cholinergic neurons to take up choline and/or a loss of cholinergic neurons.</description><subject>Acetylcholine - biosynthesis</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biological Transport</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - psychology</subject><subject>Brain injury</subject><subject>Choline</subject><subject>Choline - pharmacokinetics</subject><subject>Craniotomy</subject><subject>Extracellular Space - metabolism</subject><subject>High affinity choline uptake</subject><subject>Hippocampus</subject><subject>Hippocampus - metabolism</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Medical sciences</subject><subject>Memory Disorders - etiology</subject><subject>Memory Disorders - physiopathology</subject><subject>Microdialysis</subject><subject>Neurons - metabolism</subject><subject>Rats</subject><subject>Traumas. Diseases due to physical agents</subject><subject>Wounds, Nonpenetrating - metabolism</subject><subject>Wounds, Nonpenetrating - psychology</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi0EKtvCPwDJB4TgkGLHdpxckFBFKVKlXsoJIWvsTFiXfOGPiv33Tdhlj_Q0I83jd8bvS8grzs4549UHJpgsRCPZu0a-b5hiotBPyIbXuix0o8unZHNEnpPTGO8YY4oreUJOtF7aSm7I7jZAHiB5R20AP1I_3uWwowHb7DDSrZ_nycEwQ7_0P7cFdJ0ffdrR71Rc_XDbqfcj0jwn-IXU5kTHKVH8kwI47PvcQ6D_oB7vsY_LBhogxRfkWQd9xJeHeka-XX6-vbgqrm--fL34dF04yXUq2k51oOqSg-SyZaCsqHVtbYl1qQVWHUpRMmUtd7KtlFt-5ay1UiloGWItzsjbve4cpt8ZYzKDj-ttMOKUo9G6Zlpo_SjIq0oJVosFlHvQhSnGgJ2Zgx8g7AxnZo3GrL6b1XfTSPM3GrPqvz7oZztge3x0yGKZvznMITrouwCj8_GIibLRTKwyH_fY4iXeewwmOo-jw9YHdMm0k___HQ_SHKwT</recordid><startdate>19941024</startdate><enddate>19941024</enddate><creator>Dixon, C.Edward</creator><creator>Bao, Juliang</creator><creator>Bergmann, John S</creator><creator>Johnson, Kenneth M</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>19941024</creationdate><title>Traumatic brain injury reduces hippocampal high-affinity [ 3H]choline uptake but not extracellular choline levels in rats</title><author>Dixon, C.Edward ; Bao, Juliang ; Bergmann, John S ; Johnson, Kenneth M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-df5fa5821a414d0a5b3878bb2e8273e6fe43205bb1c4d65c564cbbb455ad0ee83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Acetylcholine - biosynthesis</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biological Transport</topic><topic>Brain Injuries - metabolism</topic><topic>Brain Injuries - psychology</topic><topic>Brain injury</topic><topic>Choline</topic><topic>Choline - pharmacokinetics</topic><topic>Craniotomy</topic><topic>Extracellular Space - metabolism</topic><topic>High affinity choline uptake</topic><topic>Hippocampus</topic><topic>Hippocampus - metabolism</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Medical sciences</topic><topic>Memory Disorders - etiology</topic><topic>Memory Disorders - physiopathology</topic><topic>Microdialysis</topic><topic>Neurons - metabolism</topic><topic>Rats</topic><topic>Traumas. Diseases due to physical agents</topic><topic>Wounds, Nonpenetrating - metabolism</topic><topic>Wounds, Nonpenetrating - psychology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dixon, C.Edward</creatorcontrib><creatorcontrib>Bao, Juliang</creatorcontrib><creatorcontrib>Bergmann, John S</creatorcontrib><creatorcontrib>Johnson, Kenneth M</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dixon, C.Edward</au><au>Bao, Juliang</au><au>Bergmann, John S</au><au>Johnson, Kenneth M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Traumatic brain injury reduces hippocampal high-affinity [ 3H]choline uptake but not extracellular choline levels in rats</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>1994-10-24</date><risdate>1994</risdate><volume>180</volume><issue>2</issue><spage>127</spage><epage>130</epage><pages>127-130</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>Hippocampal cholinergic hypofunction may contribute to memory deficits following experimental traumatic brain injury. These studies examined two important factors in acetylcholine synthesis: choline availability and neuronal uptake. No reductions in basal extracellular choline levels, using microdialysis, were observed 2 weeks after cortical impact injury. However, studies of high affinity [
3H]choline uptake in the hippocampus, measured in a synaptosomal preparation, found a reduction in the maximum velocity of choline uptake (
V
max), while no differences in affinity constants (
K
m) were found. The results suggest that post-traumatic cholinergic deficits are not attributable to decreased availability of choline, but may be associated with either a decreased ability of cholinergic neurons to take up choline and/or a loss of cholinergic neurons.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>7700564</pmid><doi>10.1016/0304-3940(94)90503-7</doi><tpages>4</tpages></addata></record> |
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subjects | Acetylcholine - biosynthesis Animals Biological and medical sciences Biological Transport Brain Injuries - metabolism Brain Injuries - psychology Brain injury Choline Choline - pharmacokinetics Craniotomy Extracellular Space - metabolism High affinity choline uptake Hippocampus Hippocampus - metabolism Injuries of the nervous system and the skull. Diseases due to physical agents Medical sciences Memory Disorders - etiology Memory Disorders - physiopathology Microdialysis Neurons - metabolism Rats Traumas. Diseases due to physical agents Wounds, Nonpenetrating - metabolism Wounds, Nonpenetrating - psychology |
title | Traumatic brain injury reduces hippocampal high-affinity [ 3H]choline uptake but not extracellular choline levels in rats |
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