CCL2-ethanol interactions and hippocampal synaptic protein expression in a transgenic mouse model
Chronic exposure to ethanol produces a number of detrimental effects on behavior. Neuroadaptive changes in brain structure or function underlie these behavioral changes and may be transient or persistent in nature. Central to the functional changes are alterations in the biology of neuronal and glia...
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Frontiers Media S.A.
2014-04-01
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Series: | Frontiers in Integrative Neuroscience |
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Online Access: | http://journal.frontiersin.org/Journal/10.3389/fnint.2014.00029/full |
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author | Donna eGruol Khanh eVo Jennifer eBray Amanda eRoberts |
author_facet | Donna eGruol Khanh eVo Jennifer eBray Amanda eRoberts |
author_sort | Donna eGruol |
collection | DOAJ |
description | Chronic exposure to ethanol produces a number of detrimental effects on behavior. Neuroadaptive changes in brain structure or function underlie these behavioral changes and may be transient or persistent in nature. Central to the functional changes are alterations in the biology of neuronal and glial cells of the brain. Recent data show that ethanol induces glial cells of the brain to produce elevated levels of neuroimmune factors including CCL2, a key innate immune chemokine. Depending on the conditions of ethanol exposure, the upregulated levels of CCL2 can be transient or persistent and outlast the period of ethanol exposure. Importantly, results indicate that the upregulated levels of CCL2 may lead to CCL2-ethanol interactions that mediate or regulate the effects of ethanol on the brain. Glial cells are in close association with neurons and regulate many neuronal functions. Therefore, effects of ethanol on glial cells may underlie some of the effects of ethanol on neurons. To investigate this possibility, we are studying the effects of chronic ethanol on hippocampal synaptic function in a transgenic mouse model that expresses elevated levels of CCL2 in the brain through enhanced glial expression, a situation know to occur in alcoholics. Both CCL2 and ethanol have been reported to alter synaptic function in the hippocampus. In the current study, we determined if interactions are evident between CCL2 and ethanol at level of hippocampal synaptic proteins. Two ethanol exposure paradigms were used; the first involved ethanol exposure by drinking and the second involved ethanol exposure in a paradigm that combines drinking plus ethanol vapor. The first paradigm does not produce dependence on ethanol, whereas the second paradigm is commonly used to produce ethanol dependence. Results show modest effects of both ethanol exposure paradigms on the level of synaptic proteins in the hippocampus of CCL2 transgenic mice compared with their non-transgenic li |
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issn | 1662-5145 |
language | English |
last_indexed | 2024-04-13T12:27:55Z |
publishDate | 2014-04-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Integrative Neuroscience |
spelling | doaj.art-55f5333bf15f480187df98da4572a5182022-12-22T02:46:57ZengFrontiers Media S.A.Frontiers in Integrative Neuroscience1662-51452014-04-01810.3389/fnint.2014.0002982286CCL2-ethanol interactions and hippocampal synaptic protein expression in a transgenic mouse modelDonna eGruol0Khanh eVo1Jennifer eBray2Amanda eRoberts3The Scripps Research InstituteThe Scripps Research InstituteThe Scripps Research InstituteThe Scripps Research InstituteChronic exposure to ethanol produces a number of detrimental effects on behavior. Neuroadaptive changes in brain structure or function underlie these behavioral changes and may be transient or persistent in nature. Central to the functional changes are alterations in the biology of neuronal and glial cells of the brain. Recent data show that ethanol induces glial cells of the brain to produce elevated levels of neuroimmune factors including CCL2, a key innate immune chemokine. Depending on the conditions of ethanol exposure, the upregulated levels of CCL2 can be transient or persistent and outlast the period of ethanol exposure. Importantly, results indicate that the upregulated levels of CCL2 may lead to CCL2-ethanol interactions that mediate or regulate the effects of ethanol on the brain. Glial cells are in close association with neurons and regulate many neuronal functions. Therefore, effects of ethanol on glial cells may underlie some of the effects of ethanol on neurons. To investigate this possibility, we are studying the effects of chronic ethanol on hippocampal synaptic function in a transgenic mouse model that expresses elevated levels of CCL2 in the brain through enhanced glial expression, a situation know to occur in alcoholics. Both CCL2 and ethanol have been reported to alter synaptic function in the hippocampus. In the current study, we determined if interactions are evident between CCL2 and ethanol at level of hippocampal synaptic proteins. Two ethanol exposure paradigms were used; the first involved ethanol exposure by drinking and the second involved ethanol exposure in a paradigm that combines drinking plus ethanol vapor. The first paradigm does not produce dependence on ethanol, whereas the second paradigm is commonly used to produce ethanol dependence. Results show modest effects of both ethanol exposure paradigms on the level of synaptic proteins in the hippocampus of CCL2 transgenic mice compared with their non-transgenic lihttp://journal.frontiersin.org/Journal/10.3389/fnint.2014.00029/fullchemokineastrocytewestern blotneuroimmunealcohol use disorderschronic treatment |
spellingShingle | Donna eGruol Khanh eVo Jennifer eBray Amanda eRoberts CCL2-ethanol interactions and hippocampal synaptic protein expression in a transgenic mouse model Frontiers in Integrative Neuroscience chemokine astrocyte western blot neuroimmune alcohol use disorders chronic treatment |
title | CCL2-ethanol interactions and hippocampal synaptic protein expression in a transgenic mouse model |
title_full | CCL2-ethanol interactions and hippocampal synaptic protein expression in a transgenic mouse model |
title_fullStr | CCL2-ethanol interactions and hippocampal synaptic protein expression in a transgenic mouse model |
title_full_unstemmed | CCL2-ethanol interactions and hippocampal synaptic protein expression in a transgenic mouse model |
title_short | CCL2-ethanol interactions and hippocampal synaptic protein expression in a transgenic mouse model |
title_sort | ccl2 ethanol interactions and hippocampal synaptic protein expression in a transgenic mouse model |
topic | chemokine astrocyte western blot neuroimmune alcohol use disorders chronic treatment |
url | http://journal.frontiersin.org/Journal/10.3389/fnint.2014.00029/full |
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