Chronic intermittent ethanol exposure alters CA1 synaptic transmission in rat hippocampal slices
We investigated the neuroadaptive changes in synaptic transmission in the CA1 region of the hippocampus as a result of chronic intermittent ethanol exposure. Male Wistar rats were exposed daily (14 h) to ethanol vapors (blood alcohol levels=150–200 mg%) for 12–14 days, and synaptic field potentials...
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| Veröffentlicht in: | Neuroscience 1999-01, Vol.94 (2), p.431-442 |
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| description | We investigated the neuroadaptive changes in synaptic transmission in the CA1 region of the hippocampus as a result of chronic intermittent ethanol exposure. Male Wistar rats were exposed daily (14
h) to ethanol vapors (blood alcohol levels=150–200
mg%) for 12–14
days, and synaptic field potentials elicited by Schaffer collateral stimulation were compared in hippocampal slices from control and chronic ethanol-treated rats. Excitatory postsynaptic responses of slices were recorded under three conditions: (i) normal physiological saline; (ii) continued presence of 33
mM (150
mg%) ethanol (chronic ethanol-treated rats only); (iii) acute exposure to 33
mM ethanol. When recorded in ethanol-free physiological saline, the mean amplitude of the dendritic synaptic potential and the somatic population spike were significantly smaller in slices from chronic ethanol-treated rats compared to slices from control rats. Under conditions of continuous ethanol exposure, somatic and dendritic synaptic responses of slices taken from chronic ethanol-treated rats were further depressed, suggesting that neural pathways in area CA1 remained sensitive to ethanol. Acute application of ethanol led to a more pronounced reduction of the mean somatic population spike amplitude in slices from chronic ethanol-treated rats than in slices from control rats. However, dendritic synaptic responses were unaffected by acute ethanol in slices from both control and chronic ethanol-treated rats. In addition, we examined the involvement of presynaptic mechanisms in the effects of chronic intermittent ethanol using paired-pulse protocols. When recorded in the continued presence of ethanol, slices from chronic ethanol-treated rats exhibited a significant reduction in paired-pulse facilitation of the dendritic synaptic response compared to slices from control rats, indicating a presynaptic component to the neuroadaptive effects of chronic intermittent ethanol exposure. Conversely, acute ethanol exposure resulted in an enhancement of paired-pulse facilitation of the dendritic synaptic response, an effect that was similar in slices from both control and chronic ethanol-treated rats. Paired-pulse facilitation of the somatic population spike amplitude was not altered by chronic ethanol treatment. However, acute ethanol exposure significantly enhanced paired-pulse facilitation of the somatic population spike in slices from chronic ethanol-treated rats. This effect of acute ethanol was not observed in slice |
| doi_str_mv | 10.1016/S0306-4522(99)00336-X |
| format | Article |
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h) to ethanol vapors (blood alcohol levels=150–200
mg%) for 12–14
days, and synaptic field potentials elicited by Schaffer collateral stimulation were compared in hippocampal slices from control and chronic ethanol-treated rats. Excitatory postsynaptic responses of slices were recorded under three conditions: (i) normal physiological saline; (ii) continued presence of 33
mM (150
mg%) ethanol (chronic ethanol-treated rats only); (iii) acute exposure to 33
mM ethanol. When recorded in ethanol-free physiological saline, the mean amplitude of the dendritic synaptic potential and the somatic population spike were significantly smaller in slices from chronic ethanol-treated rats compared to slices from control rats. Under conditions of continuous ethanol exposure, somatic and dendritic synaptic responses of slices taken from chronic ethanol-treated rats were further depressed, suggesting that neural pathways in area CA1 remained sensitive to ethanol. Acute application of ethanol led to a more pronounced reduction of the mean somatic population spike amplitude in slices from chronic ethanol-treated rats than in slices from control rats. However, dendritic synaptic responses were unaffected by acute ethanol in slices from both control and chronic ethanol-treated rats. In addition, we examined the involvement of presynaptic mechanisms in the effects of chronic intermittent ethanol using paired-pulse protocols. When recorded in the continued presence of ethanol, slices from chronic ethanol-treated rats exhibited a significant reduction in paired-pulse facilitation of the dendritic synaptic response compared to slices from control rats, indicating a presynaptic component to the neuroadaptive effects of chronic intermittent ethanol exposure. Conversely, acute ethanol exposure resulted in an enhancement of paired-pulse facilitation of the dendritic synaptic response, an effect that was similar in slices from both control and chronic ethanol-treated rats. Paired-pulse facilitation of the somatic population spike amplitude was not altered by chronic ethanol treatment. However, acute ethanol exposure significantly enhanced paired-pulse facilitation of the somatic population spike in slices from chronic ethanol-treated rats. This effect of acute ethanol was not observed in slices from control rats. Paired-pulse inhibition was not significantly altered in slices from chronic ethanol-treated rats, suggesting that GABAergic inhibitory mechanisms were not involved in the neuroadaptive effects of chronic intermittent ethanol exposure.
We suggest that chronic intermittent ethanol exposure can induce multiple neuroadaptive changes in synaptic transmission of CA1 pyramidal neurons that are detectable at both the pre- and postsynaptic levels. Alterations in paired-pulse facilitation indicate presynaptic changes involving the release of the excitatory neurotransmitter glutamate, whereas changes in dendritic synaptic responses suggest postsynaptic changes in the responsiveness of neurons to synaptic input. Moreover, differential effects of chronic ethanol treatment on synaptic responses recorded in the dendrites versus the somatic region implicate additional effects of ethanol on somatically located mechanisms of CA1 pyramidal neurons. Furthermore, we suggest that complete tolerance to ethanol does not occur in the CA1 region of the hippocampus following chronic intermittent ethanol exposure.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/S0306-4522(99)00336-X</identifier><identifier>PMID: 10579206</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>alcohol ; Alcoholism - physiopathology ; Alcoholism and acute alcohol poisoning ; Animals ; Biological and medical sciences ; Dendrites - physiology ; Electric Stimulation ; electrophysiology ; Ethanol - blood ; field potential ; hippocampus ; Hippocampus - physiology ; Hippocampus - physiopathology ; In Vitro Techniques ; Male ; Medical sciences ; Models, Neurological ; Neurons - physiology ; paired-pulse facilitation ; paired-pulse inhibition ; Pyramidal Cells - physiology ; Rats ; Rats, Wistar ; Synapses - physiology ; Synaptic Transmission - physiology ; Time Factors ; Toxicology</subject><ispartof>Neuroscience, 1999-01, Vol.94 (2), p.431-442</ispartof><rights>1999 IBRO</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-5f44386911cd937cd9870aba689c5dce4613de2fedf5c52ed9e322d0d024e3693</citedby><cites>FETCH-LOGICAL-c421t-5f44386911cd937cd9870aba689c5dce4613de2fedf5c52ed9e322d0d024e3693</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0306-4522(99)00336-X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27922,27923,45993</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1971571$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10579206$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nelson, T.E</creatorcontrib><creatorcontrib>Ur, C.L</creatorcontrib><creatorcontrib>Gruol, D.L</creatorcontrib><title>Chronic intermittent ethanol exposure alters CA1 synaptic transmission in rat hippocampal slices</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>We investigated the neuroadaptive changes in synaptic transmission in the CA1 region of the hippocampus as a result of chronic intermittent ethanol exposure. Male Wistar rats were exposed daily (14
h) to ethanol vapors (blood alcohol levels=150–200
mg%) for 12–14
days, and synaptic field potentials elicited by Schaffer collateral stimulation were compared in hippocampal slices from control and chronic ethanol-treated rats. Excitatory postsynaptic responses of slices were recorded under three conditions: (i) normal physiological saline; (ii) continued presence of 33
mM (150
mg%) ethanol (chronic ethanol-treated rats only); (iii) acute exposure to 33
mM ethanol. When recorded in ethanol-free physiological saline, the mean amplitude of the dendritic synaptic potential and the somatic population spike were significantly smaller in slices from chronic ethanol-treated rats compared to slices from control rats. Under conditions of continuous ethanol exposure, somatic and dendritic synaptic responses of slices taken from chronic ethanol-treated rats were further depressed, suggesting that neural pathways in area CA1 remained sensitive to ethanol. Acute application of ethanol led to a more pronounced reduction of the mean somatic population spike amplitude in slices from chronic ethanol-treated rats than in slices from control rats. However, dendritic synaptic responses were unaffected by acute ethanol in slices from both control and chronic ethanol-treated rats. In addition, we examined the involvement of presynaptic mechanisms in the effects of chronic intermittent ethanol using paired-pulse protocols. When recorded in the continued presence of ethanol, slices from chronic ethanol-treated rats exhibited a significant reduction in paired-pulse facilitation of the dendritic synaptic response compared to slices from control rats, indicating a presynaptic component to the neuroadaptive effects of chronic intermittent ethanol exposure. Conversely, acute ethanol exposure resulted in an enhancement of paired-pulse facilitation of the dendritic synaptic response, an effect that was similar in slices from both control and chronic ethanol-treated rats. Paired-pulse facilitation of the somatic population spike amplitude was not altered by chronic ethanol treatment. However, acute ethanol exposure significantly enhanced paired-pulse facilitation of the somatic population spike in slices from chronic ethanol-treated rats. This effect of acute ethanol was not observed in slices from control rats. Paired-pulse inhibition was not significantly altered in slices from chronic ethanol-treated rats, suggesting that GABAergic inhibitory mechanisms were not involved in the neuroadaptive effects of chronic intermittent ethanol exposure.
We suggest that chronic intermittent ethanol exposure can induce multiple neuroadaptive changes in synaptic transmission of CA1 pyramidal neurons that are detectable at both the pre- and postsynaptic levels. Alterations in paired-pulse facilitation indicate presynaptic changes involving the release of the excitatory neurotransmitter glutamate, whereas changes in dendritic synaptic responses suggest postsynaptic changes in the responsiveness of neurons to synaptic input. Moreover, differential effects of chronic ethanol treatment on synaptic responses recorded in the dendrites versus the somatic region implicate additional effects of ethanol on somatically located mechanisms of CA1 pyramidal neurons. Furthermore, we suggest that complete tolerance to ethanol does not occur in the CA1 region of the hippocampus following chronic intermittent ethanol exposure.</description><subject>alcohol</subject><subject>Alcoholism - physiopathology</subject><subject>Alcoholism and acute alcohol poisoning</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Dendrites - physiology</subject><subject>Electric Stimulation</subject><subject>electrophysiology</subject><subject>Ethanol - blood</subject><subject>field potential</subject><subject>hippocampus</subject><subject>Hippocampus - physiology</subject><subject>Hippocampus - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Models, Neurological</subject><subject>Neurons - physiology</subject><subject>paired-pulse facilitation</subject><subject>paired-pulse inhibition</subject><subject>Pyramidal Cells - physiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Synapses - physiology</subject><subject>Synaptic Transmission - physiology</subject><subject>Time Factors</subject><subject>Toxicology</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkD1vFDEQhi1ERI7ATwBtgRAUC_7ecxVFJz4iRaIApHTGsWd1Rrv24vEh8u_x5U6QLi7GxTzvzOgh5AWj7xhl-v1XKqjupeL8jTFvKRVC99ePyIqtB9EPSsrHZPUPOSVPEX_S9pQUT8gpo2ownOoV-bHZlpyi72KqUOZYK6TaQd26lKcO_iwZdwU6N7UudpsL1uFtckttiVpcwjkixpxavCuudtu4LNm7eXFTh1P0gM_IyegmhOfH_4x8__jh2-Zzf_Xl0-Xm4qr3krPaq1FKsdaGMR-MGFpZD9TdOL02XgUPUjMRgI8QRuUVh2BAcB5ooFyC0EackdeHuUvJv3aA1bbTPEyTS5B3aNmgtTSSNVAdQF8yYoHRLiXOrtxaRu1erb1Ta_ferDH2Tq29brmXxwW7mxnCvdTBZQNeHQGH3k1j0-Mj_ufMwNSw339-wKDZ-B2hWPQRkocQC_hqQ44PXPIXWJiXRw</recordid><startdate>19990101</startdate><enddate>19990101</enddate><creator>Nelson, T.E</creator><creator>Ur, C.L</creator><creator>Gruol, D.L</creator><general>Elsevier 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></search><sort><creationdate>19990101</creationdate><title>Chronic intermittent ethanol exposure alters CA1 synaptic transmission in rat hippocampal slices</title><author>Nelson, T.E ; Ur, C.L ; Gruol, D.L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-5f44386911cd937cd9870aba689c5dce4613de2fedf5c52ed9e322d0d024e3693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>alcohol</topic><topic>Alcoholism - physiopathology</topic><topic>Alcoholism and acute alcohol poisoning</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Dendrites - physiology</topic><topic>Electric Stimulation</topic><topic>electrophysiology</topic><topic>Ethanol - blood</topic><topic>field potential</topic><topic>hippocampus</topic><topic>Hippocampus - physiology</topic><topic>Hippocampus - physiopathology</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Models, Neurological</topic><topic>Neurons - physiology</topic><topic>paired-pulse facilitation</topic><topic>paired-pulse inhibition</topic><topic>Pyramidal Cells - physiology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Synapses - physiology</topic><topic>Synaptic Transmission - physiology</topic><topic>Time Factors</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nelson, T.E</creatorcontrib><creatorcontrib>Ur, C.L</creatorcontrib><creatorcontrib>Gruol, D.L</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><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nelson, T.E</au><au>Ur, C.L</au><au>Gruol, D.L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic intermittent ethanol exposure alters CA1 synaptic transmission in rat hippocampal slices</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>1999-01-01</date><risdate>1999</risdate><volume>94</volume><issue>2</issue><spage>431</spage><epage>442</epage><pages>431-442</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>We investigated the neuroadaptive changes in synaptic transmission in the CA1 region of the hippocampus as a result of chronic intermittent ethanol exposure. Male Wistar rats were exposed daily (14
h) to ethanol vapors (blood alcohol levels=150–200
mg%) for 12–14
days, and synaptic field potentials elicited by Schaffer collateral stimulation were compared in hippocampal slices from control and chronic ethanol-treated rats. Excitatory postsynaptic responses of slices were recorded under three conditions: (i) normal physiological saline; (ii) continued presence of 33
mM (150
mg%) ethanol (chronic ethanol-treated rats only); (iii) acute exposure to 33
mM ethanol. When recorded in ethanol-free physiological saline, the mean amplitude of the dendritic synaptic potential and the somatic population spike were significantly smaller in slices from chronic ethanol-treated rats compared to slices from control rats. Under conditions of continuous ethanol exposure, somatic and dendritic synaptic responses of slices taken from chronic ethanol-treated rats were further depressed, suggesting that neural pathways in area CA1 remained sensitive to ethanol. Acute application of ethanol led to a more pronounced reduction of the mean somatic population spike amplitude in slices from chronic ethanol-treated rats than in slices from control rats. However, dendritic synaptic responses were unaffected by acute ethanol in slices from both control and chronic ethanol-treated rats. In addition, we examined the involvement of presynaptic mechanisms in the effects of chronic intermittent ethanol using paired-pulse protocols. When recorded in the continued presence of ethanol, slices from chronic ethanol-treated rats exhibited a significant reduction in paired-pulse facilitation of the dendritic synaptic response compared to slices from control rats, indicating a presynaptic component to the neuroadaptive effects of chronic intermittent ethanol exposure. Conversely, acute ethanol exposure resulted in an enhancement of paired-pulse facilitation of the dendritic synaptic response, an effect that was similar in slices from both control and chronic ethanol-treated rats. Paired-pulse facilitation of the somatic population spike amplitude was not altered by chronic ethanol treatment. However, acute ethanol exposure significantly enhanced paired-pulse facilitation of the somatic population spike in slices from chronic ethanol-treated rats. This effect of acute ethanol was not observed in slices from control rats. Paired-pulse inhibition was not significantly altered in slices from chronic ethanol-treated rats, suggesting that GABAergic inhibitory mechanisms were not involved in the neuroadaptive effects of chronic intermittent ethanol exposure.
We suggest that chronic intermittent ethanol exposure can induce multiple neuroadaptive changes in synaptic transmission of CA1 pyramidal neurons that are detectable at both the pre- and postsynaptic levels. Alterations in paired-pulse facilitation indicate presynaptic changes involving the release of the excitatory neurotransmitter glutamate, whereas changes in dendritic synaptic responses suggest postsynaptic changes in the responsiveness of neurons to synaptic input. Moreover, differential effects of chronic ethanol treatment on synaptic responses recorded in the dendrites versus the somatic region implicate additional effects of ethanol on somatically located mechanisms of CA1 pyramidal neurons. Furthermore, we suggest that complete tolerance to ethanol does not occur in the CA1 region of the hippocampus following chronic intermittent ethanol exposure.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>10579206</pmid><doi>10.1016/S0306-4522(99)00336-X</doi><tpages>12</tpages></addata></record> |
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| ispartof | Neuroscience, 1999-01, Vol.94 (2), p.431-442 |
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| subjects | alcohol Alcoholism - physiopathology Alcoholism and acute alcohol poisoning Animals Biological and medical sciences Dendrites - physiology Electric Stimulation electrophysiology Ethanol - blood field potential hippocampus Hippocampus - physiology Hippocampus - physiopathology In Vitro Techniques Male Medical sciences Models, Neurological Neurons - physiology paired-pulse facilitation paired-pulse inhibition Pyramidal Cells - physiology Rats Rats, Wistar Synapses - physiology Synaptic Transmission - physiology Time Factors Toxicology |
| title | Chronic intermittent ethanol exposure alters CA1 synaptic transmission in rat hippocampal slices |
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