Sensory and Sensorimotor Gating Deficits after Neonatal Ventral Hippocampal Lesions in Rats
Neonatal ventral hippocampal lesions (NVHLs) in rats lead to reduced prepulse inhibition (PPI) of startle and other behavioral deficits in adulthood that model abnormalities in schizophrenia patients. A neurophysiological deficit in schizophrenia patients and their first-degree relatives is reduced...
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| Veröffentlicht in: | Developmental neuroscience 2012-09, Vol.34 (2-3), p.240-249 |
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| container_title | Developmental neuroscience |
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| creator | Swerdlow, Neal R. Light, Gregory A. Breier, Michelle R. Shoemaker, Jody M. Saint Marie, Richard L. Neary, Alaina C. Geyer, Mark A. Stevens, Karen E. Powell, Susan B. |
| description | Neonatal ventral hippocampal lesions (NVHLs) in rats lead to reduced prepulse inhibition (PPI) of startle and other behavioral deficits in adulthood that model abnormalities in schizophrenia patients. A neurophysiological deficit in schizophrenia patients and their first-degree relatives is reduced gating of the P50 event-related potential (ERP). N40 ERP gating in rats may be a cross-species analog of P50 gating, and is disrupted in experimental manipulations related to schizophrenia. Here, we tested whether N40 gating as well as PPI is disrupted after NVHLs, using contemporaneous measures of these two conceptually related phenomena. Male rat pups received sham or ibotenic acid NVHLs on postnatal day 7. PPI was tested on days 35 and 56, after which rats were equipped with cortical surface electrodes for ERP measurements. One week later, PPI and N40 gating were measured in a single test, using paired S1-S2 clicks spaced 500 ms apart to elicit N40 gating. Compared to sham-lesioned rats, those with NVHLs exhibited PPI deficits on days 35 and 56. NVHL rats also exhibited reduced N40 gating and reduced PPI, when measured contemporaneously at day 65. Deficits in PPI and N40 gating appeared most pronounced in rats with larger lesions, focused within the ventral hippocampus. In this first report of contemporaneous measures of two important schizophrenia-related phenotypes in NVHL rats, NVHLs reproduce both sensory (N40) and sensorimotor (PPI) gating deficits exhibited in schizophrenia. In this study, lesion effects were detected prior to pubertal onset, and were sustained well into adulthood. |
| doi_str_mv | 10.1159/000336841 |
| format | Article |
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A neurophysiological deficit in schizophrenia patients and their first-degree relatives is reduced gating of the P50 event-related potential (ERP). N40 ERP gating in rats may be a cross-species analog of P50 gating, and is disrupted in experimental manipulations related to schizophrenia. Here, we tested whether N40 gating as well as PPI is disrupted after NVHLs, using contemporaneous measures of these two conceptually related phenomena. Male rat pups received sham or ibotenic acid NVHLs on postnatal day 7. PPI was tested on days 35 and 56, after which rats were equipped with cortical surface electrodes for ERP measurements. One week later, PPI and N40 gating were measured in a single test, using paired S1-S2 clicks spaced 500 ms apart to elicit N40 gating. Compared to sham-lesioned rats, those with NVHLs exhibited PPI deficits on days 35 and 56. NVHL rats also exhibited reduced N40 gating and reduced PPI, when measured contemporaneously at day 65. Deficits in PPI and N40 gating appeared most pronounced in rats with larger lesions, focused within the ventral hippocampus. In this first report of contemporaneous measures of two important schizophrenia-related phenotypes in NVHL rats, NVHLs reproduce both sensory (N40) and sensorimotor (PPI) gating deficits exhibited in schizophrenia. In this study, lesion effects were detected prior to pubertal onset, and were sustained well into adulthood.</description><identifier>ISSN: 0378-5866</identifier><identifier>ISBN: 9783318022513</identifier><identifier>ISBN: 3318022519</identifier><identifier>EISSN: 1421-9859</identifier><identifier>EISBN: 9783318022520</identifier><identifier>EISBN: 3318022527</identifier><identifier>DOI: 10.1159/000336841</identifier><identifier>PMID: 22572564</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Acoustic Stimulation ; Animal models ; Animals ; Animals, Newborn ; Brain Injuries - physiopathology ; Electrodes ; Event-related potentials ; Gating ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - injuries ; Hippocampus - physiopathology ; Ibotenic acid ; Ibotenic Acid - pharmacology ; Male ; Mental disorders ; Neonates ; Nervous system ; Rats ; Rats, Sprague-Dawley ; Reflex, Startle - drug effects ; Reflex, Startle - physiology ; Schizophrenia ; Sensorimotor gating ; Sensory Gating - drug effects ; Sensory Gating - physiology</subject><ispartof>Developmental neuroscience, 2012-09, Vol.34 (2-3), p.240-249</ispartof><rights>2012 S. Karger AG, Basel</rights><rights>Copyright © 2012 S. Karger AG, Basel.</rights><rights>Copyright (c) 2012 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c367t-995fd4f17c166a22e8c0a3bd68ae0ebe1efad509279d2fbd3df06eec84dbd7793</citedby><cites>FETCH-LOGICAL-c367t-995fd4f17c166a22e8c0a3bd68ae0ebe1efad509279d2fbd3df06eec84dbd7793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22572564$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Swerdlow, Neal R.</creatorcontrib><creatorcontrib>Light, Gregory A.</creatorcontrib><creatorcontrib>Breier, Michelle R.</creatorcontrib><creatorcontrib>Shoemaker, Jody M.</creatorcontrib><creatorcontrib>Saint Marie, Richard L.</creatorcontrib><creatorcontrib>Neary, Alaina C.</creatorcontrib><creatorcontrib>Geyer, Mark A.</creatorcontrib><creatorcontrib>Stevens, Karen E.</creatorcontrib><creatorcontrib>Powell, Susan B.</creatorcontrib><title>Sensory and Sensorimotor Gating Deficits after Neonatal Ventral Hippocampal Lesions in Rats</title><title>Developmental neuroscience</title><addtitle>Dev Neurosci</addtitle><description>Neonatal ventral hippocampal lesions (NVHLs) in rats lead to reduced prepulse inhibition (PPI) of startle and other behavioral deficits in adulthood that model abnormalities in schizophrenia patients. A neurophysiological deficit in schizophrenia patients and their first-degree relatives is reduced gating of the P50 event-related potential (ERP). N40 ERP gating in rats may be a cross-species analog of P50 gating, and is disrupted in experimental manipulations related to schizophrenia. Here, we tested whether N40 gating as well as PPI is disrupted after NVHLs, using contemporaneous measures of these two conceptually related phenomena. Male rat pups received sham or ibotenic acid NVHLs on postnatal day 7. PPI was tested on days 35 and 56, after which rats were equipped with cortical surface electrodes for ERP measurements. One week later, PPI and N40 gating were measured in a single test, using paired S1-S2 clicks spaced 500 ms apart to elicit N40 gating. Compared to sham-lesioned rats, those with NVHLs exhibited PPI deficits on days 35 and 56. NVHL rats also exhibited reduced N40 gating and reduced PPI, when measured contemporaneously at day 65. Deficits in PPI and N40 gating appeared most pronounced in rats with larger lesions, focused within the ventral hippocampus. In this first report of contemporaneous measures of two important schizophrenia-related phenotypes in NVHL rats, NVHLs reproduce both sensory (N40) and sensorimotor (PPI) gating deficits exhibited in schizophrenia. In this study, lesion effects were detected prior to pubertal onset, and were sustained well into adulthood.</description><subject>Acoustic Stimulation</subject><subject>Animal models</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Brain Injuries - physiopathology</subject><subject>Electrodes</subject><subject>Event-related potentials</subject><subject>Gating</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - injuries</subject><subject>Hippocampus - physiopathology</subject><subject>Ibotenic acid</subject><subject>Ibotenic Acid - pharmacology</subject><subject>Male</subject><subject>Mental disorders</subject><subject>Neonates</subject><subject>Nervous system</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reflex, Startle - drug effects</subject><subject>Reflex, Startle - physiology</subject><subject>Schizophrenia</subject><subject>Sensorimotor gating</subject><subject>Sensory Gating - drug effects</subject><subject>Sensory Gating - physiology</subject><issn>0378-5866</issn><issn>1421-9859</issn><isbn>9783318022513</isbn><isbn>3318022519</isbn><isbn>9783318022520</isbn><isbn>3318022527</isbn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqN0c9rFDEUB_DUVuxae_AuEvBSD6P5_eMoVVthUVDbi4chM3kpU3eTaZI99L83stsFe_IQ3oN88uDli9BLSt5RKu17Qgjnygh6gE6tNpxTQxiTjDxBCyoY7ayR9vCfO8qP0IJwbTpplDpGz0u5JYQyy_UzdNyAZlKJBfr1A2JJ-R676PG2n9appowvXJ3iDf4IYRqnWrALFTL-Cim66lb4GmLNrV5O85xGt55bv4QypVjwFPF3V8sL9DS4VYHTXT1BV58__Ty_7JbfLr6cf1h2I1e6dtbK4EWgeqRKOcbAjMTxwSvjgMAAFILzklimrWdh8NwHogBGI_zgtbb8BJ1t58453W2g1H49lRFWKxchbUpPieVCSErNf1BlWTtSNPrmEb1NmxzbIj1lSiuliJBNvd2qMadSMoR-bh_o8n0b1f8Nr9-H1-zr3cTNsAa_lw9pNPBqC367fAN5D3bv_wBRPJe3</recordid><startdate>201209</startdate><enddate>201209</enddate><creator>Swerdlow, Neal R.</creator><creator>Light, Gregory A.</creator><creator>Breier, Michelle R.</creator><creator>Shoemaker, Jody M.</creator><creator>Saint Marie, Richard L.</creator><creator>Neary, Alaina C.</creator><creator>Geyer, Mark A.</creator><creator>Stevens, Karen E.</creator><creator>Powell, Susan B.</creator><general>S. 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Academic</collection><jtitle>Developmental neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Swerdlow, Neal R.</au><au>Light, Gregory A.</au><au>Breier, Michelle R.</au><au>Shoemaker, Jody M.</au><au>Saint Marie, Richard L.</au><au>Neary, Alaina C.</au><au>Geyer, Mark A.</au><au>Stevens, Karen E.</au><au>Powell, Susan B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sensory and Sensorimotor Gating Deficits after Neonatal Ventral Hippocampal Lesions in Rats</atitle><jtitle>Developmental neuroscience</jtitle><addtitle>Dev Neurosci</addtitle><date>2012-09</date><risdate>2012</risdate><volume>34</volume><issue>2-3</issue><spage>240</spage><epage>249</epage><pages>240-249</pages><issn>0378-5866</issn><eissn>1421-9859</eissn><isbn>9783318022513</isbn><isbn>3318022519</isbn><eisbn>9783318022520</eisbn><eisbn>3318022527</eisbn><abstract>Neonatal ventral hippocampal lesions (NVHLs) in rats lead to reduced prepulse inhibition (PPI) of startle and other behavioral deficits in adulthood that model abnormalities in schizophrenia patients. A neurophysiological deficit in schizophrenia patients and their first-degree relatives is reduced gating of the P50 event-related potential (ERP). N40 ERP gating in rats may be a cross-species analog of P50 gating, and is disrupted in experimental manipulations related to schizophrenia. Here, we tested whether N40 gating as well as PPI is disrupted after NVHLs, using contemporaneous measures of these two conceptually related phenomena. Male rat pups received sham or ibotenic acid NVHLs on postnatal day 7. PPI was tested on days 35 and 56, after which rats were equipped with cortical surface electrodes for ERP measurements. One week later, PPI and N40 gating were measured in a single test, using paired S1-S2 clicks spaced 500 ms apart to elicit N40 gating. Compared to sham-lesioned rats, those with NVHLs exhibited PPI deficits on days 35 and 56. NVHL rats also exhibited reduced N40 gating and reduced PPI, when measured contemporaneously at day 65. Deficits in PPI and N40 gating appeared most pronounced in rats with larger lesions, focused within the ventral hippocampus. In this first report of contemporaneous measures of two important schizophrenia-related phenotypes in NVHL rats, NVHLs reproduce both sensory (N40) and sensorimotor (PPI) gating deficits exhibited in schizophrenia. In this study, lesion effects were detected prior to pubertal onset, and were sustained well into adulthood.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>22572564</pmid><doi>10.1159/000336841</doi><tpages>10</tpages></addata></record> |
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| subjects | Acoustic Stimulation Animal models Animals Animals, Newborn Brain Injuries - physiopathology Electrodes Event-related potentials Gating Hippocampus Hippocampus - drug effects Hippocampus - injuries Hippocampus - physiopathology Ibotenic acid Ibotenic Acid - pharmacology Male Mental disorders Neonates Nervous system Rats Rats, Sprague-Dawley Reflex, Startle - drug effects Reflex, Startle - physiology Schizophrenia Sensorimotor gating Sensory Gating - drug effects Sensory Gating - physiology |
| title | Sensory and Sensorimotor Gating Deficits after Neonatal Ventral Hippocampal Lesions in Rats |
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