Sleep and EEG profile in neonatal hippocampal lesion model of schizophrenia

Abstract Sleep architecture, EEG power pattern and locomotor activity were investigated in a putative animal model of schizophrenia. The model was prepared by excitotoxic damage of the ventral hippocampus on postnatal day 7 (PD 7), after which locomotor activity and electroencephalographic (EEG) sle...

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Veröffentlicht in:Physiology & behavior 2007-10, Vol.92 (3), p.461-467
Hauptverfasser: Ahnaou, A, Nayak, S, Heylen, A, Ashton, D, Drinkenburg, W.H.I.M
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creator Ahnaou, A
Nayak, S
Heylen, A
Ashton, D
Drinkenburg, W.H.I.M
description Abstract Sleep architecture, EEG power pattern and locomotor activity were investigated in a putative animal model of schizophrenia. The model was prepared by excitotoxic damage of the ventral hippocampus on postnatal day 7 (PD 7), after which locomotor activity and electroencephalographic (EEG) sleep profile were compared between lesioned and sham operated animals respectively, at prepuberty (postnatal day PD 35) and postpuberty (PD 56). An enhancement of locomotor activity was observed in lesioned adult PD 56, but not in juvenile PD 35 rats. Spontaneous EEG/EMG recordings during 24 h showed no major differences between both groups at PD 35 and at PD 56. However, quantitative analysis of the EEG revealed an enhancement of power in delta ( δ ), theta ( θ ) and alpha ( α ) activities in lesioned animals at PD 35 during wakefulness in both light and dark phases. At PD 56, the power in the δ and θ bands was increased during the light and dark periods in both wakefulness and non-REM sleep. These findings suggest that ventral hippocampus lesion is not associated with disturbance of sleep architecture in rats, while consistent changes were observed in the dynamic of EEG slow wave frequency domain. Thus, the data indicate that neonatal lesion of ventral hippocampus did not mimic sleep abnormalities observed in schizophrenia, however this rodent model may model some EEG features seen in schizophrenia such as a frontally pronounced slowing of the slow EEG activity in δ and θ frequency bands.
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Psychology</subject><subject>Hippocampus - injuries</subject><subject>Hippocampus - pathology</subject><subject>Hippocampus lesion</subject><subject>Ibotenic Acid</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Motor Activity - physiology</subject><subject>Pregnancy</subject><subject>Psychiatry</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychology. Psychophysiology</subject><subject>Psychopathology. Psychiatry</subject><subject>Psychoses</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Schizophrenia</subject><subject>Schizophrenia - chemically induced</subject><subject>Schizophrenia - pathology</subject><subject>Schizophrenia - physiopathology</subject><subject>Sleep</subject><subject>Sleep - physiology</subject><subject>Statistics, Nonparametric</subject><issn>0031-9384</issn><issn>1873-507X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkVuL1DAUgIMo7rj6E5S-iE-tJ5c27Ysiy7iKCz6sgm8hTU9pxjSpyYww_npTprDgi4GQQL5zyXcIeUmhokCbt4dqmc6px6liALICUQGDR2RHW8nLGuSPx2QHwGnZ8VZckWcpHSAvLvhTckVlzYTgYke-3DvEpdB-KPb722KJYbQOC-sLj8Hro3bFZJclGD0v-e4w2eCLOQzoijAWyUz2T1imiN7q5-TJqF3CF9t5Tb5_3H-7-VTefb39fPPhrjSihWOJIHqo21qMDeOdpMAG1nbQD5q3ppZ8bPuBI-jemPyUd9N1_aj1IJlk6xeuyZtL3tztrxOmo5ptMuiczj2fkmobKXlb05WsL6SJIaWIo1qinXU8Kwpq1agOatOoVo0KhMoac9yrrcKpn3F4iNq8ZeD1BuhktBuj9samB66jnWBAM_f-wmH28dtiVMlY9AYHG9Ec1RDsf1t5908G46y3uehPPGM6hFP0WbaiKjEF6n6d-TpykAC0bgT_C8k9p0E</recordid><startdate>20071022</startdate><enddate>20071022</enddate><creator>Ahnaou, A</creator><creator>Nayak, S</creator><creator>Heylen, A</creator><creator>Ashton, D</creator><creator>Drinkenburg, W.H.I.M</creator><general>Elsevier Inc</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>7QG</scope><scope>7TK</scope></search><sort><creationdate>20071022</creationdate><title>Sleep and EEG profile in neonatal hippocampal lesion model of schizophrenia</title><author>Ahnaou, A ; Nayak, S ; Heylen, A ; Ashton, D ; Drinkenburg, W.H.I.M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c480t-e04b05854f62397102d2890bda38c573f8bd3e0abcc02dc02699bfaad72720003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult and adolescent clinical studies</topic><topic>Age Factors</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Behavioral psychophysiology</topic><topic>Biological and medical sciences</topic><topic>Disease Models, Animal</topic><topic>EEG</topic><topic>Electroencephalography</topic><topic>Electromyography</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. 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Psychiatry</topic><topic>Psychoses</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Schizophrenia</topic><topic>Schizophrenia - chemically induced</topic><topic>Schizophrenia - pathology</topic><topic>Schizophrenia - physiopathology</topic><topic>Sleep</topic><topic>Sleep - physiology</topic><topic>Statistics, Nonparametric</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ahnaou, A</creatorcontrib><creatorcontrib>Nayak, S</creatorcontrib><creatorcontrib>Heylen, A</creatorcontrib><creatorcontrib>Ashton, D</creatorcontrib><creatorcontrib>Drinkenburg, W.H.I.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>Animal Behavior Abstracts</collection><collection>Neurosciences Abstracts</collection><jtitle>Physiology &amp; behavior</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ahnaou, A</au><au>Nayak, S</au><au>Heylen, A</au><au>Ashton, D</au><au>Drinkenburg, W.H.I.M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sleep and EEG profile in neonatal hippocampal lesion model of schizophrenia</atitle><jtitle>Physiology &amp; behavior</jtitle><addtitle>Physiol Behav</addtitle><date>2007-10-22</date><risdate>2007</risdate><volume>92</volume><issue>3</issue><spage>461</spage><epage>467</epage><pages>461-467</pages><issn>0031-9384</issn><eissn>1873-507X</eissn><abstract>Abstract Sleep architecture, EEG power pattern and locomotor activity were investigated in a putative animal model of schizophrenia. The model was prepared by excitotoxic damage of the ventral hippocampus on postnatal day 7 (PD 7), after which locomotor activity and electroencephalographic (EEG) sleep profile were compared between lesioned and sham operated animals respectively, at prepuberty (postnatal day PD 35) and postpuberty (PD 56). An enhancement of locomotor activity was observed in lesioned adult PD 56, but not in juvenile PD 35 rats. Spontaneous EEG/EMG recordings during 24 h showed no major differences between both groups at PD 35 and at PD 56. However, quantitative analysis of the EEG revealed an enhancement of power in delta ( δ ), theta ( θ ) and alpha ( α ) activities in lesioned animals at PD 35 during wakefulness in both light and dark phases. At PD 56, the power in the δ and θ bands was increased during the light and dark periods in both wakefulness and non-REM sleep. These findings suggest that ventral hippocampus lesion is not associated with disturbance of sleep architecture in rats, while consistent changes were observed in the dynamic of EEG slow wave frequency domain. Thus, the data indicate that neonatal lesion of ventral hippocampus did not mimic sleep abnormalities observed in schizophrenia, however this rodent model may model some EEG features seen in schizophrenia such as a frontally pronounced slowing of the slow EEG activity in δ and θ frequency bands.</abstract><cop>Cambridge</cop><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>17524434</pmid><doi>10.1016/j.physbeh.2007.04.020</doi><tpages>7</tpages></addata></record>
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source MEDLINE; Access via ScienceDirect (Elsevier)
subjects Adult and adolescent clinical studies
Age Factors
Animals
Animals, Newborn
Behavioral psychophysiology
Biological and medical sciences
Disease Models, Animal
EEG
Electroencephalography
Electromyography
Female
Fundamental and applied biological sciences. Psychology
Hippocampus - injuries
Hippocampus - pathology
Hippocampus lesion
Ibotenic Acid
Male
Medical sciences
Motor Activity - physiology
Pregnancy
Psychiatry
Psychology. Psychoanalysis. Psychiatry
Psychology. Psychophysiology
Psychopathology. Psychiatry
Psychoses
Rat
Rats
Rats, Sprague-Dawley
Schizophrenia
Schizophrenia - chemically induced
Schizophrenia - pathology
Schizophrenia - physiopathology
Sleep
Sleep - physiology
Statistics, Nonparametric
title Sleep and EEG profile in neonatal hippocampal lesion model of schizophrenia
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