Generation of cortical event-related slow potentials in the rat involves nucleus basalis cholinergic innervation

These experiments were conducted to gather information regarding the role of cholinergic innervation to the cortex in the generation of event-related slow potentials. The effects of unilateral drug treatments or lesions on ipsilateral and contralateral frontal cortex slow potential (SP) responses we...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Electroencephalography and clinical neurophysiology 1986-05, Vol.63 (5), p.464-475
Hauptverfasser: Pirch, J.H, Corbus, M.J, Rigdon, G.C, Lyness, W.H
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 475
container_issue 5
container_start_page 464
container_title Electroencephalography and clinical neurophysiology
container_volume 63
creator Pirch, J.H
Corbus, M.J
Rigdon, G.C
Lyness, W.H
description These experiments were conducted to gather information regarding the role of cholinergic innervation to the cortex in the generation of event-related slow potentials. The effects of unilateral drug treatments or lesions on ipsilateral and contralateral frontal cortex slow potential (SP) responses were examined in rats. The SP responses were recorded with silver-silver chloride electrodes and were generated by a 2 sec light cue which preceded medial forebrain bundle stimulation. The following approaches were used: (1) microinjection of GABA, procaine or saline into the nucleus basalis magnocellularis; (2) microinjection of atropine or saline subdurally in the SP recording area; (3) electrolytic lesion of the nucleus basalis area; and (4) kainic acid lesion of the nucleus basalis area. The following bilateral measurements were obtained in the lesion studies: choline acetyltransferase (ChAT) in cortex and hippocampus; serotonin in cortex, hippocampus, striatum and nucleus accumbens; norepinephrine in cortex and hippocampus; dopamine in striatum and nucleus accumbens; and metabolites of serotonin, norepinephrine and dopamine in these areas. The cortical SP responses were reduced on the side ipsilateral to the injections of GABA and procaine into the nucleus basalis, and on the side of the subdural atropine injection. With either type of lesion, the SP responses on the lesioned side were significantly reduced as compared to the non-lesioned side. Reductions in cortical ChAT and other measures were observed ipsilateral to the electrolytic lesion, but only cortical ChAT activity was reduced in the kainic acid-lesioned animals. Thus, pharmacological depression of nucleus basalis neurons, blockade of cholinergic muscarinic receptors in the cortex, and nucleus basalis lesions that reduce cortical choline acetyltransferase activity depress event-related slow potentials in the rat frontal cortex. These results provide evidence that cortical slow potential responses in the rat are dependent upon cholinergic innervation from the nucleus basalis. Ces travaux ont été effectués pour obtenir des données sur le rôle de l'innervation cholinergique afférente au cortex dans la production de potentiels lents liés à l'événement. On a recherché les effets d'injections unilatérales de drogues ou de lésions unilatérales sur les potentiels lents (PL) des cortex frontaux ipsi- et contralatéral. Les PL ont été enregistrés à l'aide d'électrodes d'argent-chlorure d'argent et ont été prod
doi_str_mv 10.1016/0013-4694(86)90128-8
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_76766388</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>0013469486901288</els_id><sourcerecordid>76766388</sourcerecordid><originalsourceid>FETCH-LOGICAL-c386t-de9f2930f4b52300d1f4e196011ff13d0688339a82d481208e3284d345acf933</originalsourceid><addsrcrecordid>eNp9kE1rVDEUhoModVr9BwpZiOji6snH5OZuClLsBxTcdB8yuSc2krkZk9xb-u_NdIZZusoh53nfhIeQDwy-MWDqOwATnVSD_KLV1wEY151-RVZM97xTQsNrsjohb8l5KX8AgDPen5EzLjmsFV-R3Q1OmG0NaaLJU5dyDc5GigtOtcsYbcWRlpie6C7VdhdsLDRMtD4ibbk2LikuWOg0u4hzoRtbbAyFuscUQ-v-HVyD2rC8vPKOvPGtAt8fzwvycP3z4eq2u_91c3f1475zQqvajTh4PgjwcrPmAmBkXiIbFDDmPRMjKK2FGKzmo9SMg0bBtRyFXFvnByEuyOdD7S6nvzOWarahOIzRTpjmYnrVqyZJN1AeQJdTKRm92eWwtfnZMDB7z2Yv0ewlGq3Mi2ezj3089s-bLY6n0FFs23867m1pPn22kwvlhGkQivWyYZcHDJuKJWA2xQWcHI4ho6tmTOH___gHAt2aVw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>76766388</pqid></control><display><type>article</type><title>Generation of cortical event-related slow potentials in the rat involves nucleus basalis cholinergic innervation</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Pirch, J.H ; Corbus, M.J ; Rigdon, G.C ; Lyness, W.H</creator><creatorcontrib>Pirch, J.H ; Corbus, M.J ; Rigdon, G.C ; Lyness, W.H</creatorcontrib><description>These experiments were conducted to gather information regarding the role of cholinergic innervation to the cortex in the generation of event-related slow potentials. The effects of unilateral drug treatments or lesions on ipsilateral and contralateral frontal cortex slow potential (SP) responses were examined in rats. The SP responses were recorded with silver-silver chloride electrodes and were generated by a 2 sec light cue which preceded medial forebrain bundle stimulation. The following approaches were used: (1) microinjection of GABA, procaine or saline into the nucleus basalis magnocellularis; (2) microinjection of atropine or saline subdurally in the SP recording area; (3) electrolytic lesion of the nucleus basalis area; and (4) kainic acid lesion of the nucleus basalis area. The following bilateral measurements were obtained in the lesion studies: choline acetyltransferase (ChAT) in cortex and hippocampus; serotonin in cortex, hippocampus, striatum and nucleus accumbens; norepinephrine in cortex and hippocampus; dopamine in striatum and nucleus accumbens; and metabolites of serotonin, norepinephrine and dopamine in these areas. The cortical SP responses were reduced on the side ipsilateral to the injections of GABA and procaine into the nucleus basalis, and on the side of the subdural atropine injection. With either type of lesion, the SP responses on the lesioned side were significantly reduced as compared to the non-lesioned side. Reductions in cortical ChAT and other measures were observed ipsilateral to the electrolytic lesion, but only cortical ChAT activity was reduced in the kainic acid-lesioned animals. Thus, pharmacological depression of nucleus basalis neurons, blockade of cholinergic muscarinic receptors in the cortex, and nucleus basalis lesions that reduce cortical choline acetyltransferase activity depress event-related slow potentials in the rat frontal cortex. These results provide evidence that cortical slow potential responses in the rat are dependent upon cholinergic innervation from the nucleus basalis. Ces travaux ont été effectués pour obtenir des données sur le rôle de l'innervation cholinergique afférente au cortex dans la production de potentiels lents liés à l'événement. On a recherché les effets d'injections unilatérales de drogues ou de lésions unilatérales sur les potentiels lents (PL) des cortex frontaux ipsi- et contralatéral. Les PL ont été enregistrés à l'aide d'électrodes d'argent-chlorure d'argent et ont été produits par un signal lumineux de 2 sec qui précédait une récompense par stimulation du faisceau médian du télencéphale. Les approches suivantes ont été utilisées: (1) microinjection de GABA, procaïne ou liquide physiologique dans le noyau basal magnocellulaire; (2) microinjection subdurale d'atropine ou de liquide physiologique dans la région d'enregistrement des PL; (3) lésion électrolytique de la région du noyau basal; et (4) lésion chimique à l'acide kaïnique de la région de noyau basal. On a effectué bilatéralement les mesures suivantes pour les études lésionnelles: acétylcholine transférase (AChT) dans le cortex et l'hippocampe; sérotonine dans le cortex, l'hippocampe, le noyau caudé et le noyau accumbens; norépinéphrine dans le cortex et l'hippocampe; dopamine dans le noyau caudé et le noyau accumbens; métabolites de la sérotonine, de la norépinéphrine et de la dopamine dans ces régions. On a noté une diminution des PL corticaux du côté ipsilatéral aux injections de GABA et de procaïne dans le noyau basal, et du côté de l'injection subdurale d'atropine. Quel que soit le type de lésion, les réponses PL ipsilatérales à la lésion ont été significativement réduites par rapport aux réponses contralatérales. Du côté ipsilatéral à la lésion électrolytique on a aussi observé des diminutions de l'AChT corticale et des autres valeurs; mais seule l'activité AChT corticale était réduite si la lésion était kaïnique. Ainsi, la dépression pharmacologique des neurones du noyau basal, le blocage des récepteurs cholinergiques muscariniques corticaux et les lésions du noyau basal qui réduisent l'activité de AChT réduisent les potentiels lents liés à l'événement, du cortex frontal chez le rat. D'après ces résultats, les potentiels lents corticaux chez le rat seraient dépendants de l'innervation cholinergic du noyau basal.</description><identifier>ISSN: 0013-4694</identifier><identifier>EISSN: 1872-6380</identifier><identifier>DOI: 10.1016/0013-4694(86)90128-8</identifier><identifier>PMID: 2420562</identifier><identifier>CODEN: ECNEAZ</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Acetylcholine - physiology ; Action Potentials - drug effects ; Animals ; Atropine - pharmacology ; Biological and medical sciences ; Central nervous system ; cortical slow potentials ; Electroencephalography ; Electrophysiology ; event-related slow potentials ; Frontal Lobe - drug effects ; Frontal Lobe - physiology ; Fundamental and applied biological sciences. Psychology ; gamma-Aminobutyric Acid - pharmacology ; Male ; nucleus basalis ; Rats ; Rats, Inbred Strains ; Space life sciences ; Vertebrates: nervous system and sense organs ; Vestibular Nuclei - physiology</subject><ispartof>Electroencephalography and clinical neurophysiology, 1986-05, Vol.63 (5), p.464-475</ispartof><rights>1986</rights><rights>1987 INIST-CNRS</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-de9f2930f4b52300d1f4e196011ff13d0688339a82d481208e3284d345acf933</citedby><cites>FETCH-LOGICAL-c386t-de9f2930f4b52300d1f4e196011ff13d0688339a82d481208e3284d345acf933</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=8036174$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2420562$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pirch, J.H</creatorcontrib><creatorcontrib>Corbus, M.J</creatorcontrib><creatorcontrib>Rigdon, G.C</creatorcontrib><creatorcontrib>Lyness, W.H</creatorcontrib><title>Generation of cortical event-related slow potentials in the rat involves nucleus basalis cholinergic innervation</title><title>Electroencephalography and clinical neurophysiology</title><addtitle>Electroencephalogr Clin Neurophysiol</addtitle><description>These experiments were conducted to gather information regarding the role of cholinergic innervation to the cortex in the generation of event-related slow potentials. The effects of unilateral drug treatments or lesions on ipsilateral and contralateral frontal cortex slow potential (SP) responses were examined in rats. The SP responses were recorded with silver-silver chloride electrodes and were generated by a 2 sec light cue which preceded medial forebrain bundle stimulation. The following approaches were used: (1) microinjection of GABA, procaine or saline into the nucleus basalis magnocellularis; (2) microinjection of atropine or saline subdurally in the SP recording area; (3) electrolytic lesion of the nucleus basalis area; and (4) kainic acid lesion of the nucleus basalis area. The following bilateral measurements were obtained in the lesion studies: choline acetyltransferase (ChAT) in cortex and hippocampus; serotonin in cortex, hippocampus, striatum and nucleus accumbens; norepinephrine in cortex and hippocampus; dopamine in striatum and nucleus accumbens; and metabolites of serotonin, norepinephrine and dopamine in these areas. The cortical SP responses were reduced on the side ipsilateral to the injections of GABA and procaine into the nucleus basalis, and on the side of the subdural atropine injection. With either type of lesion, the SP responses on the lesioned side were significantly reduced as compared to the non-lesioned side. Reductions in cortical ChAT and other measures were observed ipsilateral to the electrolytic lesion, but only cortical ChAT activity was reduced in the kainic acid-lesioned animals. Thus, pharmacological depression of nucleus basalis neurons, blockade of cholinergic muscarinic receptors in the cortex, and nucleus basalis lesions that reduce cortical choline acetyltransferase activity depress event-related slow potentials in the rat frontal cortex. These results provide evidence that cortical slow potential responses in the rat are dependent upon cholinergic innervation from the nucleus basalis. Ces travaux ont été effectués pour obtenir des données sur le rôle de l'innervation cholinergique afférente au cortex dans la production de potentiels lents liés à l'événement. On a recherché les effets d'injections unilatérales de drogues ou de lésions unilatérales sur les potentiels lents (PL) des cortex frontaux ipsi- et contralatéral. Les PL ont été enregistrés à l'aide d'électrodes d'argent-chlorure d'argent et ont été produits par un signal lumineux de 2 sec qui précédait une récompense par stimulation du faisceau médian du télencéphale. Les approches suivantes ont été utilisées: (1) microinjection de GABA, procaïne ou liquide physiologique dans le noyau basal magnocellulaire; (2) microinjection subdurale d'atropine ou de liquide physiologique dans la région d'enregistrement des PL; (3) lésion électrolytique de la région du noyau basal; et (4) lésion chimique à l'acide kaïnique de la région de noyau basal. On a effectué bilatéralement les mesures suivantes pour les études lésionnelles: acétylcholine transférase (AChT) dans le cortex et l'hippocampe; sérotonine dans le cortex, l'hippocampe, le noyau caudé et le noyau accumbens; norépinéphrine dans le cortex et l'hippocampe; dopamine dans le noyau caudé et le noyau accumbens; métabolites de la sérotonine, de la norépinéphrine et de la dopamine dans ces régions. On a noté une diminution des PL corticaux du côté ipsilatéral aux injections de GABA et de procaïne dans le noyau basal, et du côté de l'injection subdurale d'atropine. Quel que soit le type de lésion, les réponses PL ipsilatérales à la lésion ont été significativement réduites par rapport aux réponses contralatérales. Du côté ipsilatéral à la lésion électrolytique on a aussi observé des diminutions de l'AChT corticale et des autres valeurs; mais seule l'activité AChT corticale était réduite si la lésion était kaïnique. Ainsi, la dépression pharmacologique des neurones du noyau basal, le blocage des récepteurs cholinergiques muscariniques corticaux et les lésions du noyau basal qui réduisent l'activité de AChT réduisent les potentiels lents liés à l'événement, du cortex frontal chez le rat. D'après ces résultats, les potentiels lents corticaux chez le rat seraient dépendants de l'innervation cholinergic du noyau basal.</description><subject>Acetylcholine - physiology</subject><subject>Action Potentials - drug effects</subject><subject>Animals</subject><subject>Atropine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Central nervous system</subject><subject>cortical slow potentials</subject><subject>Electroencephalography</subject><subject>Electrophysiology</subject><subject>event-related slow potentials</subject><subject>Frontal Lobe - drug effects</subject><subject>Frontal Lobe - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>gamma-Aminobutyric Acid - pharmacology</subject><subject>Male</subject><subject>nucleus basalis</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Space life sciences</subject><subject>Vertebrates: nervous system and sense organs</subject><subject>Vestibular Nuclei - physiology</subject><issn>0013-4694</issn><issn>1872-6380</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1rVDEUhoModVr9BwpZiOji6snH5OZuClLsBxTcdB8yuSc2krkZk9xb-u_NdIZZusoh53nfhIeQDwy-MWDqOwATnVSD_KLV1wEY151-RVZM97xTQsNrsjohb8l5KX8AgDPen5EzLjmsFV-R3Q1OmG0NaaLJU5dyDc5GigtOtcsYbcWRlpie6C7VdhdsLDRMtD4ibbk2LikuWOg0u4hzoRtbbAyFuscUQ-v-HVyD2rC8vPKOvPGtAt8fzwvycP3z4eq2u_91c3f1475zQqvajTh4PgjwcrPmAmBkXiIbFDDmPRMjKK2FGKzmo9SMg0bBtRyFXFvnByEuyOdD7S6nvzOWarahOIzRTpjmYnrVqyZJN1AeQJdTKRm92eWwtfnZMDB7z2Yv0ewlGq3Mi2ezj3089s-bLY6n0FFs23867m1pPn22kwvlhGkQivWyYZcHDJuKJWA2xQWcHI4ho6tmTOH___gHAt2aVw</recordid><startdate>19860501</startdate><enddate>19860501</enddate><creator>Pirch, J.H</creator><creator>Corbus, M.J</creator><creator>Rigdon, G.C</creator><creator>Lyness, W.H</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>7X8</scope></search><sort><creationdate>19860501</creationdate><title>Generation of cortical event-related slow potentials in the rat involves nucleus basalis cholinergic innervation</title><author>Pirch, J.H ; Corbus, M.J ; Rigdon, G.C ; Lyness, W.H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-de9f2930f4b52300d1f4e196011ff13d0688339a82d481208e3284d345acf933</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>Acetylcholine - physiology</topic><topic>Action Potentials - drug effects</topic><topic>Animals</topic><topic>Atropine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Central nervous system</topic><topic>cortical slow potentials</topic><topic>Electroencephalography</topic><topic>Electrophysiology</topic><topic>event-related slow potentials</topic><topic>Frontal Lobe - drug effects</topic><topic>Frontal Lobe - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>gamma-Aminobutyric Acid - pharmacology</topic><topic>Male</topic><topic>nucleus basalis</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Space life sciences</topic><topic>Vertebrates: nervous system and sense organs</topic><topic>Vestibular Nuclei - physiology</topic><toplevel>online_resources</toplevel><creatorcontrib>Pirch, J.H</creatorcontrib><creatorcontrib>Corbus, M.J</creatorcontrib><creatorcontrib>Rigdon, G.C</creatorcontrib><creatorcontrib>Lyness, W.H</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>MEDLINE - Academic</collection><jtitle>Electroencephalography and clinical neurophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pirch, J.H</au><au>Corbus, M.J</au><au>Rigdon, G.C</au><au>Lyness, W.H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Generation of cortical event-related slow potentials in the rat involves nucleus basalis cholinergic innervation</atitle><jtitle>Electroencephalography and clinical neurophysiology</jtitle><addtitle>Electroencephalogr Clin Neurophysiol</addtitle><date>1986-05-01</date><risdate>1986</risdate><volume>63</volume><issue>5</issue><spage>464</spage><epage>475</epage><pages>464-475</pages><issn>0013-4694</issn><eissn>1872-6380</eissn><coden>ECNEAZ</coden><abstract>These experiments were conducted to gather information regarding the role of cholinergic innervation to the cortex in the generation of event-related slow potentials. The effects of unilateral drug treatments or lesions on ipsilateral and contralateral frontal cortex slow potential (SP) responses were examined in rats. The SP responses were recorded with silver-silver chloride electrodes and were generated by a 2 sec light cue which preceded medial forebrain bundle stimulation. The following approaches were used: (1) microinjection of GABA, procaine or saline into the nucleus basalis magnocellularis; (2) microinjection of atropine or saline subdurally in the SP recording area; (3) electrolytic lesion of the nucleus basalis area; and (4) kainic acid lesion of the nucleus basalis area. The following bilateral measurements were obtained in the lesion studies: choline acetyltransferase (ChAT) in cortex and hippocampus; serotonin in cortex, hippocampus, striatum and nucleus accumbens; norepinephrine in cortex and hippocampus; dopamine in striatum and nucleus accumbens; and metabolites of serotonin, norepinephrine and dopamine in these areas. The cortical SP responses were reduced on the side ipsilateral to the injections of GABA and procaine into the nucleus basalis, and on the side of the subdural atropine injection. With either type of lesion, the SP responses on the lesioned side were significantly reduced as compared to the non-lesioned side. Reductions in cortical ChAT and other measures were observed ipsilateral to the electrolytic lesion, but only cortical ChAT activity was reduced in the kainic acid-lesioned animals. Thus, pharmacological depression of nucleus basalis neurons, blockade of cholinergic muscarinic receptors in the cortex, and nucleus basalis lesions that reduce cortical choline acetyltransferase activity depress event-related slow potentials in the rat frontal cortex. These results provide evidence that cortical slow potential responses in the rat are dependent upon cholinergic innervation from the nucleus basalis. Ces travaux ont été effectués pour obtenir des données sur le rôle de l'innervation cholinergique afférente au cortex dans la production de potentiels lents liés à l'événement. On a recherché les effets d'injections unilatérales de drogues ou de lésions unilatérales sur les potentiels lents (PL) des cortex frontaux ipsi- et contralatéral. Les PL ont été enregistrés à l'aide d'électrodes d'argent-chlorure d'argent et ont été produits par un signal lumineux de 2 sec qui précédait une récompense par stimulation du faisceau médian du télencéphale. Les approches suivantes ont été utilisées: (1) microinjection de GABA, procaïne ou liquide physiologique dans le noyau basal magnocellulaire; (2) microinjection subdurale d'atropine ou de liquide physiologique dans la région d'enregistrement des PL; (3) lésion électrolytique de la région du noyau basal; et (4) lésion chimique à l'acide kaïnique de la région de noyau basal. On a effectué bilatéralement les mesures suivantes pour les études lésionnelles: acétylcholine transférase (AChT) dans le cortex et l'hippocampe; sérotonine dans le cortex, l'hippocampe, le noyau caudé et le noyau accumbens; norépinéphrine dans le cortex et l'hippocampe; dopamine dans le noyau caudé et le noyau accumbens; métabolites de la sérotonine, de la norépinéphrine et de la dopamine dans ces régions. On a noté une diminution des PL corticaux du côté ipsilatéral aux injections de GABA et de procaïne dans le noyau basal, et du côté de l'injection subdurale d'atropine. Quel que soit le type de lésion, les réponses PL ipsilatérales à la lésion ont été significativement réduites par rapport aux réponses contralatérales. Du côté ipsilatéral à la lésion électrolytique on a aussi observé des diminutions de l'AChT corticale et des autres valeurs; mais seule l'activité AChT corticale était réduite si la lésion était kaïnique. Ainsi, la dépression pharmacologique des neurones du noyau basal, le blocage des récepteurs cholinergiques muscariniques corticaux et les lésions du noyau basal qui réduisent l'activité de AChT réduisent les potentiels lents liés à l'événement, du cortex frontal chez le rat. D'après ces résultats, les potentiels lents corticaux chez le rat seraient dépendants de l'innervation cholinergic du noyau basal.</abstract><cop>Shannon</cop><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>2420562</pmid><doi>10.1016/0013-4694(86)90128-8</doi><tpages>12</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0013-4694
ispartof Electroencephalography and clinical neurophysiology, 1986-05, Vol.63 (5), p.464-475
issn 0013-4694
1872-6380
language eng
recordid cdi_proquest_miscellaneous_76766388
source MEDLINE; Alma/SFX Local Collection
subjects Acetylcholine - physiology
Action Potentials - drug effects
Animals
Atropine - pharmacology
Biological and medical sciences
Central nervous system
cortical slow potentials
Electroencephalography
Electrophysiology
event-related slow potentials
Frontal Lobe - drug effects
Frontal Lobe - physiology
Fundamental and applied biological sciences. Psychology
gamma-Aminobutyric Acid - pharmacology
Male
nucleus basalis
Rats
Rats, Inbred Strains
Space life sciences
Vertebrates: nervous system and sense organs
Vestibular Nuclei - physiology
title Generation of cortical event-related slow potentials in the rat involves nucleus basalis cholinergic innervation
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T13%3A44%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Generation%20of%20cortical%20event-related%20slow%20potentials%20in%20the%20rat%20involves%20nucleus%20basalis%20cholinergic%20innervation&rft.jtitle=Electroencephalography%20and%20clinical%20neurophysiology&rft.au=Pirch,%20J.H&rft.date=1986-05-01&rft.volume=63&rft.issue=5&rft.spage=464&rft.epage=475&rft.pages=464-475&rft.issn=0013-4694&rft.eissn=1872-6380&rft.coden=ECNEAZ&rft_id=info:doi/10.1016/0013-4694(86)90128-8&rft_dat=%3Cproquest_cross%3E76766388%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=76766388&rft_id=info:pmid/2420562&rft_els_id=0013469486901288&rfr_iscdi=true