Smooth-Pursuit Eye-Movement Deficits With Chemical Lesions in Macaque Nucleus Reticularis Tegmenti Pontis
1 Department of Ophthalmology, Indiana University School of Medicine, Indianapolis, Indiana 46202; and 2 Department of Ophthalmology, Kitasato University, Kitasato 228, Japan Suzuki, David A., Tetsuto Yamada, Rebecca Hoedema, and Robert D. Yee. Smooth-Pursuit Eye-Movement Deficits With Chemical...
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creator | Suzuki, David A Yamada, Tetsuto Hoedema, Rebecca Yee, Robert D |
description | 1 Department of Ophthalmology, Indiana
University School of Medicine, Indianapolis, Indiana 46202; and
2 Department of Ophthalmology, Kitasato
University, Kitasato 228, Japan
Suzuki, David A.,
Tetsuto Yamada,
Rebecca Hoedema, and
Robert D. Yee.
Smooth-Pursuit Eye-Movement Deficits With Chemical Lesions in
Macaque Nucleus Reticularis Tegmenti Pontis. J. Neurophysiol. 82: 1178-1186, 1999. Anatomic and
neuronal recordings suggest that the nucleus reticularis tegmenti
pontis (NRTP) of macaques may be a major pontine component of a
cortico-ponto-cerebellar pathway that subserves the control of
smooth-pursuit eye movements. The existence of such a pathway was
implicated by the lack of permanent pursuit impairment after bilateral
lesions in the dorsolateral pontine nucleus. To provide more direct
evidence that NRTP is involved with regulating smooth-pursuit eye
movements, chemical lesions were made in macaque NRTP by injecting
either lidocaine or ibotenic acid. Injection sites first were
identified by the recording of smooth-pursuit-related modulations in
neuronal activity. The resulting lesions caused significant deficits in
both the maintenance and the initiation of smooth-pursuit eye
movements. After lesion formation, the gain of constant-velocity,
maintained smooth-pursuit eye movements decreased, on the average, by
44%. Recovery of the ability to maintain smooth-pursuit eye movements
occurred over ~3 days when maintained pursuit gains attained normal
values. The step-ramp, "Rashbass" task was used to investigate the
effects of the lesions on the initiation of smooth-pursuit eye
movements. Eye accelerations averaged over the initial 80 ms of pursuit
initiation were determined and found to be decremented, on the average,
by 48% after the administration of ibotenic acid. Impairments in the
initiation and maintenance of smooth-pursuit eye movements were
directional in nature. Upward pursuit seemed to be the most vulnerable
and was impaired in all cases independent of lesioning agent and type of pursuit investigated. Downward smooth pursuit seemed more resistant to the effects of chemical lesions in NRTP. Impairments in horizontal tracking were observed with examples of deficits in ipsilaterally and
contralaterally directed pursuit. The results provide behavioral support for the physiologically and anatomic-based conclusion that NRTP
is a component of a cortico-ponto-cerebellar circuit that presumably
involves the pursuit area of the frontal eye field (FEF) a |
doi_str_mv | 10.1152/jn.1999.82.3.1178 |
format | Article |
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University School of Medicine, Indianapolis, Indiana 46202; and
2 Department of Ophthalmology, Kitasato
University, Kitasato 228, Japan
Suzuki, David A.,
Tetsuto Yamada,
Rebecca Hoedema, and
Robert D. Yee.
Smooth-Pursuit Eye-Movement Deficits With Chemical Lesions in
Macaque Nucleus Reticularis Tegmenti Pontis. J. Neurophysiol. 82: 1178-1186, 1999. Anatomic and
neuronal recordings suggest that the nucleus reticularis tegmenti
pontis (NRTP) of macaques may be a major pontine component of a
cortico-ponto-cerebellar pathway that subserves the control of
smooth-pursuit eye movements. The existence of such a pathway was
implicated by the lack of permanent pursuit impairment after bilateral
lesions in the dorsolateral pontine nucleus. To provide more direct
evidence that NRTP is involved with regulating smooth-pursuit eye
movements, chemical lesions were made in macaque NRTP by injecting
either lidocaine or ibotenic acid. Injection sites first were
identified by the recording of smooth-pursuit-related modulations in
neuronal activity. The resulting lesions caused significant deficits in
both the maintenance and the initiation of smooth-pursuit eye
movements. After lesion formation, the gain of constant-velocity,
maintained smooth-pursuit eye movements decreased, on the average, by
44%. Recovery of the ability to maintain smooth-pursuit eye movements
occurred over ~3 days when maintained pursuit gains attained normal
values. The step-ramp, "Rashbass" task was used to investigate the
effects of the lesions on the initiation of smooth-pursuit eye
movements. Eye accelerations averaged over the initial 80 ms of pursuit
initiation were determined and found to be decremented, on the average,
by 48% after the administration of ibotenic acid. Impairments in the
initiation and maintenance of smooth-pursuit eye movements were
directional in nature. Upward pursuit seemed to be the most vulnerable
and was impaired in all cases independent of lesioning agent and type of pursuit investigated. Downward smooth pursuit seemed more resistant to the effects of chemical lesions in NRTP. Impairments in horizontal tracking were observed with examples of deficits in ipsilaterally and
contralaterally directed pursuit. The results provide behavioral support for the physiologically and anatomic-based conclusion that NRTP
is a component of a cortico-ponto-cerebellar circuit that presumably
involves the pursuit area of the frontal eye field (FEF) and projects
to ocular motor-related areas of the cerebellum. This
FEF-NRTP-cerebellum path would parallel a middle and medial superior
temporal cerebral cortical area-dorsolateral pontine nucleus-cerebellum
pathway also known to be involved with regulating smooth-pursuit eye movements.</description><identifier>ISSN: 0022-3077</identifier><identifier>EISSN: 1522-1598</identifier><identifier>DOI: 10.1152/jn.1999.82.3.1178</identifier><identifier>PMID: 10482737</identifier><language>eng</language><publisher>United States: Am Phys Soc</publisher><subject>Animals ; Brain Mapping ; Excitatory Amino Acid Agonists - pharmacology ; Eye Movements - physiology ; Ibotenic Acid - pharmacology ; Macaca ; Macaca fascicularis ; Macaca nemestrina ; Pons - drug effects ; Pons - pathology ; Pons - physiology ; Pursuit, Smooth - physiology ; reticular nuclei ; smooth pursuit eye movements</subject><ispartof>Journal of neurophysiology, 1999-09, Vol.82 (3), p.1178-1186</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c404t-d255a2c6ecc661051944bde477bf36004172a438f6098240a150aa01ae4a9ad23</citedby><cites>FETCH-LOGICAL-c404t-d255a2c6ecc661051944bde477bf36004172a438f6098240a150aa01ae4a9ad23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10482737$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Suzuki, David A</creatorcontrib><creatorcontrib>Yamada, Tetsuto</creatorcontrib><creatorcontrib>Hoedema, Rebecca</creatorcontrib><creatorcontrib>Yee, Robert D</creatorcontrib><title>Smooth-Pursuit Eye-Movement Deficits With Chemical Lesions in Macaque Nucleus Reticularis Tegmenti Pontis</title><title>Journal of neurophysiology</title><addtitle>J Neurophysiol</addtitle><description> 1 Department of Ophthalmology, Indiana
University School of Medicine, Indianapolis, Indiana 46202; and
2 Department of Ophthalmology, Kitasato
University, Kitasato 228, Japan
Suzuki, David A.,
Tetsuto Yamada,
Rebecca Hoedema, and
Robert D. Yee.
Smooth-Pursuit Eye-Movement Deficits With Chemical Lesions in
Macaque Nucleus Reticularis Tegmenti Pontis. J. Neurophysiol. 82: 1178-1186, 1999. Anatomic and
neuronal recordings suggest that the nucleus reticularis tegmenti
pontis (NRTP) of macaques may be a major pontine component of a
cortico-ponto-cerebellar pathway that subserves the control of
smooth-pursuit eye movements. The existence of such a pathway was
implicated by the lack of permanent pursuit impairment after bilateral
lesions in the dorsolateral pontine nucleus. To provide more direct
evidence that NRTP is involved with regulating smooth-pursuit eye
movements, chemical lesions were made in macaque NRTP by injecting
either lidocaine or ibotenic acid. Injection sites first were
identified by the recording of smooth-pursuit-related modulations in
neuronal activity. The resulting lesions caused significant deficits in
both the maintenance and the initiation of smooth-pursuit eye
movements. After lesion formation, the gain of constant-velocity,
maintained smooth-pursuit eye movements decreased, on the average, by
44%. Recovery of the ability to maintain smooth-pursuit eye movements
occurred over ~3 days when maintained pursuit gains attained normal
values. The step-ramp, "Rashbass" task was used to investigate the
effects of the lesions on the initiation of smooth-pursuit eye
movements. Eye accelerations averaged over the initial 80 ms of pursuit
initiation were determined and found to be decremented, on the average,
by 48% after the administration of ibotenic acid. Impairments in the
initiation and maintenance of smooth-pursuit eye movements were
directional in nature. Upward pursuit seemed to be the most vulnerable
and was impaired in all cases independent of lesioning agent and type of pursuit investigated. Downward smooth pursuit seemed more resistant to the effects of chemical lesions in NRTP. Impairments in horizontal tracking were observed with examples of deficits in ipsilaterally and
contralaterally directed pursuit. The results provide behavioral support for the physiologically and anatomic-based conclusion that NRTP
is a component of a cortico-ponto-cerebellar circuit that presumably
involves the pursuit area of the frontal eye field (FEF) and projects
to ocular motor-related areas of the cerebellum. This
FEF-NRTP-cerebellum path would parallel a middle and medial superior
temporal cerebral cortical area-dorsolateral pontine nucleus-cerebellum
pathway also known to be involved with regulating smooth-pursuit eye movements.</description><subject>Animals</subject><subject>Brain Mapping</subject><subject>Excitatory Amino Acid Agonists - pharmacology</subject><subject>Eye Movements - physiology</subject><subject>Ibotenic Acid - pharmacology</subject><subject>Macaca</subject><subject>Macaca fascicularis</subject><subject>Macaca nemestrina</subject><subject>Pons - drug effects</subject><subject>Pons - pathology</subject><subject>Pons - physiology</subject><subject>Pursuit, Smooth - physiology</subject><subject>reticular nuclei</subject><subject>smooth pursuit eye movements</subject><issn>0022-3077</issn><issn>1522-1598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAURi1ERYfCA7BBXsEq0-ufxMkSDS0gTUsFg1haHudm4pGTTGMHmLevo6lQN4iNbV2d78i6HyFvGCwZy_nlvl-yqqqWJV-KNFHlM7JIc56xvCqfkwVAegtQ6py8DGEPACoH_oKcM5AlV0ItiPveDUNss7tpDJOL9OqI2c3wCzvsI_2IjbMuBvrTxZauWuycNZ6uMbihD9T19MZYcz8hvZ2sxynQbxidnbwZXaAb3M0WR--GdIZX5KwxPuDrx_uC_Li-2qw-Z-uvn76sPqwzK0HGrOZ5brgt0NqiYJCzSsptjVKpbSMKAMkUN1KUTQFVySUYloMxwAxKU5maiwvy7uQ9jEP6Woi6c8Gi96bHYQpaAYhC5Oy_IFOiLJRUCWQn0I5DCCM2-jC6zoxHzUDPReh9r-cidMm10HMRKfP2UT5tO6yfJE6bT8D7E9C6XfvbjagP7THt1Q-74-x7qhL_Jq8n7zf4J6bI34Q-1I14AFespKQ</recordid><startdate>19990901</startdate><enddate>19990901</enddate><creator>Suzuki, David A</creator><creator>Yamada, Tetsuto</creator><creator>Hoedema, Rebecca</creator><creator>Yee, Robert D</creator><general>Am Phys Soc</general><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><scope>7X8</scope></search><sort><creationdate>19990901</creationdate><title>Smooth-Pursuit Eye-Movement Deficits With Chemical Lesions in Macaque Nucleus Reticularis Tegmenti Pontis</title><author>Suzuki, David A ; Yamada, Tetsuto ; Hoedema, Rebecca ; Yee, Robert D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c404t-d255a2c6ecc661051944bde477bf36004172a438f6098240a150aa01ae4a9ad23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Brain Mapping</topic><topic>Excitatory Amino Acid Agonists - pharmacology</topic><topic>Eye Movements - physiology</topic><topic>Ibotenic Acid - pharmacology</topic><topic>Macaca</topic><topic>Macaca fascicularis</topic><topic>Macaca nemestrina</topic><topic>Pons - drug effects</topic><topic>Pons - pathology</topic><topic>Pons - physiology</topic><topic>Pursuit, Smooth - physiology</topic><topic>reticular nuclei</topic><topic>smooth pursuit eye movements</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Suzuki, David A</creatorcontrib><creatorcontrib>Yamada, Tetsuto</creatorcontrib><creatorcontrib>Hoedema, Rebecca</creatorcontrib><creatorcontrib>Yee, Robert D</creatorcontrib><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><collection>MEDLINE - Academic</collection><jtitle>Journal of neurophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Suzuki, David A</au><au>Yamada, Tetsuto</au><au>Hoedema, Rebecca</au><au>Yee, Robert D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Smooth-Pursuit Eye-Movement Deficits With Chemical Lesions in Macaque Nucleus Reticularis Tegmenti Pontis</atitle><jtitle>Journal of neurophysiology</jtitle><addtitle>J Neurophysiol</addtitle><date>1999-09-01</date><risdate>1999</risdate><volume>82</volume><issue>3</issue><spage>1178</spage><epage>1186</epage><pages>1178-1186</pages><issn>0022-3077</issn><eissn>1522-1598</eissn><abstract> 1 Department of Ophthalmology, Indiana
University School of Medicine, Indianapolis, Indiana 46202; and
2 Department of Ophthalmology, Kitasato
University, Kitasato 228, Japan
Suzuki, David A.,
Tetsuto Yamada,
Rebecca Hoedema, and
Robert D. Yee.
Smooth-Pursuit Eye-Movement Deficits With Chemical Lesions in
Macaque Nucleus Reticularis Tegmenti Pontis. J. Neurophysiol. 82: 1178-1186, 1999. Anatomic and
neuronal recordings suggest that the nucleus reticularis tegmenti
pontis (NRTP) of macaques may be a major pontine component of a
cortico-ponto-cerebellar pathway that subserves the control of
smooth-pursuit eye movements. The existence of such a pathway was
implicated by the lack of permanent pursuit impairment after bilateral
lesions in the dorsolateral pontine nucleus. To provide more direct
evidence that NRTP is involved with regulating smooth-pursuit eye
movements, chemical lesions were made in macaque NRTP by injecting
either lidocaine or ibotenic acid. Injection sites first were
identified by the recording of smooth-pursuit-related modulations in
neuronal activity. The resulting lesions caused significant deficits in
both the maintenance and the initiation of smooth-pursuit eye
movements. After lesion formation, the gain of constant-velocity,
maintained smooth-pursuit eye movements decreased, on the average, by
44%. Recovery of the ability to maintain smooth-pursuit eye movements
occurred over ~3 days when maintained pursuit gains attained normal
values. The step-ramp, "Rashbass" task was used to investigate the
effects of the lesions on the initiation of smooth-pursuit eye
movements. Eye accelerations averaged over the initial 80 ms of pursuit
initiation were determined and found to be decremented, on the average,
by 48% after the administration of ibotenic acid. Impairments in the
initiation and maintenance of smooth-pursuit eye movements were
directional in nature. Upward pursuit seemed to be the most vulnerable
and was impaired in all cases independent of lesioning agent and type of pursuit investigated. Downward smooth pursuit seemed more resistant to the effects of chemical lesions in NRTP. Impairments in horizontal tracking were observed with examples of deficits in ipsilaterally and
contralaterally directed pursuit. The results provide behavioral support for the physiologically and anatomic-based conclusion that NRTP
is a component of a cortico-ponto-cerebellar circuit that presumably
involves the pursuit area of the frontal eye field (FEF) and projects
to ocular motor-related areas of the cerebellum. This
FEF-NRTP-cerebellum path would parallel a middle and medial superior
temporal cerebral cortical area-dorsolateral pontine nucleus-cerebellum
pathway also known to be involved with regulating smooth-pursuit eye movements.</abstract><cop>United States</cop><pub>Am Phys Soc</pub><pmid>10482737</pmid><doi>10.1152/jn.1999.82.3.1178</doi><tpages>9</tpages></addata></record> |
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source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; American Physiological Society Paid |
subjects | Animals Brain Mapping Excitatory Amino Acid Agonists - pharmacology Eye Movements - physiology Ibotenic Acid - pharmacology Macaca Macaca fascicularis Macaca nemestrina Pons - drug effects Pons - pathology Pons - physiology Pursuit, Smooth - physiology reticular nuclei smooth pursuit eye movements |
title | Smooth-Pursuit Eye-Movement Deficits With Chemical Lesions in Macaque Nucleus Reticularis Tegmenti Pontis |
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