{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/82545"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/82545","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Dependence of Visuomotor Behavior on Individual Layers of the Cat Lateral Geniculate Nucleus in the Normal Brain and Following Recovery From Destruction of Individual Layers","abstract":"\"The general goal of this thesis is to better understand the ways individual layers of the cat lateral geniculate nucleus (LGN) contribute to visuomotor behavior. This thesis has two main outcomes. First, the normal contribution of dorsal and ventral layers of the LGN to visuomotor behavior parallels their contributions to cortical activity, as revealed in previous experiments with anesthetized animals. Namely, the A layers have a much stronger role than the C layers for both visually guided saccades and for the activity of the cells in cortex which project to the superior colliculus, the structure generating saccades. During layer-A reversible inactivations, saccade success rate fell from 82.4% to 26.8%. Inactivations lowered amplitude and peak velocity, and increased saccade latency. In contrast, inactivating C layers had no affect on performance. All saccades from layer A and C-layers inactivations fell along the same velocity/amplitude function, suggesting that saccade motor circuits were not affected. The second major outcome is that when cortex is deprived of input from the A layers, other parallel afferent pathways can quickly (often within 24 hours) compensate for the behavioral deficit. The C-layers clearly have this capability, although our data raise the possibility that compensation can take place if the C layers are damaged as well, perhaps via the medial interlaminar nucleus. Reversibly inactivating C layers under a layer-A lesion led to a significant decrease in saccade success rate (73.2% normal; 29.2% blocked) and peak velocity (130°/s normal; 91°/s blocked), but did not abolish saccades. The velocity/amplitude data prior to and during the reversible inactivation fell along the same \"\"main sequence\"\" suggesting that the motor circuits were not disrupted. These results suggest that in the intact animal, as well as in animals with damaged LGN, the balance of control of cortical cells by parallel geniculate inputs may be dynamically determined, perhaps by competition between the parallel inputs. An implication of this work is that behavioral results regarding the functional specialization of parvocellular and magnocellular pathways following LGN lesions in the monkey may underestimate the true functional independence of these pathways. Supported by NIH grant EY02695.\"","abstract_html":""The general goal of this thesis is to better understand the ways individual layers of the cat lateral geniculate nucleus (LGN) contribute to visuomotor behavior. This thesis has two main outcomes. First, the normal contribution of dorsal and ventral layers of the LGN to visuomotor behavior parallels their contributions to cortical activity, as revealed in previous experiments with anesthetized animals. Namely, the A layers have a much stronger role than the C layers for both visually guided saccades and for the activity of the cells in cortex which project to the superior colliculus, the structure generating saccades. During layer-A reversible inactivations, saccade success rate fell from 82.4% to 26.8%. Inactivations lowered amplitude and peak velocity, and increased saccade latency. In contrast, inactivating C layers had no affect on performance. All saccades from layer A and C-layers inactivations fell along the same velocity/amplitude function, suggesting that saccade motor circuits were not affected. The second major outcome is that when cortex is deprived of input from the A layers, other parallel afferent pathways can quickly (often within 24 hours) compensate for the behavioral deficit. The C-layers clearly have this capability, although our data raise the possibility that compensation can take place if the C layers are damaged as well, perhaps via the medial interlaminar nucleus. Reversibly inactivating C layers under a layer-A lesion led to a significant decrease in saccade success rate (73.2% normal; 29.2% blocked) and peak velocity (130°/s normal; 91°/s blocked), but did not abolish saccades. The velocity/amplitude data prior to and during the reversible inactivation fell along the same ""main sequence"" suggesting that the motor circuits were not disrupted. These results suggest that in the intact animal, as well as in animals with damaged LGN, the balance of control of cortical cells by parallel geniculate inputs may be dynamically determined, perhaps by competition between the parallel inputs. An implication of this work is that behavioral results regarding the functional specialization of parvocellular and magnocellular pathways following LGN lesions in the monkey may underestimate the true functional independence of these pathways. Supported by NIH grant EY02695."","abstract_has_math":false,"creators":["Tate, Andrew Kenichi"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Neuroscience","degree_department":null,"school":null,"contributors":["Malpeli, Joseph G.","William Greenough"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-25T20:45:47Z","date_published":"2015-09-25T20:45:47Z","updated_at":"2026-07-22T22:26:18Z","subjects":["Biology, Neuroscience"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI9971201"],"render_values":[{"text":"(MiAaPQ)AAI9971201","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/82545","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Malpeli, Joseph G.","William Greenough"]},{"key":"dc:creator","label":"Author","values":["Tate, Andrew Kenichi"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-25T20:45:47Z","10000-01-01","2000"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Neuroscience"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Neuroscience"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/82545","(MiAaPQ)AAI9971201"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["\"The general goal of this thesis is to better understand the ways individual layers of the cat lateral geniculate nucleus (LGN) contribute to visuomotor behavior. This thesis has two main outcomes. First, the normal contribution of dorsal and ventral layers of the LGN to visuomotor behavior parallels their contributions to cortical activity, as revealed in previous experiments with anesthetized animals. Namely, the A layers have a much stronger role than the C layers for both visually guided saccades and for the activity of the cells in cortex which project to the superior colliculus, the structure generating saccades. During layer-A reversible inactivations, saccade success rate fell from 82.4% to 26.8%. Inactivations lowered amplitude and peak velocity, and increased saccade latency. In contrast, inactivating C layers had no affect on performance. All saccades from layer A and C-layers inactivations fell along the same velocity/amplitude function, suggesting that saccade motor circuits were not affected. The second major outcome is that when cortex is deprived of input from the A layers, other parallel afferent pathways can quickly (often within 24 hours) compensate for the behavioral deficit. The C-layers clearly have this capability, although our data raise the possibility that compensation can take place if the C layers are damaged as well, perhaps via the medial interlaminar nucleus. Reversibly inactivating C layers under a layer-A lesion led to a significant decrease in saccade success rate (73.2% normal; 29.2% blocked) and peak velocity (130°/s normal; 91°/s blocked), but did not abolish saccades. The velocity/amplitude data prior to and during the reversible inactivation fell along the same \"\"main sequence\"\" suggesting that the motor circuits were not disrupted. These results suggest that in the intact animal, as well as in animals with damaged LGN, the balance of control of cortical cells by parallel geniculate inputs may be dynamically determined, perhaps by competition between the parallel inputs. An implication of this work is that behavioral results regarding the functional specialization of parvocellular and magnocellular pathways following LGN lesions in the monkey may underestimate the true functional independence of these pathways. Supported by NIH grant EY02695.\"","Made available in DSpace on 2015-09-25T20:45:47Z (GMT). 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This thesis has two main outcomes. First, the normal contribution of dorsal and ventral layers of the LGN to visuomotor behavior parallels their contributions to cortical activity, as revealed in previous experiments with anesthetized animals. Namely, the A layers have a much stronger role than the C layers for both visually guided saccades and for the activity of the cells in cortex which project to the superior colliculus, the structure generating saccades. During layer-A reversible inactivations, saccade success rate fell from 82.4% to 26.8%. Inactivations lowered amplitude and peak velocity, and increased saccade latency. In contrast, inactivating C layers had no affect on performance. All saccades from layer A and C-layers inactivations fell along the same velocity/amplitude function, suggesting that saccade motor circuits were not affected. The second major outcome is that when cortex is deprived of input from the A layers, other parallel afferent pathways can quickly (often within 24 hours) compensate for the behavioral deficit. The C-layers clearly have this capability, although our data raise the possibility that compensation can take place if the C layers are damaged as well, perhaps via the medial interlaminar nucleus. Reversibly inactivating C layers under a layer-A lesion led to a significant decrease in saccade success rate (73.2% normal; 29.2% blocked) and peak velocity (130°/s normal; 91°/s blocked), but did not abolish saccades. The velocity/amplitude data prior to and during the reversible inactivation fell along the same \"\"main sequence\"\" suggesting that the motor circuits were not disrupted. These results suggest that in the intact animal, as well as in animals with damaged LGN, the balance of control of cortical cells by parallel geniculate inputs may be dynamically determined, perhaps by competition between the parallel inputs. An implication of this work is that behavioral results regarding the functional specialization of parvocellular and magnocellular pathways following LGN lesions in the monkey may underestimate the true functional independence of these pathways. Supported by NIH grant EY02695.\"","Made available in DSpace on 2015-09-25T20:45:47Z (GMT). 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