<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-09-20T02:48:06Z</responseDate><request verb="GetRecord" identifier="oai:dspace.mit.edu:1721.1/42946" metadataPrefix="dim">https://dspace.mit.edu/server/oai/request</request><GetRecord><record><header><identifier>oai:dspace.mit.edu:1721.1/42946</identifier><datestamp>2022-01-13T07:54:17Z</datestamp><setSpec>com_1721.1_7582</setSpec><setSpec>com_1721.1_7581</setSpec><setSpec>col_1721.1_131022</setSpec></header><metadata><dim:dim xmlns:dim="http://www.dspace.org/xmlns/dspace/dim" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.dspace.org/xmlns/dspace/dim http://www.dspace.org/schema/dim.xsd">
   <dim:field mdschema="dc" element="contributor" qualifier="advisor" lang="en_US">Mark F. Bear.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="author" lang="en_US">Linden, Monica L. (Monica Loryn)</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="other" lang="en_US">Massachusetts Institute of Technology. Dept. of Brain and Cognitive Sciences.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="department">Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="accessioned">2008-11-07T14:12:50Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="available">2008-11-07T14:12:50Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="issued" lang="en_US">2008</dim:field>
   <dim:field mdschema="dc" element="identifier" qualifier="uri">http://hdl.handle.net/1721.1/42946</dim:field>
   <dim:field mdschema="dc" element="identifier" qualifier="oclc" lang="en_US">259207712</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2008.</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">This electronic version was submitted by the student author.  The certified thesis is available in the Institute Archives and Special Collections.</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">"June 2008."</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Includes bibliographical references.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="abstract" lang="en_US">Perturbations of sensory experience in young animals are known to cause lasting changes in adult brain function. For example, monocular visual deprivation by lid closure (MC) leads to a loss of cortical responsiveness of the deprived eye and a concomitant visual impairment. This ocular dominance (OD) plasticity is a well-studied model of experience-dependent cortical plasticity. While much is known about the anatomical, physiological and biochemical changes that occur in primary visual cortex following OD plasticity, the input patterns that lead to these changes have not been characterized. Visual input travels from the retina through the dorsal lateral geniculate nucleus (dLGN) of the thalamus and then into visual cortex. Several models of the thalamic activity patterns which drive OD plasticity have been proposed, but the assumptions about the pattern and amount of input activity from thalamus to cortex during deprivation have not been experimentally validated. Therefore, we performed extracellular recordings from the dLGN of animals during periods of visual manipulation. Contrary to previous hypotheses, the present findings demonstrate that MC does not alter the overall firing rate of neural activity in the dLGN. Instead, MC alters the pattern of neural spike trains such that there is a decrease in simultaneous firing of neighboring neurons. Moreover, the elimination of visual input from the retina, a form of deprivation which does not lead to deprived-eye depression, leads to a dramatic increase in thalamic bursting. Additionally, there are subtle qualitative differences between dLGN activity in juveniles and adults during MC, and this may contribute to differences in OD plasticity with age.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="statementofresponsibility" lang="en_US">by Monica L. Linden.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="degree" lang="en_US">Ph.D.</dim:field>
   <dim:field mdschema="dc" element="format" qualifier="extent" lang="en_US">155 p.</dim:field>
   <dim:field mdschema="dc" element="language" qualifier="iso" lang="en_US">eng</dim:field>
   <dim:field mdschema="dc" element="publisher" lang="en_US">Massachusetts Institute of Technology</dim:field>
   <dim:field mdschema="dc" element="rights" lang="en_US">M.I.T. theses are protected by 
copyright. They may be viewed from this source for any purpose, but 
reproduction or distribution in any format is prohibited without written 
permission. See provided URL for inquiries about permission.</dim:field>
   <dim:field mdschema="dc" element="rights" qualifier="uri" lang="en_US">http://dspace.mit.edu/handle/1721.1/7582</dim:field>
   <dim:field mdschema="dc" element="subject" lang="en_US">Brain and Cognitive Sciences.</dim:field>
   <dim:field mdschema="dc" element="title" lang="en_US">LGN activity patterns during ocular dominance plasticity in vivo</dim:field>
   <dim:field mdschema="dc" element="title" qualifier="alternative" lang="en_US">(cont.) These findings substantially alter the interpretation of previous studies and define the activity patterns that govern cortical plasticity in vivo. Furthermore, this work may have important implications for treatments of developmental disorders including ambylopia.</dim:field>
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   	&lt;Title>LGN activity patterns during ocular dominance plasticity in vivo&lt;/Title>
   	&lt;Subtitle>(cont.) These findings substantially alter the interpretation of previous studies and define the activity patterns that govern cortical plasticity in vivo. Furthermore, this work may have important implications for treatments of developmental disorders including ambylopia.&lt;/Subtitle>
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   	&lt;PublicationDate>2008&lt;/PublicationDate>
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        	&lt;DisplayName>Linden, Monica L. (Monica Loryn)&lt;/DisplayName>
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    &lt;Keyword>Brain and Cognitive Sciences.&lt;/Keyword>
   	&lt;Abstract>Perturbations of sensory experience in young animals are known to cause lasting changes in adult brain function. For example, monocular visual deprivation by lid closure (MC) leads to a loss of cortical responsiveness of the deprived eye and a concomitant visual impairment. This ocular dominance (OD) plasticity is a well-studied model of experience-dependent cortical plasticity. While much is known about the anatomical, physiological and biochemical changes that occur in primary visual cortex following OD plasticity, the input patterns that lead to these changes have not been characterized. Visual input travels from the retina through the dorsal lateral geniculate nucleus (dLGN) of the thalamus and then into visual cortex. Several models of the thalamic activity patterns which drive OD plasticity have been proposed, but the assumptions about the pattern and amount of input activity from thalamus to cortex during deprivation have not been experimentally validated. Therefore, we performed extracellular recordings from the dLGN of animals during periods of visual manipulation. Contrary to previous hypotheses, the present findings demonstrate that MC does not alter the overall firing rate of neural activity in the dLGN. Instead, MC alters the pattern of neural spike trains such that there is a decrease in simultaneous firing of neighboring neurons. Moreover, the elimination of visual input from the retina, a form of deprivation which does not lead to deprived-eye depression, leads to a dramatic increase in thalamic bursting. Additionally, there are subtle qualitative differences between dLGN activity in juveniles and adults during MC, and this may contribute to differences in OD plasticity with age.&lt;/Abstract>
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