<?xml version="1.0" encoding="UTF-8"?>

<rdf:RDF
   xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
   xmlns:rdfs="http://www.w3.org/2000/01/rdf-schema#"
   xmlns="http://purl.org/rss/1.0/"
   xmlns:dc="http://purl.org/dc/elements/1.1/"
   xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
   xmlns:dcterms="http://purl.org/dc/terms/"

>
<channel rdf:about="http://www.citeulike.org/about">
<pubDate>Sat, 26 Jul 2008 07:43:43 BST</pubDate>


	<title>CiteULike: nelmor's Brown</title>
	<description>CiteULike: nelmor's Brown</description>


	<link>http://www.citeulike.org/user/nelmor/author/Brown</link>
	<dc:publisher>CiteULike.org</dc:publisher>
	<dc:language>en-gb</dc:language>
	<dc:rights>Copyright &#169; 2004-2008 citeulike.org</dc:rights>
	<items>
    <rdf:Seq>
        <rdf:li rdf:resource="http://www.citeulike.org/user/nelmor/article/2797291"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/nelmor/article/2744750"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/nelmor/article/2365533"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/nelmor/article/1430211"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/nelmor/article/1070682"/>

	</rdf:Seq>
	</items>
	</channel>


<item rdf:about="http://www.citeulike.org/user/nelmor/article/2797291">
    <title>Analysis of Between-Trial and Within-Trial Neural Spiking Dynamics</title>
    <link>http://www.citeulike.org/user/nelmor/article/2797291</link>
    <description>&lt;i&gt;J Neurophysiol, Vol. 99, No. 5. (1 May 2008), pp. 2672-2693.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Recording single-neuron activity from a specific brain region across multiple trials in response to the same stimulus or execution of the same behavioral task is a common neurophysiology protocol. The raster plots of the spike trains often show strong between-trial and within-trial dynamics, yet the standard analysis of these data with the peristimulus time histogram (PSTH) and ANOVA do not consider between-trial dynamics. By itself, the PSTH does not provide a framework for statistical inference. We present a state-space generalized linear model (SS-GLM) to formulate a point process representation of between-trial and within-trial neural spiking dynamics. Our model has the PSTH as a special case. We provide a framework for model estimation, model selection, goodness-of-fit analysis, and inference. In an analysis of hippocampal neural activity recorded from a monkey performing a location-scene association task, we demonstrate how the SS-GLM may be used to answer frequently posed neurophysiological questions including, What is the nature of the between-trial and within-trial task-specific modulation of the neural spiking activity? How can we characterize learning-related neural dynamics? What are the timescales and characteristics of the neuron's biophysical properties? Our results demonstrate that the SS-GLM is a more informative tool than the PSTH and ANOVA for analysis of multiple trial neural responses and that it provides a quantitative characterization of the between-trial and withintrial neural dynamics readily visible in raster plots, as well as the less apparent fast (1-10 ms), intermediate (11-20 ms), and longer (&#62;20 ms) timescale features of the neuron's biophysical properties. 10.1152/jn.00343.2007</description>
    <dc:title>Analysis of Between-Trial and Within-Trial Neural Spiking Dynamics</dc:title>

    <dc:creator>Gabriela Czanner</dc:creator>
    <dc:creator>Uri Eden</dc:creator>
    <dc:creator>Sylvia Wirth</dc:creator>
    <dc:creator>Marianna Yanike</dc:creator>
    <dc:creator>Wendy Suzuki</dc:creator>
    <dc:creator>Emery Brown</dc:creator>
    <dc:identifier>doi:10.1152/jn.00343.2007</dc:identifier>
    <dc:source>J Neurophysiol, Vol. 99, No. 5. (1 May 2008), pp. 2672-2693.</dc:source>
    <dc:date>2008-05-14T09:52:24-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>J Neurophysiol</prism:publicationName>
    <prism:volume>99</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>2672</prism:startingPage>
    <prism:endingPage>2693</prism:endingPage>
    <prism:category>analysis</prism:category>
    <prism:category>in-vivo</prism:category>
    <prism:category>learning</prism:category>
    <prism:category>methods</prism:category>
    <prism:category>time</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/nelmor/article/2744750">
    <title>Disrupted Dopamine Transmission and the Emergence of Exaggerated Beta Oscillations in Subthalamic Nucleus and Cerebral Cortex</title>
    <link>http://www.citeulike.org/user/nelmor/article/2744750</link>
    <description>&lt;i&gt;J. Neurosci., Vol. 28, No. 18. (30 April 2008), pp. 4795-4806.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;In the subthalamic nucleus (STN) of Parkinson's disease (PD) patients, a pronounced synchronization of oscillatory activity at beta frequencies (15-30 Hz) accompanies movement difficulties. Abnormal beta oscillations and motor symptoms are concomitantly and acutely suppressed by dopaminergic therapies, suggesting that these inappropriate rhythms might also emerge acutely from disrupted dopamine transmission. The neural basis of these abnormal beta oscillations is unclear, and how they might compromise information processing, or how they arise, is unknown. Using a 6-hydroxydopamine-lesioned rodent model of PD, we demonstrate that beta oscillations are inappropriately exaggerated, compared with controls, in a brain-state-dependent manner after chronic dopamine loss. Exaggerated beta oscillations are expressed at the levels of single neurons and small neuronal ensembles, and are focally present and spatially distributed within STN. They are also expressed in synchronous population activities, as evinced by oscillatory local field potentials, in STN and cortex. Excessively synchronized beta oscillations reduce the information coding capacity of STN neuronal ensembles, which may contribute to parkinsonian motor impairment. Acute disruption of dopamine transmission in control animals with antagonists of D1/D2 receptors did not exaggerate STN or cortical beta oscillations. Moreover, beta oscillations were not exaggerated until several days after 6-hydroxydopamine injections. Thus, contrary to predictions, abnormally amplified beta oscillations in cortico-STN circuits do not result simply from an acute absence of dopamine receptor stimulation, but are instead delayed sequelae of chronic dopamine depletion. Targeting the plastic processes underlying the delayed emergence of pathological beta oscillations after continuing dopaminergic dysfunction may offer considerable therapeutic promise. 10.1523/JNEUROSCI.0123-08.2008</description>
    <dc:title>Disrupted Dopamine Transmission and the Emergence of Exaggerated Beta Oscillations in Subthalamic Nucleus and Cerebral Cortex</dc:title>

    <dc:creator>Nicolas Mallet</dc:creator>
    <dc:creator>Alek Pogosyan</dc:creator>
    <dc:creator>Andrew Sharott</dc:creator>
    <dc:creator>Jozsef Csicsvari</dc:creator>
    <dc:creator>Paul Bolam</dc:creator>
    <dc:creator>Peter Brown</dc:creator>
    <dc:creator>Peter Magill</dc:creator>
    <dc:identifier>doi:10.1523/JNEUROSCI.0123-08.2008</dc:identifier>
    <dc:source>J. Neurosci., Vol. 28, No. 18. (30 April 2008), pp. 4795-4806.</dc:source>
    <dc:date>2008-05-02T08:52:58-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>J. Neurosci.</prism:publicationName>
    <prism:volume>28</prism:volume>
    <prism:number>18</prism:number>
    <prism:startingPage>4795</prism:startingPage>
    <prism:endingPage>4806</prism:endingPage>
    <prism:category>dopamine</prism:category>
    <prism:category>oscillations</prism:category>
    <prism:category>parkinson</prism:category>
    <prism:category>plasticity</prism:category>
    <prism:category>stn</prism:category>
    <prism:category>synchronization</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/nelmor/article/2365533">
    <title>Methods for whole-cell recording from visually preselected neurons of perirhinal cortex in brain slices from young and aging rats</title>
    <link>http://www.citeulike.org/user/nelmor/article/2365533</link>
    <description>&lt;i&gt;Journal of Neuroscience Methods, Vol. 86, No. 1. (31 December 1998), pp. 35-54.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This manuscript describes methods for preparing, visualizing, and recording from healthy perirhinal cortex neurons in brain slices from young and aging rats. We focused on perirhinal cortex because of its role in learning, memory, and aging-related cognitive decline. Detailed accounts of our dissection procedures are reported. Procedures that reliably yielded healthy neurons from juvenile rats were not conducive to obtaining healthy, readily-patchable neurons from aging rats, suggesting a procedure-by-age interaction. Performing an intracardiac perfusion, using a temperature-controlled vibratome, matching osmolarity between the cutting and incubation saline, using a slow cutting speed, and incubating slices at a warm temperature for 30 min were important when working with older tissue. Excellent visualization of neurons at depths of up to 100 [mu]m was achieved in slices from all ages (without tissue clearing)--avoiding the need to record from surface neurons, which are more likely to have truncated processes. Whole-cell recordings typically remained stable for several hours in neurons prepared from rats at all ages. These procedures should benefit neuroscientists interested in applying visually-guided whole-cell patch-clamp techniques to brain slice experiments using aged tissue. These methods should also facilitate the application of fluorescent imaging technology to brain slices for studying aging-related changes.</description>
    <dc:title>Methods for whole-cell recording from visually preselected neurons of perirhinal cortex in brain slices from young and aging rats</dc:title>

    <dc:creator>James Moyer</dc:creator>
    <dc:creator>Thomas Brown</dc:creator>
    <dc:identifier>doi:10.1016/S0165-0270(98)00143-5</dc:identifier>
    <dc:source>Journal of Neuroscience Methods, Vol. 86, No. 1. (31 December 1998), pp. 35-54.</dc:source>
    <dc:date>2008-02-12T10:42:09-00:00</dc:date>
    <prism:publicationYear>1998</prism:publicationYear>
    <prism:publicationName>Journal of Neuroscience Methods</prism:publicationName>
    <prism:volume>86</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>35</prism:startingPage>
    <prism:endingPage>54</prism:endingPage>
    <prism:category>in-vitro</prism:category>
    <prism:category>methods</prism:category>
    <prism:category>physiology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/nelmor/article/1430211">
    <title>Pathological synchronization in Parkinson's disease: networks, models and treatments</title>
    <link>http://www.citeulike.org/user/nelmor/article/1430211</link>
    <description>&lt;i&gt;Trends in Neurosciences, Vol. 30, No. 7. (July 2007), pp. 357-364.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Parkinson's disease is a common and disabling disorder of movement owing to dopaminergic denervation of the striatum. However, it is still unclear how this denervation perverts normal functioning to cause slowing of voluntary movements. Recent work using tissue slice preparations, animal models and in humans with Parkinson's disease has demonstrated abnormally synchronized oscillatory activity at multiple levels of the basal ganglia-cortical loop. This excessive synchronization correlates with motor deficit, and its suppression by dopaminergic therapies, ablative surgery or deep-brain stimulation might provide the basic mechanism whereby diverse therapeutic strategies ameliorate motor impairment in patients with Parkinson's disease. This review is part of the INMED/TINS special issue, Physiogenic and pathogenic oscillations: the beauty and the beast, based on presentations at the annual INMED/TINS symposium (http://inmednet.com/).</description>
    <dc:title>Pathological synchronization in Parkinson's disease: networks, models and treatments</dc:title>

    <dc:creator>Constance Hammond</dc:creator>
    <dc:creator>Hagai Bergman</dc:creator>
    <dc:creator>Peter Brown</dc:creator>
    <dc:identifier>doi:10.1016/j.tins.2007.05.004</dc:identifier>
    <dc:source>Trends in Neurosciences, Vol. 30, No. 7. (July 2007), pp. 357-364.</dc:source>
    <dc:date>2007-07-03T08:13:20-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Trends in Neurosciences</prism:publicationName>
    <prism:volume>30</prism:volume>
    <prism:number>7</prism:number>
    <prism:startingPage>357</prism:startingPage>
    <prism:endingPage>364</prism:endingPage>
    <prism:category>oscillations</prism:category>
    <prism:category>parkinson</prism:category>
    <prism:category>synchronization</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/nelmor/article/1070682">
    <title>Inducing motor skill improvements with a declarative task</title>
    <link>http://www.citeulike.org/user/nelmor/article/1070682</link>
    <description>&lt;i&gt;Nature Neuroscience, Vol. 10, No. 2. (21 January 2007), pp. 148-149.&lt;/i&gt;</description>
    <dc:title>Inducing motor skill improvements with a declarative task</dc:title>

    <dc:creator>Rachel Brown</dc:creator>
    <dc:creator>Edwin Robertson</dc:creator>
    <dc:identifier>doi:10.1038/nn1836</dc:identifier>
    <dc:source>Nature Neuroscience, Vol. 10, No. 2. (21 January 2007), pp. 148-149.</dc:source>
    <dc:date>2007-01-27T11:53:32-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Nature Neuroscience</prism:publicationName>
    <prism:issn>1097-6256</prism:issn>
    <prism:volume>10</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>148</prism:startingPage>
    <prism:endingPage>149</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>conditioning</prism:category>
    <prism:category>implicit-learning</prism:category>
    <prism:category>learning</prism:category>
    <prism:category>memory</prism:category>
    <prism:category>psychphysics</prism:category>
</item>



</rdf:RDF>

