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<pubDate>Sun, 20 Jul 2008 21:39:26 BST</pubDate>


	<title>CiteULike: nelmor Jackson</title>
	<description>CiteULike: nelmor Jackson</description>


	<link>http://www.citeulike.org/user/nelmor/author/Jackson</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/nelmor/article/2882425"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/nelmor/article/2744824"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/nelmor/article/968547"/>

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<item rdf:about="http://www.citeulike.org/user/nelmor/article/2882425">
    <title>Median Raphe Stimulation Disrupts Hippocampal Theta Via Rapid Inhibition and State-Dependent Phase Reset of Theta-Related Neural Circuitry</title>
    <link>http://www.citeulike.org/user/nelmor/article/2882425</link>
    <description>&lt;i&gt;J Neurophysiol, Vol. 99, No. 6. (1 June 2008), pp. 3009-3026.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Evidence has accumulated suggesting that the median raphe (MR) mediates hippocampal theta desynchronization. However, few studies have evaluated theta-related neural circuitry during MR manipulation. In urethane-anesthetized rats, we investigated the effects of MR stimulation on hippocampal field and cell activity using high-frequency (100 Hz), theta burst (TBS), and slow-frequency electrical stimulation (0.5 Hz). We demonstrated that high-frequency stimulation of the MR did not elicit deactivated patterns in the forebrain, but rather elicited low-voltage activity in the neocortex and small-amplitude irregular activity (SIA) in the hippocampus. Both hippocampal phasic theta-ON and -OFF cells were inhibited by high-frequency MR stimulation, although MR stimulation failed to affect cells that had neither state or phase relationships with theta field activity. TBS of the MR-induced theta field activity phase locked to the stimulation. Slow-frequency stimulation elicited a state-dependent reset of theta phase through a short-latency inhibition (5 ms) in phasic theta-ON cells. Subpopulations of phasic theta-ON cells responded in either oscillatory or nonoscillatory patterns to MR pulses, depending on their intraburst interval. OFF cells exhibited a state-dependent modulation of cell firing occurring preferentially during nontheta. The magnitude of MR-induced reset varied as a function of the phase of the theta oscillation when the pulse was administered. Therefore high-frequency stimulation of the MR appears to disrupt hippocampal theta through a state-dependent, short-latency inhibition of rhythmic cell populations in the hippocampus functioning to switch theta oscillations to an activated SIA field state. 10.1152/jn.00065.2008</description>
    <dc:title>Median Raphe Stimulation Disrupts Hippocampal Theta Via Rapid Inhibition and State-Dependent Phase Reset of Theta-Related Neural Circuitry</dc:title>

    <dc:creator>Jesse Jackson</dc:creator>
    <dc:creator>Clayton Dickson</dc:creator>
    <dc:creator>Brian Bland</dc:creator>
    <dc:identifier>doi:10.1152/jn.00065.2008</dc:identifier>
    <dc:source>J Neurophysiol, Vol. 99, No. 6. (1 June 2008), pp. 3009-3026.</dc:source>
    <dc:date>2008-06-11T10:03:23-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>J Neurophysiol</prism:publicationName>
    <prism:volume>99</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>3009</prism:startingPage>
    <prism:endingPage>3026</prism:endingPage>
    <prism:category>hippocampus</prism:category>
    <prism:category>in-vivo</prism:category>
    <prism:category>raphe</prism:category>
    <prism:category>theta</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/nelmor/article/2744824">
    <title>Artificial dural sealant that allows multiple penetrations of implantable brain probes</title>
    <link>http://www.citeulike.org/user/nelmor/article/2744824</link>
    <description>&lt;i&gt;Journal of Neuroscience Methods, Vol. 171, No. 1. (15 June 2008), pp. 147-152.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This study reports extensive characterization of the silicone gel (3-4680, Dow Corning, Midland, MI), for potential use as an artificial dural sealant in long-term electrophysiological experiments in neurophysiology. Dural sealants are important to preserve the integrity of the intracranial space after a craniotomy and in prolonging the lifetime and functionality of implanted brain probes. In this study, we report results of our tests on a commercially available silicone gel with unique properties that make it an ideal dural substitute. The substitute is transparent, elastic, easy to apply, and has re-sealing capabilities, which makes it desirable for applications where multiple penetrations by the brain probe is desirable over an extended period of time. Cytotoxicity tests (for up to 10 days) with fibroblasts and in vivo tests (for 12 weeks) show that the gel is non-toxic and does not produce any significant neuronal degeneration when applied to the rodent cortex even after 12 weeks. In vivo humidity testing showed no sign of CSF leakage for up to 6 weeks. The gel also allows silicon microprobes to penetrate with forces less than 0.5 mN, and a 200-[mu]m diameter stainless steel microprobe with a blunt tip to penetrate with a force less than 2.5 mN. The force dependency on the velocity of penetration and thickness of the gel was also quantified and empirically modeled. The above results demonstrate that the silicone gel (3-4680) can be a viable dural substitute in long-term electrophysiology of the brain.</description>
    <dc:title>Artificial dural sealant that allows multiple penetrations of implantable brain probes</dc:title>

    <dc:creator>Nathan Jackson</dc:creator>
    <dc:creator>Jit Muthuswamy</dc:creator>
    <dc:identifier>doi:10.1016/j.jneumeth.2008.02.018</dc:identifier>
    <dc:source>Journal of Neuroscience Methods, Vol. 171, No. 1. (15 June 2008), pp. 147-152.</dc:source>
    <dc:date>2008-05-02T09:35:28-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Journal of Neuroscience Methods</prism:publicationName>
    <prism:volume>171</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>147</prism:startingPage>
    <prism:endingPage>152</prism:endingPage>
    <prism:category>extracellular-recordings</prism:category>
    <prism:category>methods</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/nelmor/article/968547">
    <title>Hippocampal Sharp Waves and Reactivation during Awake States Depend on Repeated Sequential Experience</title>
    <link>http://www.citeulike.org/user/nelmor/article/968547</link>
    <description>&lt;i&gt;J. Neurosci., Vol. 26, No. 48. (29 November 2006), pp. 12415-12426.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Hippocampal firing patterns during behavior are reactivated during rest and subsequent slow-wave sleep. These reactivations occur during transient local field potential (LFP) events, termed sharp waves. Theories of hippocampal processing suggest that sharp waves arise from strengthened plasticity, and that the strengthened plasticity depends on repeated cofiring of pyramidal cells. We tested these predictions by recording neural ensembles and LFPs from rats running tasks requiring different levels of behavioral repetition. The number of sharp waves emitted increased during sessions with more regular behaviors. Reactivation became more similar to behavioral firing patterns across the session. This enhanced reactivation also depended on the regularity of the behavior. Additional studies in CA3 and CA1 found that the number of sharp waves emitted also increased in CA3 recordings as well as CA1, but that the time courses were different between the two structures. 10.1523/JNEUROSCI.4118-06.2006</description>
    <dc:title>Hippocampal Sharp Waves and Reactivation during Awake States Depend on Repeated Sequential Experience</dc:title>

    <dc:creator>Jadin Jackson</dc:creator>
    <dc:creator>Adam Johnson</dc:creator>
    <dc:creator>David Redish</dc:creator>
    <dc:identifier>doi:10.1523/JNEUROSCI.4118</dc:identifier>
    <dc:source>J. Neurosci., Vol. 26, No. 48. (29 November 2006), pp. 12415-12426.</dc:source>
    <dc:date>2006-11-30T11:07:27-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>J. Neurosci.</prism:publicationName>
    <prism:volume>26</prism:volume>
    <prism:number>48</prism:number>
    <prism:startingPage>12415</prism:startingPage>
    <prism:endingPage>12426</prism:endingPage>
    <prism:category>consolidation</prism:category>
    <prism:category>hippocampus</prism:category>
    <prism:category>memory</prism:category>
    <prism:category>spw-r</prism:category>
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