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<pubDate>Sun, 20 Jul 2008 13:58:19 BST</pubDate>


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


	<link>http://www.citeulike.org/user/nelmor/author/Ji</link>
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<item rdf:about="http://www.citeulike.org/user/nelmor/article/2744777">
    <title>Firing Rate Dynamics in the Hippocampus Induced by Trajectory Learning</title>
    <link>http://www.citeulike.org/user/nelmor/article/2744777</link>
    <description>&lt;i&gt;J. Neurosci., Vol. 28, No. 18. (30 April 2008), pp. 4679-4689.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The hippocampus is essential for spatial navigation, which may involve sequential learning. However, how the hippocampus encodes new sequences in familiar environments is unknown. To study the impact of novel spatial sequences on the activity of hippocampal neurons, we monitored hippocampal ensembles while rats learned to switch from two familiar trajectories to a new one in a familiar environment. Here, we show that this novel spatial experience induces two types of changes in firing rates, but not locations of hippocampal place cells. First, place-cell firing rates on the two familiar trajectories start to change before the actual behavioral switch to the new trajectory. Second, repeated exposure on the new trajectory is associated with an increased dependence of place-cell firing rates on immediate past locations. The result suggests that sequence encoding in the hippocampus may involve integration of information about the recent past into current state. 10.1523/JNEUROSCI.4597-07.2008</description>
    <dc:title>Firing Rate Dynamics in the Hippocampus Induced by Trajectory Learning</dc:title>

    <dc:creator>Daoyun Ji</dc:creator>
    <dc:creator>Matthew Wilson</dc:creator>
    <dc:identifier>doi:10.1523/JNEUROSCI.4597-07.2008</dc:identifier>
    <dc:source>J. Neurosci., Vol. 28, No. 18. (30 April 2008), pp. 4679-4689.</dc:source>
    <dc:date>2008-05-02T09:18:17-00:00</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>4679</prism:startingPage>
    <prism:endingPage>4689</prism:endingPage>
    <prism:category>hippocampus</prism:category>
    <prism:category>navigation</prism:category>
    <prism:category>place-cell</prism:category>
    <prism:category>rate-remapping</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/nelmor/article/1418865">
    <title>Lateral Habenula Stimulation Inhibits Rat Midbrain Dopamine Neurons through a GABAA Receptor-Mediated Mechanism</title>
    <link>http://www.citeulike.org/user/nelmor/article/1418865</link>
    <description>&lt;i&gt;J. Neurosci., Vol. 27, No. 26. (27 June 2007), pp. 6923-6930.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Transient changes in the activity of midbrain dopamine neurons encode an error signal that contributes to associative learning. Although considerable attention has been devoted to the mechanisms contributing to phasic increases in dopamine activity, less is known about the origin of the transient cessation in firing accompanying the unexpected loss of a predicted reward. Recent studies suggesting that the lateral habenula (LHb) may contribute to this type of signaling in humans prompted us to evaluate the effects of LHb stimulation on the activity of dopamine and non-dopamine neurons of the anesthetized rat. Single-pulse stimulation of the LHb (0.5 mA, 100 micros) transiently suppressed the activity of 97% of the dopamine neurons recorded in the substantia nigra and ventral tegmental area. The duration of the cessation averaged [~]85 ms and did not differ between the two regions. Identical stimuli transiently excited 52% of the non-dopamine neurons in the ventral midbrain. Electrolytic lesions of the fasciculus retroflexus blocked the effects of LHb stimulation on dopamine neurons. Local application of bicuculline but not the SK-channel blocker apamin attenuated the effects of LHb stimulation on dopamine cells, indicating that the response is mediated by GABAA receptors. These data suggest that LHb-induced suppression of dopamine cell activity is mediated indirectly by orthodromic activation of putative GABAergic neurons in the ventral midbrain. The habenulomesencephalic pathway, which is capable of transiently suppressing the activity of dopamine neurons at a population level, may represent an important component of the circuitry involved in encoding reward expectancy. 10.1523/JNEUROSCI.0958-07.2007</description>
    <dc:title>Lateral Habenula Stimulation Inhibits Rat Midbrain Dopamine Neurons through a GABAA Receptor-Mediated Mechanism</dc:title>

    <dc:creator>Huifang Ji</dc:creator>
    <dc:creator>Paul Shepard</dc:creator>
    <dc:identifier>doi:10.1523/JNEUROSCI.0958-07.2007</dc:identifier>
    <dc:source>J. Neurosci., Vol. 27, No. 26. (27 June 2007), pp. 6923-6930.</dc:source>
    <dc:date>2007-06-28T09:44:04-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>J. Neurosci.</prism:publicationName>
    <prism:volume>27</prism:volume>
    <prism:number>26</prism:number>
    <prism:startingPage>6923</prism:startingPage>
    <prism:endingPage>6930</prism:endingPage>
    <prism:category>dopamine</prism:category>
    <prism:category>lateral_habenula</prism:category>
    <prism:category>physiology</prism:category>
    <prism:category>snc</prism:category>
    <prism:category>vta</prism:category>
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