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<pubDate>Thu, 21 Aug 2008 00:50:25 BST</pubDate>


	<title>CiteULike: morven's photoreceptors</title>
	<description>CiteULike: morven's photoreceptors</description>


	<link>http://www.citeulike.org/user/morven/tag/photoreceptors</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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	<dc:rights>Copyright &#169; 2004-2008 citeulike.org</dc:rights>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/morven/article/706222"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/morven/article/706099"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/morven/article/706097"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/morven/article/343404"/>

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<item rdf:about="http://www.citeulike.org/user/morven/article/706222">
    <title>Non-visual ocular photoreception.</title>
    <link>http://www.citeulike.org/user/morven/article/706222</link>
    <description>&lt;i&gt;Ophthalmic Genet, Vol. 22, No. 4. (December 2001), pp. 195-205.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;At least six light-regulated phenomena are preserved in the eyes of retinally degenerate mice, including the entrainment of circadian rhythms, the gating of ocular immune response, and pupillary reactivity. Some of these phenomena have also been observed in blind human patients. These findings have prompted the search for a non-visual ocular phototransduction mechanism. Molecular genetic studies have identified several candidate genes for these effects. These include genes encoding novel ocular opsins, such as melanopsin, as well as potential flavin-based photopigments. Data linking these potential photoreceptors to these phenomena are discussed, and the clinical implications of these findings are explored.</description>
    <dc:title>Non-visual ocular photoreception.</dc:title>

    <dc:creator>RN Van Gelder</dc:creator>
    <dc:source>Ophthalmic Genet, Vol. 22, No. 4. (December 2001), pp. 195-205.</dc:source>
    <dc:date>2006-06-21T19:03:21-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Ophthalmic Genet</prism:publicationName>
    <prism:issn>1381-6810</prism:issn>
    <prism:volume>22</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>195</prism:startingPage>
    <prism:endingPage>205</prism:endingPage>
    <prism:category>photoreceptors</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/morven/article/706099">
    <title>Neither functional rod photoreceptors nor rod or cone outer segments are required for the photic inhibition of pineal melatonin.</title>
    <link>http://www.citeulike.org/user/morven/article/706099</link>
    <description>&lt;i&gt;Endocrinology, Vol. 140, No. 4. (April 1999), pp. 1520-1524.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Pineal melatonin production is rapidly suppressed by light. In mammals, the photoreceptors mediating this response are ocular; however, definitive information regarding their nature and precise location is absent. In an attempt to define these photoreceptors, we examined the sensitivity of pineal melatonin production to inhibition by controlled irradiance monochromatic green light (lambda max 509 nm) in C3H mice bearing either of two mutations affecting the retina: retinal degeneration (rd), a disruption of rod phototransduction, and retinal degeneration slow (rds), an ablation of photoreceptor outer segments. Diurnal profiles of pineal melatonin content were similar in both mutant genotypes and in wild-type mice; melatonin peaked between 3-5 h before lights on. All three genotypes exhibited irradiance dependent inhibition of pineal melatonin content; 2.6 x 10(-2) microwatts/cm2 509 nm light induced complete suppression in all three genotypes, whereas lower irradiances were ineffective in all cases. Bilateral enucleation abolished responses even to 6 microwatts/cm2 509 nm light. These results demonstrate that the process of irradiance detection for pineal melatonin inhibition is buffered against considerable loss of photoreceptive capacity and that neither rod photoreceptors nor rod or cone outer segments are required for mediating this response in mice.</description>
    <dc:title>Neither functional rod photoreceptors nor rod or cone outer segments are required for the photic inhibition of pineal melatonin.</dc:title>

    <dc:creator>RJ Lucas</dc:creator>
    <dc:creator>RG Foster</dc:creator>
    <dc:source>Endocrinology, Vol. 140, No. 4. (April 1999), pp. 1520-1524.</dc:source>
    <dc:date>2006-06-21T18:07:23-00:00</dc:date>
    <prism:publicationYear>1999</prism:publicationYear>
    <prism:publicationName>Endocrinology</prism:publicationName>
    <prism:issn>0013-7227</prism:issn>
    <prism:volume>140</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>1520</prism:startingPage>
    <prism:endingPage>1524</prism:endingPage>
    <prism:category>melatonin</prism:category>
    <prism:category>photoreceptors</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/morven/article/706097">
    <title>Circadian oscillation of photopigment transcript levels in the mouse retina.</title>
    <link>http://www.citeulike.org/user/morven/article/706097</link>
    <description>&lt;i&gt;Brain Res Mol Brain Res, Vol. 72, No. 1. (8 September 1999), pp. 108-114.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The mammalian retina contains an autonomous circadian oscillator that can sustain rhythms in outer segment disc shedding and melatonin synthesis even in the absence of cues from the central oscillator in the suprachiasmatic nucleus (SCN). The present investigation aimed to ascertain whether the steady-state levels of rod and cone opsin mRNA exhibited a circadian oscillation in the mouse, and if so, to characterise this oscillation with regard to phase. Retinas were collected from mice free-running in constant darkness at circadian times (CT) 0, 4, 12, 16, and 20. RNA was extracted for the production of Northern blots, which were sequentially hybridised with probes for alpha-tubulin (control), ultraviolet opsin, and rhodopsin. Whereas no significant oscillation was detected in the levels of alpha-tubulin, the levels of both ultraviolet opsin and rhodopsin transcripts oscillated with an amplitude of at least 3-fold. The highest levels were found at around CT12 (which corresponds to the subjective evening, the time of activity onset in the mouse). These results show that the levels of rod and cone photopigment mRNA are under circadian control. The significance of the rhythms and their phasing is discussed. These findings have potential clinical implications both with regard to nocturnal light treatment of phase asynchrony, and in the timing of chemo- and radiotherapy.</description>
    <dc:title>Circadian oscillation of photopigment transcript levels in the mouse retina.</dc:title>

    <dc:creator>M von Schantz</dc:creator>
    <dc:creator>RJ Lucas</dc:creator>
    <dc:creator>RG Foster</dc:creator>
    <dc:source>Brain Res Mol Brain Res, Vol. 72, No. 1. (8 September 1999), pp. 108-114.</dc:source>
    <dc:date>2006-06-21T18:06:48-00:00</dc:date>
    <prism:publicationYear>1999</prism:publicationYear>
    <prism:publicationName>Brain Res Mol Brain Res</prism:publicationName>
    <prism:issn>0169-328X</prism:issn>
    <prism:volume>72</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>108</prism:startingPage>
    <prism:endingPage>114</prism:endingPage>
    <prism:category>circadian</prism:category>
    <prism:category>photoreceptors</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/morven/article/343404">
    <title>Activation, deactivation, and adaptation in vertebrate photoreceptor cells.</title>
    <link>http://www.citeulike.org/user/morven/article/343404</link>
    <description>&lt;i&gt;Annu Rev Neurosci, Vol. 24 (2001), pp. 779-805.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Visual transduction captures widespread interest because its G-protein signaling motif recurs throughout nature yet is uniquely accessible for study in the photoreceptor cells. The light-activated currents generated at the photoreceptor outer segment provide an easily observed real-time measure of the output of the signaling cascade, and the ease of obtaining pure samples of outer segments in reasonable quantity facilitates biochemical experiments. A quiet revolution in the study of the mechanism has occurred during the past decade with the advent of gene-targeting techniques. These have made it possible to observe how transduction is perturbed by the deletion, overexpression, or mutation of specific components of the transduction apparatus.</description>
    <dc:title>Activation, deactivation, and adaptation in vertebrate photoreceptor cells.</dc:title>

    <dc:creator>ME Burns</dc:creator>
    <dc:creator>DA Baylor</dc:creator>
    <dc:identifier>doi:10.1146/annurev.neuro.24.1.779</dc:identifier>
    <dc:source>Annu Rev Neurosci, Vol. 24 (2001), pp. 779-805.</dc:source>
    <dc:date>2005-10-07T09:52:17-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Annu Rev Neurosci</prism:publicationName>
    <prism:issn>0147-006X</prism:issn>
    <prism:volume>24</prism:volume>
    <prism:startingPage>779</prism:startingPage>
    <prism:endingPage>805</prism:endingPage>
    <prism:category>photoreceptors</prism:category>
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