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		<title>Phenocyclidine Related Disorders</title>
		<description><![CDATA[Behavioral Health Central - Articles and Resources for the Behavioral Healthcare Industry.]]></description>
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			<title>Phenocyclidine Related Disorders</title>
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			<description>Behavioral Health Central - Articles and Resources for the Behavioral Healthcare Industry.</description>
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			<title>Contribution of Cystine-Glutamate Antiporters to the Psychotomimetic Effects of Phencyclidine </title>
			<link>http://behavioralhealthcentral.com/index.php/20090522232/Phencyclidine-latest/contribution-of-cystine-glutamate-antiporters-to-the-psychotomimetic-effects-of-phencyclidine.html?Itemid=</link>
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			<description><![CDATA[<span id="dnn_ctr1404_ViewBHC_Article_lblArticleDetails">By Baker D.A.;  Madayag A.;  Kristiansen L.V.;  Meador-Woodruff J.H.;  Haroutunian V.;  Raju I.<br /><br /> Altered glutamate signaling contributes to a myriad of neural disorders, including schizophrenia. While synaptic levels are intensely studied, nonvesicular release mechanisms, including cystine-glutamate exchange, maintain high steady-state glutamate levels in the extrasynaptic space. The existence of extrasynaptic receptors, including metabotropic group II glutamate receptors (mGluR), pose nonvesicular release mechanisms as unrecognized targets capable of contributing to pathological glutamate signaling. We tested the hypothesis that activation of cystine-glutamate antiporters using the cysteine prodrug N-acetylcysteine would blunt psychotomimetic effects in the rodent phencyclidine (PCP) model of schizophrenia. <br /> <br /> First, we demonstrate that PCP elevates extracellular glutamate in the prefrontal cortex, an effect that is blocked by N-acetylcysteine pretreatment. To determine the relevance of the above finding, we assessed social interaction and found that N-acetylcysteine reverses social withdrawal produced...]]></description>
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			<pubDate>Fri, 22 May 2009 12:51:13 +0000</pubDate>
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			<title>Disordered Eating and Substance Use in High-School Students</title>
			<link>http://behavioralhealthcentral.com/index.php/20090522231/Phencyclidine-latest/disordered-eating-and-substance-use-in-high-school-students.html?Itemid=</link>
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			<description><![CDATA[<span id="dnn_ctr1404_ViewBHC_Article_lblArticleDetails"><span style="font-weight: bold; color: #144878;">Results from the Youth Risk Behavior Surveillance System <br /><br /></span> By Pisetsky E.M.;  Chao Y.M.;  Dierker L.C.;  May A.M.; Striegel-Moore R.H.<br /><br /> Objective: To examine the association between disordered eating (fasting, diet product use, and vomiting or laxative use) and use of 10 substances (cigarettes, alcohol, marijuana, cocaine, inhalants, heroin, methamphetamines, ecstasy, steroids, and hallucinogens) in a nationally representative adolescent sample. <br /> <br /> Method: Participants were 13,917 U.S. high-school students participating in the 2005 Youth Risk Behavior Surveillance System. <br /> <br /> Results: Disordered eating was significantly associated with the use of each substance. Using effect size estimates that take base rates into consideration, for female students, associations between substance use and disordered eating were weak for all but three forms of substance use: current smoking, binge drinking, and inhalants. Among male students, strong (marijuana, steroids, and...]]></description>
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			<pubDate>Fri, 22 May 2009 12:50:22 +0000</pubDate>
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			<title>Contribution of Cystine-Glutamate Antiporters to the Psychotomimetic Effects of Phencyclidine</title>
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			<description><![CDATA[Altered glutamate signaling contributes to a myriad of neural disorders, including schizophrenia. While synaptic levels are intensely studied, nonvesicular release mechanisms, including cystine-glutamate exchange, maintain high steady-state glutamate levels in the extrasynaptic space. The existence of extrasynaptic receptors, including metabotropic group II glutamate receptors (mGluR), pose nonvesicular release mechanisms as unrecognized targets capable of contributing to pathological glutamate signaling. We tested the hypothesis that activation of cystine-glutamate antiporters using the cysteine prodrug N-acetylcysteine would blunt psychotomimetic effects in the rodent phencyclidine (PCP) model of schizophrenia. <br /><br /><br /><br />First, we demonstrate that PCP elevates extracellular glutamate in the prefrontal cortex, an effect that is blocked by N-acetylcysteine pretreatment. To determine the relevance of the above finding, we assessed social interaction and found that N-acetylcysteine reverses social withdrawal produced by repeated PCP. In a separate paradigm, acute PCP resulted in working memory deficits assessed using a discrete trial t-maze task,...]]></description>
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