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	<title>Cerebral Plasy Information &#187; Dopaminergic Medicine</title>
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	<link>http://cerebralpalsysocial.com</link>
	<description>the most up to date information about cerebral palsy</description>
	<lastBuildDate>Mon, 31 Jan 2011 06:52:40 +0000</lastBuildDate>
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		<title>Using the self-administration of apomorphine and cocaine to measure the pharmacodynamic potencies and pharmacokinetics of competitive dopamine receptor antagonists.</title>
		<link>http://cerebralpalsysocial.com/2011/01/using-the-self-administration-of-apomorphine-and-cocaine-to-measure-the-pharmacodynamic-potencies-and-pharmacokinetics-of-competitive-dopamine-receptor-antagonists/</link>
		<comments>http://cerebralpalsysocial.com/2011/01/using-the-self-administration-of-apomorphine-and-cocaine-to-measure-the-pharmacodynamic-potencies-and-pharmacokinetics-of-competitive-dopamine-receptor-antagonists/#comments</comments>
		<pubDate>Mon, 31 Jan 2011 06:51:57 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Dopaminergic Medicine]]></category>

		<guid isPermaLink="false">http://cerebralpalsysocial.com/2011/01/using-the-self-administration-of-apomorphine-and-cocaine-to-measure-the-pharmacodynamic-potencies-and-pharmacokinetics-of-competitive-dopamine-receptor-antagonists/</guid>
		<description><![CDATA[Competitive dopamine receptor antagonists accelerate psychomotor stimulant self-administration. According to pharmacological theory of competitive antagonism antagonists raise the equiactive agonist concentration. In the self-administration paradigm this is assumed to be the satiety threshold or C(min). The magnitude of the proportional increase in satiety threshold (agonist concentration ratio) as a function of antagonist dose should reflect [...]]]></description>
		<wfw:commentRss>http://cerebralpalsysocial.com/2011/01/using-the-self-administration-of-apomorphine-and-cocaine-to-measure-the-pharmacodynamic-potencies-and-pharmacokinetics-of-competitive-dopamine-receptor-antagonists/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Activities of bone morphogenetic proteins in prolactin regulation by somatostatin analogs in rat pituitary GH3 cells.</title>
		<link>http://cerebralpalsysocial.com/2011/01/activities-of-bone-morphogenetic-proteins-in-prolactin-regulation-by-somatostatin-analogs-in-rat-pituitary-gh3-cells/</link>
		<comments>http://cerebralpalsysocial.com/2011/01/activities-of-bone-morphogenetic-proteins-in-prolactin-regulation-by-somatostatin-analogs-in-rat-pituitary-gh3-cells/#comments</comments>
		<pubDate>Mon, 31 Jan 2011 06:51:55 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Dopaminergic Medicine]]></category>

		<guid isPermaLink="false">http://cerebralpalsysocial.com/2011/01/activities-of-bone-morphogenetic-proteins-in-prolactin-regulation-by-somatostatin-analogs-in-rat-pituitary-gh3-cells/</guid>
		<description><![CDATA[Involvement of the pituitary BMP system in the modulation of prolactin (PRL) secretion regulated by somatostatin analogs, including octreotide (OCT) and pasireotide (SOM230), and a dopamine agonist, bromocriptine (BRC), were examined in GH3 cells. GH3 cells are rat pituitary somato-lactotrope tumor cells that express somatostatin receptors (SSTRs) and BMP system molecules including BMP-4 and -6. [...]]]></description>
		<wfw:commentRss>http://cerebralpalsysocial.com/2011/01/activities-of-bone-morphogenetic-proteins-in-prolactin-regulation-by-somatostatin-analogs-in-rat-pituitary-gh3-cells/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Prenatal depression effects on early development: A review.</title>
		<link>http://cerebralpalsysocial.com/2011/01/prenatal-depression-effects-on-early-development-a-review/</link>
		<comments>http://cerebralpalsysocial.com/2011/01/prenatal-depression-effects-on-early-development-a-review/#comments</comments>
		<pubDate>Mon, 31 Jan 2011 06:51:53 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Dopaminergic Medicine]]></category>

		<guid isPermaLink="false">http://cerebralpalsysocial.com/2011/01/prenatal-depression-effects-on-early-development-a-review/</guid>
		<description><![CDATA[This review of recent research on prenatal depression suggests that it is a strong predictor of postpartum depression and is more common than postpartum depression. Prenatal depression has been associated with excessive activity and growth delays in the fetus as well as prematurity, low birthweight, disorganized sleep and less responsiveness to stimulation in the neonate. [...]]]></description>
		<wfw:commentRss>http://cerebralpalsysocial.com/2011/01/prenatal-depression-effects-on-early-development-a-review/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>POSTTRANSLATIONAL MODIFICATION OF GLUTAMIC ACID DECARBOXYLASE 67 BY INTERMITTENT HYPOXIA: Evidence for the involvement of dopamine D1 receptor signaling($).</title>
		<link>http://cerebralpalsysocial.com/2011/01/posttranslational-modification-of-glutamic-acid-decarboxylase-67-by-intermittent-hypoxia-evidence-for-the-involvement-of-dopamine-d1-receptor-signaling/</link>
		<comments>http://cerebralpalsysocial.com/2011/01/posttranslational-modification-of-glutamic-acid-decarboxylase-67-by-intermittent-hypoxia-evidence-for-the-involvement-of-dopamine-d1-receptor-signaling/#comments</comments>
		<pubDate>Mon, 31 Jan 2011 06:51:52 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Dopaminergic Medicine]]></category>

		<guid isPermaLink="false">http://cerebralpalsysocial.com/2011/01/posttranslational-modification-of-glutamic-acid-decarboxylase-67-by-intermittent-hypoxia-evidence-for-the-involvement-of-dopamine-d1-receptor-signaling/</guid>
		<description><![CDATA[Intermittent hypoxia (IH) associated with sleep apnea leads to cardio-respiratory morbidities. Previous studies have shown that IH alters the synthesis of neurotransmitters including catecholamines and neuropeptides in brainstem regions associated with regulation of cardio-respiratory functions. GABA, a major inhibitory neurotransmitter in the central nervous system, has been implicated in cardio-respiratory control. GABA synthesis is primarily [...]]]></description>
		<wfw:commentRss>http://cerebralpalsysocial.com/2011/01/posttranslational-modification-of-glutamic-acid-decarboxylase-67-by-intermittent-hypoxia-evidence-for-the-involvement-of-dopamine-d1-receptor-signaling/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Nigral and striatal regulation of angiotensin receptor expression by dopamine and angiotensin in rodents: implications for progression of Parkinson&#8217;s disease.</title>
		<link>http://cerebralpalsysocial.com/2011/01/nigral-and-striatal-regulation-of-angiotensin-receptor-expression-by-dopamine-and-angiotensin-in-rodents-implications-for-progression-of-parkinsons-disease/</link>
		<comments>http://cerebralpalsysocial.com/2011/01/nigral-and-striatal-regulation-of-angiotensin-receptor-expression-by-dopamine-and-angiotensin-in-rodents-implications-for-progression-of-parkinsons-disease/#comments</comments>
		<pubDate>Mon, 31 Jan 2011 06:51:49 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Dopaminergic Medicine]]></category>

		<guid isPermaLink="false">http://cerebralpalsysocial.com/2011/01/nigral-and-striatal-regulation-of-angiotensin-receptor-expression-by-dopamine-and-angiotensin-in-rodents-implications-for-progression-of-parkinsons-disease/</guid>
		<description><![CDATA[The basal ganglia have a local renin-angiotensin system and it has been shown that the loss of dopaminergic neurons induced by neurotoxins is amplified by local angiotensin II (AII) via angiotensin type 1 receptors (AT1) and nicotinamide adenine dinucleotide phosphate (NADPH) complex activation. Recent studies have revealed a high degree of counter-regulatory interactions between dopamine [...]]]></description>
		<wfw:commentRss>http://cerebralpalsysocial.com/2011/01/nigral-and-striatal-regulation-of-angiotensin-receptor-expression-by-dopamine-and-angiotensin-in-rodents-implications-for-progression-of-parkinsons-disease/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Test-retest variability of [(11)C]raclopride binding potential in nontreatment-seeking alcoholics.</title>
		<link>http://cerebralpalsysocial.com/2011/01/test-retest-variability-of-11craclopride-binding-potential-in-nontreatment-seeking-alcoholics/</link>
		<comments>http://cerebralpalsysocial.com/2011/01/test-retest-variability-of-11craclopride-binding-potential-in-nontreatment-seeking-alcoholics/#comments</comments>
		<pubDate>Mon, 31 Jan 2011 06:51:47 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Dopaminergic Medicine]]></category>

		<guid isPermaLink="false">http://cerebralpalsysocial.com/2011/01/test-retest-variability-of-11craclopride-binding-potential-in-nontreatment-seeking-alcoholics/</guid>
		<description><![CDATA[Knowledge of the reproducibility of striatal [(11)C]raclopride (RAC) binding is important for studies that use RAC PET paradigms to estimate changes in striatal dopamine during pharmacological and cognitive challenges. To our knowledge, no baseline test-retest data exist for nontreatment-seeking alcoholics (NTS). We determined the test-retest reproducibility of baseline RAC binding potential (BP(ND)) in twelve male [...]]]></description>
		<wfw:commentRss>http://cerebralpalsysocial.com/2011/01/test-retest-variability-of-11craclopride-binding-potential-in-nontreatment-seeking-alcoholics/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Discrimination of prolactinoma from hyperprolactinemic non-functioning adenoma.</title>
		<link>http://cerebralpalsysocial.com/2011/01/discrimination-of-prolactinoma-from-hyperprolactinemic-non-functioning-adenoma/</link>
		<comments>http://cerebralpalsysocial.com/2011/01/discrimination-of-prolactinoma-from-hyperprolactinemic-non-functioning-adenoma/#comments</comments>
		<pubDate>Mon, 31 Jan 2011 06:51:46 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Dopaminergic Medicine]]></category>

		<guid isPermaLink="false">http://cerebralpalsysocial.com/2011/01/discrimination-of-prolactinoma-from-hyperprolactinemic-non-functioning-adenoma/</guid>
		<description><![CDATA[The objective of this study was to evaluate characteristics that discriminate prolactinoma from non-functioning pituitary macroadenoma with hyperprolactinemia. We included 117 patients with hyperprolactinemic pituitary macroadenomas. Patients were divided into three groups according to treatment outcomes and pathologic results: (A) prolactinoma that responded to dopamine agonist (DA) treatment (PRDA); (B) prolactinoma requiring surgical treatment (PRS); [...]]]></description>
		<wfw:commentRss>http://cerebralpalsysocial.com/2011/01/discrimination-of-prolactinoma-from-hyperprolactinemic-non-functioning-adenoma/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Prolonged Attenuation of the Reinforcing Strength of Cocaine by Chronic d-Amphetamine in Rhesus Monkeys.</title>
		<link>http://cerebralpalsysocial.com/2011/01/prolonged-attenuation-of-the-reinforcing-strength-of-cocaine-by-chronic-d-amphetamine-in-rhesus-monkeys/</link>
		<comments>http://cerebralpalsysocial.com/2011/01/prolonged-attenuation-of-the-reinforcing-strength-of-cocaine-by-chronic-d-amphetamine-in-rhesus-monkeys/#comments</comments>
		<pubDate>Mon, 31 Jan 2011 06:51:43 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Dopaminergic Medicine]]></category>

		<guid isPermaLink="false">http://cerebralpalsysocial.com/2011/01/prolonged-attenuation-of-the-reinforcing-strength-of-cocaine-by-chronic-d-amphetamine-in-rhesus-monkeys/</guid>
		<description><![CDATA[Chronic treatment with the indirect dopamine agonist d-amphetamine can reduce cocaine use in clinical trials and, in preclinical studies in laboratory animals, attenuates daily cocaine self-administration. The present study extended previous results to conditions designed to reflect a more clinically relevant experience of cocaine exposure and d-amphetamine treatment. Each morning, monkeys pressed a lever to [...]]]></description>
		<wfw:commentRss>http://cerebralpalsysocial.com/2011/01/prolonged-attenuation-of-the-reinforcing-strength-of-cocaine-by-chronic-d-amphetamine-in-rhesus-monkeys/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Comment on &#8220;paroxetine prevents loss of nigrostriatal dopaminergic neurons by inhibiting brain inflammation and oxidative stress in an experimental model of Parkinson&#8217;s disease&#8221;.</title>
		<link>http://cerebralpalsysocial.com/2011/01/comment-on-paroxetine-prevents-loss-of-nigrostriatal-dopaminergic-neurons-by-inhibiting-brain-inflammation-and-oxidative-stress-in-an-experimental-model-of-parkinsons-disease/</link>
		<comments>http://cerebralpalsysocial.com/2011/01/comment-on-paroxetine-prevents-loss-of-nigrostriatal-dopaminergic-neurons-by-inhibiting-brain-inflammation-and-oxidative-stress-in-an-experimental-model-of-parkinsons-disease/#comments</comments>
		<pubDate>Mon, 31 Jan 2011 06:51:42 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Dopaminergic Medicine]]></category>

		<guid isPermaLink="false">http://cerebralpalsysocial.com/2011/01/comment-on-paroxetine-prevents-loss-of-nigrostriatal-dopaminergic-neurons-by-inhibiting-brain-inflammation-and-oxidative-stress-in-an-experimental-model-of-parkinsons-disease/</guid>
		<description><![CDATA[Share and Enjoy: Tags: Dopaminergic Medicine]]></description>
		<wfw:commentRss>http://cerebralpalsysocial.com/2011/01/comment-on-paroxetine-prevents-loss-of-nigrostriatal-dopaminergic-neurons-by-inhibiting-brain-inflammation-and-oxidative-stress-in-an-experimental-model-of-parkinsons-disease/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Human immunodeficiency virus-1 Tat activates calpain proteases via the ryanodine receptor to enhance surface dopamine transporter levels and increase transporter-specific uptake and Vmax.</title>
		<link>http://cerebralpalsysocial.com/2011/01/human-immunodeficiency-virus-1-tat-activates-calpain-proteases-via-the-ryanodine-receptor-to-enhance-surface-dopamine-transporter-levels-and-increase-transporter-specific-uptake-and-vmax/</link>
		<comments>http://cerebralpalsysocial.com/2011/01/human-immunodeficiency-virus-1-tat-activates-calpain-proteases-via-the-ryanodine-receptor-to-enhance-surface-dopamine-transporter-levels-and-increase-transporter-specific-uptake-and-vmax/#comments</comments>
		<pubDate>Mon, 31 Jan 2011 06:51:40 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Dopaminergic Medicine]]></category>

		<guid isPermaLink="false">http://cerebralpalsysocial.com/2011/01/human-immunodeficiency-virus-1-tat-activates-calpain-proteases-via-the-ryanodine-receptor-to-enhance-surface-dopamine-transporter-levels-and-increase-transporter-specific-uptake-and-vmax/</guid>
		<description><![CDATA[Human immunodeficiency virus-associated neurological disease (HAND) still causes significant morbidity, despite success reducing viral loads with combination antiretroviral therapy. The dopamine (DA) system is particularly vulnerable in HAND. We hypothesize that early, &#8220;reversible&#8221; DAergic synaptic dysfunction occurs long before DAergic neuron loss. As such, aging human immunodeficiency virus (HIV)-infected individuals may be vulnerable to other [...]]]></description>
		<wfw:commentRss>http://cerebralpalsysocial.com/2011/01/human-immunodeficiency-virus-1-tat-activates-calpain-proteases-via-the-ryanodine-receptor-to-enhance-surface-dopamine-transporter-levels-and-increase-transporter-specific-uptake-and-vmax/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
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