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<title>Psychopharmacology RSS : Gourt</title>
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<dc:rights>Copyright 2007, Gourt.com</dc:rights>
<dc:date>2012-02-07T06:20+53:00
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<dc:publisher>rtruog@gourt.com</dc:publisher>
<dc:creator>rtruog@gourt.com</dc:creator>
<dc:subject>Psychopharmacology RSS : Gourt</dc:subject>
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<title>Agmatine, an endogenous ligand of imidazoline receptor protects against memory impairment and biochemical alterations in streptozotocin-induced diabetic rats.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=22300747&#x26;dopt=Abstract</link>
<description><![CDATA[
	
        Agmatine, an endogenous ligand of imidazoline receptor protects against memory impairment and biochemical alterations in streptozotocin-induced diabetic rats.
        Prog Neuropsychopharmacol Biol Psychiatry. 2012 Jan 25;
        Authors:  Bhutada P, Mundhada Y, Humane V, Rahigude A, Deshmukh P, Latad S, Jain K
        Abstract
        Agmatine, a polycationic amine synthesized via decarboxylation of l-arginine by arginine decarboxylase is reported to exhibit anti-hyperglycemic, antioxidant and memory enhancing effects. Therefore, we tested its influence against cognitive dysfunction in streptozotocin-induced diabetic rats using Morris water maze and object recognition paradigm. Lipid peroxidation and glutathione levels as parameters of oxidative stress and choline esterase (ChE) activity as a marker of cholinergic function were assessed in the cerebral cortex and hippocampus. Thirty days after diabetes induction rats showed a severe deficit in learning and memory associated with increased lipid peroxidation, decreased reduced glutathione, and elevated ChE activity. In contrast, chronic treatment with agmatine (5-10mg/kg, i.p. for 30days) improved cognitive performance, lowered hyperglycemia, oxidative stress, and ChE activity in diabetic rats. Further, memory improving effects of agmatine were independent of adrenal I(2) imidazoline receptors. In a separate set, agmatine treatment for an initial 15days after diabetes confirmation also significantly reduced memory impairment during training trials after 30days of diabetes confirmation. Moreover, treatment during training trials (30days after diabetes) also significantly reduced memory impairment in diabetic rats. In conclusion, the present study demonstrates that treatment with agmatine prevents changes in oxidative stress and ChE activity, and probably consequent memory impairment in diabetic rats.
        PMID: 22300747 [PubMed - as supplied by publisher]
    ]]></description>
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<title>Interactions between the cannabinoid and dopaminergic systems: Evidence from animal studies.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=22300746&#x26;dopt=Abstract</link>
<description><![CDATA[
	
        Interactions between the cannabinoid and dopaminergic systems: Evidence from animal studies.
        Prog Neuropsychopharmacol Biol Psychiatry. 2012 Jan 20;
        Authors:  El Khoury MA, Gorgievski V, Moutsimilli L, Giros B, Tzavara ET
        Abstract
        There is a prominent role of the cannabinoid system to control basal ganglia function, in respect to reward, psychomotor function and motor control. Cannabinoid dysregulations might have a pathogenetic role in dopamine- and basal ganglia related neuropsychiatric disorders, such as drug addiction, psychosis, Parkinson's disease and Huntington's disease. This review highlights interactions between cannabinoids, and dopamine, to modulate neurotransmitter release and synaptic plasticity in the context of drug addiction, psychosis and cognition. Modulating endocannabinoid function, as a plasticity based therapeutic strategy, in the above pathologies with particular focus on cannabinoid receptor type 1 (CB1 receptor) antagonists/inverse agonists, is discussed. On the basis of the existing literature and of new experimental evidence presented here, CB1 receptor antagonists might be beneficial in disease states associated with hedonic dysregulation, and with cognitive dysfunction in particular in the context of psychosis. It is suggested that this effects might be mediated via a hyperglutamatergic state through metabotropic glutamate activation. Indications for endocannabinoid catabolism inhibitors in psychiatric disorders, that might be CB1 receptor independent and might involve TRPV1 receptors, are also discussed.
        PMID: 22300746 [PubMed - as supplied by publisher]
    ]]></description>
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<title>Involvement of descending serotonergic and noradrenergic pathways in CB(1) receptor-mediated antinociception.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=22300745&#x26;dopt=Abstract</link>
<description><![CDATA[
	
        Involvement of descending serotonergic and noradrenergic pathways in CB(1) receptor-mediated antinociception.
        Prog Neuropsychopharmacol Biol Psychiatry. 2012 Jan 24;
        Authors:  Dogrul A, Seyrek M, Yalcin B, Ulugol A
        Abstract
        Cannabinoids produce antinociceptive and antihyperalgesic effects mainly through activation of the inhibitory CB1 receptors. The demonstration that antinociceptive effects of systemic cannabinoids are significantly diminished following surgical dorsolateral funiculus lesion provides evidence that supraspinal sites and descending pain modulatory pathways play crucial roles in systemic cannabinoid analgesia. In this review, we will firstly provide a background, brief overview of descending modulatory pathways followed by descending pathways implicated in cannabinoid analgesia. We will then describe the recent evidence of the involvement of descending serotonergic and noradrenergic pathways in CB1 receptor-mediated antinociception. This review will provide evidences that systemically administered cannabinoids reinforce the descending serotonergic and noradrenergic pathways to produce acute antinociceptive effects via spinal 5-HT7, 5-HT2A and alpha-2 adrenoceptors activation.
        PMID: 22300745 [PubMed - as supplied by publisher]
    ]]></description>
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