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G D Shorten - One of the best experts on this subject based on the ideXlab platform.

Anna Dreber - One of the best experts on this subject based on the ideXlab platform.

  • the 7r polymorphism in the Dopamine Receptor d4 gene drd4 is associated with financial risk taking in men
    Evolution and Human Behavior, 2009
    Co-Authors: Anna Dreber, Coren L Apicella, Daniel Eisenberg, Justin R Garcia, Richard S Zamore, Benjamin C Campbell
    Abstract:

    Individuals exhibit substantial heterogeneity in financial risk aversion. Recent work on twins demonstrated that some variation is influenced by individual heritable differences. Despite this, there has been no study investigating possible genetic loci associated with financial risk taking in healthy individuals. Here, we examined whether there is an association between financial risk preferences, elicited experimentally in a game with real monetary payoffs, and the presence of the 7-repeat allele (7R+) in the Dopamine Receptor D4 gene as well as the presence of the A1 allele (A1+) in the Dopamine Receptor D2 gene in 94 young men. Although we found no association between the A1

Jeancharles Schwartz - One of the best experts on this subject based on the ideXlab platform.

Benjamin C Campbell - One of the best experts on this subject based on the ideXlab platform.

  • the 7r polymorphism in the Dopamine Receptor d4 gene drd4 is associated with financial risk taking in men
    Evolution and Human Behavior, 2009
    Co-Authors: Anna Dreber, Coren L Apicella, Daniel Eisenberg, Justin R Garcia, Richard S Zamore, Benjamin C Campbell
    Abstract:

    Individuals exhibit substantial heterogeneity in financial risk aversion. Recent work on twins demonstrated that some variation is influenced by individual heritable differences. Despite this, there has been no study investigating possible genetic loci associated with financial risk taking in healthy individuals. Here, we examined whether there is an association between financial risk preferences, elicited experimentally in a game with real monetary payoffs, and the presence of the 7-repeat allele (7R+) in the Dopamine Receptor D4 gene as well as the presence of the A1 allele (A1+) in the Dopamine Receptor D2 gene in 94 young men. Although we found no association between the A1

Benjamin Weiss - One of the best experts on this subject based on the ideXlab platform.

  • Intrastriatal administration of an oligodeoxynucleotide antisense to the D2 Dopamine Receptor mRNA inhibits D2 Dopamine Receptor-mediated behavior and D2 Dopamine Receptors in normal mice and in mice lesioned with 6-hydroxyDopamine
    Neurochemistry International, 1996
    Co-Authors: Long-wu Zhou, Sui-po Zhang, Benjamin Weiss
    Abstract:

    Abstract Previous studies have shown that the intracerebroventricular injection of antisense oligodeoxynucleotides targeted to the mRNAs encoding the different subtypes of Dopamine Receptors inhibited behaviors mediated by these Receptors. The present studies were designed to determine whether such antisense oligodeoxynucleotides could produce similar effects when injected into a discrete brain area. A D 2 Dopamine Receptor antisense oligodeoxynucleotide (D 2 antisense) was repeatedly injected into one corpus striatum of either normal mice or mice with unilateral lesions of the striatum induced by 6-hydroxyDopamine. In the latter, intrastriatal injection of D 2 antisense blocked the contralateral rotational behavior induced by the parenteral administration of the D 2 Dopamine Receptor agonist quinpirole. The inhibitory effect of D 2 antisense was dose- and time-related and was reversed upon cessation of D 2 antisense treatment. This inhibitory effect was also selective in that D 2 antisense treatment inhibited the rotational behavior induced by quinpirole but not that induced by the D 1 Dopamine Receptor agonist SKF 38393 or by the muscarinic cholinergic agonist oxotremorine. Following repeated intrastriatal injections of D 2 antisense into normal mice, parenteral administration of quinpirole caused rotational behavior ipsilateral to the side in which the D 2 antisense was injected. No such rotational behavior was seen when similarly treated mice were challenged with SKF 38393 or oxotremorine. The quinpirole-induced rotational behavior in mice given intrastriatal injections of D 2 antisense disappeared upon cessation of D 2 antisense treatment. Repeated intrastriatal administration of D 2 antisense also caused a significant reduction in the levels of D 2 , but not D 1 , Dopamine Receptors in striatum, as determined by Receptor autoradiography. The levels of D 2 Dopamine Receptors returned to normal upon cessation of D 2 antisense treatment. Intrastriatal administration of an oligodeoxynucleotide with randomly placed nucleotides failed to alter the rotational response to quinpirole in either 6-hydroxyDopamine-lesioned or normal mice and failed to alter the levels of D 2 Dopamine Receptors in striatum. These results show that selective inhibition of behavioral responses mediated by D 2 Dopamine Receptors can be achieved by the direct injection of a D 2 antisense oligodeoxynucleotide into a discrete brain area. Copyright © 1996 Elsevier Science Ltd

  • Uptake and distribution of fluorescein-labeled D_2 Dopamine Receptor antisense oligodeoxynucleotide in mouse brain
    Journal of Molecular Neuroscience, 1996
    Co-Authors: Sui-po Zhang, Long-wu Zhou, Mark Morabito, Rick C. S. Lin, Benjamin Weiss
    Abstract:

    To determine the uptake and distribution of oligodeoxynucleotides in brain, a 20-mer phosphorothioated oligodeoxynucleotide complementary to a portion of the D_2 Dopamine Receptor mRNA was fluorescently labeled with fluorescein isothiocyanate (FITC) and injected into the lateral cerebral ventricles of mice. At various survival times after the injection, the brains were removed, fixed, sectioned, and viewed under a fluorescent microscope. The results showed that the oligodeoxynucleotide was rapidly taken up into the brain. Initially the label was relatively diffusely spread throughout the interstitial spaces of the brain, then became redistributed to the cellular compartments. The signal extended from those forebrain nuclei located immediately in contact with the ventricles, such as the corpus striatum, septum, and hippocampus, to areas further removed from the ventricles, such as the cerebral cortex, nucleus accumbens, and substantia nigra. When the FITC-labeled D_2 antisense oligodeoxynucleotide was given once daily for 4 d, the signal intensity seen 24 h after the last injection appeared to be of greater intensity overall compared to that seen after a single injection. At early time-points the oligodeoxynucleotide signals appeared to be punctuated and were found in cell bodies as well as in proximal dendritic processes. However, not all cells were equally labeled, suggesting an uneven uptake and accumulation of the D_2 antisense into the various cell types. At later time-points the fluorescent signal appeared granular; at these times the injected material was largely degraded. These studies show that a D_2 Dopamine Receptor antisense oligodeoxynucleotide is rapidly taken up from cerebral ventricles into brain, becomes widely distributed throughout the brain tissue to areas far removed from direct contact with the ventricles, and appears to accumulate to a different extent in the various brain areas and cell types.

  • Irreversible blockade of D2 Dopamine Receptors by fluphenazine-N-mustard increases D2 Dopamine Receptor mRNA and proenkephalin mRNA and decreases D1 Dopamine Receptor mRNA and mu and delta opioid Receptors in rat striatum.
    Neurochemistry International, 1994
    Co-Authors: Jiang Fan Chen, Vincent J. Aloyo, Benjamin Weiss
    Abstract:

    Abstract The consequences of irreversibly-inhibiting D2 Dopaminergic Receptors on the expression of D1 and D2 Dopamine Receptor mRNAs and proenkephalin mRNA and on the level of μ- and δ-opioid Receptors in rat striatum were studied following single or repeated administration of the irreversibly-acting D2 Dopamine Receptor antagonist, fluphenazine-N-mustard (FNM). The density of Dopamine and opioid Receptors was determined by Receptor autoradiography and the levels of the mRNA for the D1 and D2 Dopamine Receptors and proenkephalin were measured by in situ hybridization histochemistry. Repeated treatment of rats with FNM for 6 days produced more than 80% inhibition of D2 Dopamine Receptors but less than 25% inhibition of D1 Dopamine Receptors. Repeated treatment with FNM also resulted in statistically significant increases in D2 Dopamine Receptor mRNA but decreases in D1 Dopamine Receptor mRNA. In contrast, acute treatment with FNM for 3 h had no significant effects on D1 or D2 Dopamine Receptor mRNAs in striatum. An examination of the effects of FNM on the opioid system showed that repeated treatment with FNM for 6 days produced more than a 2-fold increase in the expression of proenkephalin mRNA in striatum. This was accompanied by significant decreases in μ- and δ-opioid Receptors in striatum, mainly by reducing the size of the patch compartment of striatum. Acute treatment with FNM for 3 h produced small increases in proenkephalin mRNA and μ-opioid Receptors in striatum but had no significant effects on δ-opioid Receptors. These results suggest that persistent inhibition of D2 Dopamine Receptors differentially regulates the expression of D1 and D2 Dopamine Receptor mRNA in striatum, and that the magnitude, duration and interval of inhibiting Dopaminergic transmission may be important factors in regulating Dopamine Receptor mRNA expression. These results also suggest that D2 Dopamine antagonists indirectly down-regulate opioid Receptors by increasing the expression of proenkephalin mRNA, thereby increasing enkephalin which, in turn, decreases opioid Receptors in striatum.

  • D2 Dopamine Receptor messenger RNA is altered to a greater extent by blockade of glutamate Receptors than by blockade of Dopamine Receptors
    Neuroscience, 1994
    Co-Authors: L.-w. Zhou, Benjamin Weiss
    Abstract:

    Abstract To study further the molecular mechanisms by which glutamate and Dopamine interact to regulate the functions of the basal ganglia, the effects of persistently inhibiting Dopamine Receptors and glutamate N -methyl- d -aspartate Receptors on the density of D 1 and D 2 Dopamine Receptors and on the level of their transcripts were examined in mouse brain. To block Dopamine Receptors, mice were treated with N -ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline once daily for two and six days, or were treated with fluphenazine- N -mustard once daily for five days. To block N -methyl- d -aspartate Receptors, mice were treated with dizocilpine by continuous infusion with osmotic mini-pumps for two and six days. The density of D 1 and D 2 Dopamine Receptors was measured by Receptor autoradiography, and the level of D 1 and D 2 Dopamine Receptor messenger RNA was measured by in situ hybridization histochemistry. The results showed that N -ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline blocked about 90% of both D 1 and D 2 Dopamine Receptors, but had no significant effect on the level of either D 1 or D 2 Dopamine Receptor messenger RNA. Fluphenazine- N -mustard, which was as effective as N -ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline in blocking D 2 Dopamine Receptors but had little effect on D 1 Dopamine Receptors, also had no significant effect on the level of D 1 and D 2 Dopamine Receptor messenger RNAs. By contrast, continuously infusing dizocilpine significantly decreased the levels of D 2 Dopamine Receptor messenger RNA in striatum, nucleus accumbens and olfactory tubercle. Dizocilpine also caused small decreases in the density of D 2 Dopamine Receptors, but only in posterior striatum was this decrease statistically significant. Dizocilpine slightly and transiently decreased the levels of D 1 Dopamine Receptor messenger RNA in striatum but had no significant effect on the density of D 1 Dopamine Receptors in any region examined. This study demonstrates that persistent blockade of D 1 and D 2 Dopamine Receptors has relatively little effect on the levels of D 1 and D 2 Dopamine Receptor messenger RNA, but that blockade of N -methyl- d -aspartate Receptors produces a rapid and profound decrease in the levels of D 2 Dopamine Receptor messenger RNA and a smaller decrease in the density of D 2 Dopamine Receptors. These results suggest that N -methyl- d -aspartate Receptors play an important role in the expression of D 2 Dopamine Receptors in basal ganglia.

  • In vivo administration of an oligodeoxynucleotide antisense to the D2 Dopamine Receptor messenger RNA inhibits D2 Dopamine Receptor-mediated behavior and the expression of D2 Dopamine Receptors in mouse striatum.
    Journal of Pharmacology and Experimental Therapeutics, 1994
    Co-Authors: Long-wu Zhou, Sui-po Zhang, Benjamin Weiss
    Abstract:

    A 20-mer phosphorothioate oligodeoxynucleotide (D2 antisense) to the D2 antisense Dopamine Receptor messenger RNA (mRNA) was administered i.c.v. to mice with unilateral 6-hydroxyDopamine lesions of the corpus striatum. The mice were then challenged with acute injections of various agents that cause contralateral rotational behavior, and the levels of D1 and D2 Dopamine Receptors and their respective mRNAs were determined in the corpus striatum. Administering the D2 antisense inhibited rotations induced by the D2 Dopamine Receptor agonists quinpirole and N-propyl-N-2-thienylethylamine-5-hydroxytetralin but did not block rotations induced by the D1 Dopamine Receptor agonist 1-phenyl-2,3,4,5-tetrahydro-1H-3 benzazepine-7,8-diol HCl or by the muscarinic cholinergic Receptor agonist oxotremorine. The reduction in quinpirole-induced rotational behavior was related to the amount and length of time the D2 antisense was given. Significant reductions in behavior were seen within 1 day of repeated injections of D2 antisense, and almost complete inhibition was seen after 6 days of treatment. Recovery from inhibition occurred by 2 days after cessation of antisense treatment. Repeated treatment with D2 antisense significantly reduced the levels of D2 Dopamine Receptors and D2 Dopamine Receptor mRNA, but not the levels of D1 Receptors or D1 mRNA, in the dorsolateral area of the lesioned striatum. Treatment with an oligodeoxynucleotide with randomly placed nucleotides did not inhibit quinpirole-induced rotations or alter D2 Dopamine Receptors or D2 Dopamine Receptor mRNA in either area of striatum.(ABSTRACT TRUNCATED AT 250 WORDS)