D2-Like Receptor

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Praful S Singru - One of the best experts on this subject based on the ideXlab platform.

  • transient Receptor potential vanilloid 3 trpv3 in the ventral tegmental area of rat role in modulation of the mesolimbic dopamine reward pathway
    Neuropharmacology, 2016
    Co-Authors: Uday Singh, Santosh Kumar, Gajanan P Shelkar, Manoj Yadav, Dadasaheb M Kokare, Chandan Goswami, Ronald M Lechan, Praful S Singru
    Abstract:

    Abstract While dopamine (DA) neurons in the ventral tegmental area (VTA) drive the mesolimbic-reward pathway, confluent lines of evidence underscore the importance of transient Receptor potential vanilloid (TRPV) channels as novel regulators of these neurons. Among the TRPV-subfamily, TRPV3 is of particular interest in reward, since active ingredients of flavour-enhancing spices in food serve as TRPV3 agonists and modulate DAergic neurotransmission. The nature of TRPV3 elements in the VTA and their role in driving the mesolimbic-DA-reward pathway has however, remained unexplored. We observed TRPV3 mRNA as well as TRPV3-immunoreactive neurons in the VTA of Wistar rats. We therefore explored whether these ion channels participate in modulating mesolimbic-DA reward pathway. In the posterior VTA (pVTA), 82 ± 2.6% of the TRPV3 neurons co-express tyrosine hydroxylase and 68 ± 5.5% of these neurons project to the nucleus accumbens shell (Acb shell). While ex vivo treatment of midbrain slices with TRPV3-agonist, thymol increased [Ca2+]i-activity in pVTA neurons, intra-pVTA injections of thymol in freely-moving, satiated rats enhanced positive reinforcement for active lever pressings in an operant chamber to self-administer sweet pellets. This behavior was attenuated by prior treatment with intra-Acb shell DA D1- and D2-Like Receptor antagonists. These results demonstrate a role for TRPV3 in driving mesolimbic-DA food-reward pathway, and underscores the importance of these channels in the VTA as key components processing reward.

Richard J. Davidson - One of the best experts on this subject based on the ideXlab platform.

  • PET Evidence for a Role for Striatal Dopamine in the Attentional Blink: Functional Implications
    Journal of Cognitive Neuroscience, 2012
    Co-Authors: Heleen A. Slagter, Rachel Tomer, Bradley T. Christian, Lorenza S. Colzato, Carlye R. King, Dhanabalan Murali, Richard J. Davidson
    Abstract:

    Our outside world changes continuously, for example, when driving through traffic. An important question is how our brain deals with this constant barrage of rapidly changing sensory input and flexibly selects only newly goal-relevant information for further capacity-limited processing in working memory. The challenge our brain faces is experimentally captured by the attentional blink (AB): an impairment in detecting the second of two target stimuli presented in close temporal proximity among distracters. Many theories have been proposed to explain this deficit in processing goal-relevant information, with some attributing the AB to capacity limitations related to encoding of the first target and others assigning a critical role to on-line selection mechanisms that control access to working memory. The current study examined the role of striatal dopamine in the AB, given its known role in regulating the contents of working memory. Specifically, participants performed an AB task and their basal level of dopamine D2-Like Receptor binding was measured using PET and [F-18]fallypride. As predicted, individual differences analyses showed that greater D2-Like Receptor binding in the striatum was associated with a larger AB, implicating striatal dopamine and mechanisms that control access to working memory in the AB. Specifically, we propose that striatal dopamine may determine the AB by regulating the threshold for working memory updating, providing a testable physiological basis for this deficit in gating rapidly changing visual information. A challenge for current models of the AB lies in connecting more directly to these neurobiological data.

Ronald M Lechan - One of the best experts on this subject based on the ideXlab platform.

  • transient Receptor potential vanilloid 3 trpv3 in the ventral tegmental area of rat role in modulation of the mesolimbic dopamine reward pathway
    Neuropharmacology, 2016
    Co-Authors: Uday Singh, Santosh Kumar, Gajanan P Shelkar, Manoj Yadav, Dadasaheb M Kokare, Chandan Goswami, Ronald M Lechan, Praful S Singru
    Abstract:

    Abstract While dopamine (DA) neurons in the ventral tegmental area (VTA) drive the mesolimbic-reward pathway, confluent lines of evidence underscore the importance of transient Receptor potential vanilloid (TRPV) channels as novel regulators of these neurons. Among the TRPV-subfamily, TRPV3 is of particular interest in reward, since active ingredients of flavour-enhancing spices in food serve as TRPV3 agonists and modulate DAergic neurotransmission. The nature of TRPV3 elements in the VTA and their role in driving the mesolimbic-DA-reward pathway has however, remained unexplored. We observed TRPV3 mRNA as well as TRPV3-immunoreactive neurons in the VTA of Wistar rats. We therefore explored whether these ion channels participate in modulating mesolimbic-DA reward pathway. In the posterior VTA (pVTA), 82 ± 2.6% of the TRPV3 neurons co-express tyrosine hydroxylase and 68 ± 5.5% of these neurons project to the nucleus accumbens shell (Acb shell). While ex vivo treatment of midbrain slices with TRPV3-agonist, thymol increased [Ca2+]i-activity in pVTA neurons, intra-pVTA injections of thymol in freely-moving, satiated rats enhanced positive reinforcement for active lever pressings in an operant chamber to self-administer sweet pellets. This behavior was attenuated by prior treatment with intra-Acb shell DA D1- and D2-Like Receptor antagonists. These results demonstrate a role for TRPV3 in driving mesolimbic-DA food-reward pathway, and underscores the importance of these channels in the VTA as key components processing reward.

Rosario Moratalla - One of the best experts on this subject based on the ideXlab platform.

  • dopamine d3 Receptor modulates l dopa induced dyskinesia by targeting d1 Receptor mediated striatal signaling
    Cerebral Cortex, 2015
    Co-Authors: Ming Xu, Oscar Solis, Jose Ruben Garciamontes, Aldo Gonzalezgranillo, Rosario Moratalla
    Abstract:

    The dopamine D3 Receptor (D3R) belongs to the dopamine D2-Like Receptor family and is principally located in the ventral striatum. However, previous studies reported D3R overexpression in the dorsal striatum following l-DOPA treatment in parkinsonian animals. This fact has drawn attention in the importance of D3R in l-DOPA-induced dyskinesia (LID). Here, we used D3R knockout mice to assess the role of D3R in LID and rotational sensitization in the hemiparkinsonian model. Mice lacking D3R presented a reduction in dyskinesia without interfering with the antiparkinsonian l-DOPA effect and were accompanied by a reduction in the l-DOPA-induced rotations. Interestingly, deleting D3R attenuated important molecular markers in the D1R-neurons such as FosB, extracellular signal-regulated kinase, and histone-3 (H3)-activation. Colocalization studies in D1R-tomato and D2R-green fluorescent protein BAC-transgenic mice indicated that l-DOPA-induced D3R overexpression principally occurs in D1R-containing neurons although it is also present in the D2R-neurons. Moreover, D3R pharmacological blockade with PG01037 reduced dyskinesia and the molecular markers expressed in D1R-neurons. In addition, this antagonist further reduced dyskinetic symptoms in D1R heterozygous mice, indicating a direct interaction between D1R and D3R. Together, our results demonstrate that D3R modulates the development of dyskinesia by targeting D1R-mediated intracellular signaling and suggest that decreasing D3R activity may help to ameliorate LID.

Toshitaka Nabeshima - One of the best experts on this subject based on the ideXlab platform.

  • discriminative stimulus effects of methamphetamine and morphine in rats are attenuated by camp related compounds
    Behavioural Brain Research, 2006
    Co-Authors: Yijin Yan, Atsumi Nitta, Tomoko Mizuno, Akira Nakajima, Kiyofumi Yamada, Toshitaka Nabeshima
    Abstract:

    Animal models of drug discrimination have been used to examine the subjective effects of addictive substances. The cAMP system is a crucial downstream signaling pathway implicated in the long-lasting neuroadaptations induced by addictive drugs. We examined effects of rolipram, nefiracetam, and dopamine D2-Like Receptor antagonists, all of which have been reported to modulate cAMP level in vivo, on the discriminative-stimulus effects of methamphetamine (METH) and morphine in rats. All these compounds inhibited the discriminative-stimulus effects of METH, while only rolipram and nefiracetam attenuated the discriminative-stimulus effects of morphine. In addition, neither nifedipine nor neomycin, two voltage-sensitive calcium channel blockers, was found to modulate the effect of nefiracetam on METH-associated discriminative stimuli, suggesting that the inhibitory effect of nefiracetam may not involve the activation of calcium channels. These findings suggest that the cAMP signaling cascade may play a key role in the discriminative-stimulus effects of METH and morphine and may be a potential target for the development of therapeutics to counter drugs of abuse.