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Dopamine Modulation (dopamine + modulation)

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Life Sciences	100%

Selected Abstracts

Dopamine modulation of the In vivo acetylcholine response in the Drosophila mushroom body

DEVELOPMENTAL NEUROBIOLOGY, Issue 11 2009
Vitold Tsydzik
Abstract Olfactory sensory information in Drosophila is transmitted through antennal lobe projections to Mushroom Body neurons (Kenyon cells) by means of cholinergic synapses. Application of acetylcholine (ACh) and odors produce significant increases in intracellular calcium ([Ca2+]i) in these neurons. Behavioral studies show that Kenyon cell activity is modulated by dopaminergic inputs and this modulation is thought to be the basis for an olfactory conditioned response. However, quantitative assessment of the synaptic inputs to Kenyon cells is currently lacking. To assess neuronal activity under in vivo conditions, we have used the endogenously-expressed camgaroo reporter to measure [Ca2+]i in these neurons. We report here the dose-response relationship of Kenyon cells for ACh and dopamine (DA). Importantly, we also show that simultaneous application of ACh and DA results in a significant decrease in the response to ACh alone. In addition, we show inhibition of the ACh response by cyclic adenosine monophosphate. This is the first quantitative assessment of the effects of these two important transmitters in this system, and it provides an important basis for future analysis of the cellular mechanisms of this well established model for associative olfactory learning. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2009 [source]

Dopamine modulation of excitatory currents in the striatum is dictated by the expression of D1 or D2 receptors and modified by endocannabinoids

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2010
Véronique M. André
Abstract Striatal medium-sized spiny neurons (MSSNs) receive glutamatergic inputs modulated presynaptically and postsynaptically by dopamine. Mice expressing the gene for enhanced green fluorescent protein as a reporter gene to identify MSSNs containing D1 or D2 receptor subtypes were used to examine dopamine modulation of spontaneous excitatory postsynaptic currents (sEPSCs) in slices and postsynaptic N -methyl- d -aspartate (NMDA) and ,-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) currents in acutely isolated cells. The results demonstrated dopamine receptor-specific modulation of sEPSCs. Dopamine and D1 agonists increased sEPSC frequency in D1 receptor-expressing MSSNs (D1 cells), whereas dopamine and D2 agonists decreased sEPSC frequency in D2 receptor-expressing MSSNs (D2 cells). These effects were fully (D1 cells) or partially (D2 cells) mediated through retrograde signaling via endocannabinoids. A cannabinoid 1 receptor (CB1R) agonist and a blocker of anandamide transporter prevented the D1 receptor-mediated increase in sEPSC frequency in D1 cells, whereas a CB1R antagonist partially blocked the decrease in sEPSC frequency in D2 cells. At the postsynaptic level, low concentrations of a D1 receptor agonist consistently increased NMDA and AMPA currents in acutely isolated D1 cells, whereas a D2 receptor agonist decreased these currents in acutely isolated D2 cells. These results show that both glutamate release and postsynaptic excitatory currents are regulated in opposite directions by activation of D1 or D2 receptors. The direction of this regulation is also specific to D1 and D2 cells. We suggest that activation of postsynaptic dopamine receptors controls endocannabinoid mobilization, acting on presynaptic CB1Rs, thus modulating glutamate release differently in glutamate terminals projecting to D1 and D2 cells. [source]

Suppression of excitatory cholinergic synaptic transmission by Drosophila dopamine D1-like receptors

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2007
Ning Yuan
Abstract The physiological function of dopamine is mediated through its G-protein-coupled receptor family. In Drosophila, four dopamine receptors have been molecularly characterized so far. However, due largely to the absence of a suitable preparation, the role of Drosophila dopamine receptors in modulating central synaptic transmission has not been examined. The present study investigated mechanisms by which dopamine modulates excitatory cholinergic synaptic transmission in Drosophila using primary neuronal cultures. Whole-cell recordings demonstrated that cholinergic excitatory postsynaptic currents (EPSCs) were down-regulated by focally applied dopamine (10,500 µm). The vertebrate D1 specific agonists SKF38393 and 6-chloro-APB (10 µm) mimicked dopamine-mediated suppression of cholinergic synaptic transmission with higher potency. In contrast, the D2 agonists quinpirole and bromocriptine did not alter cholinergic EPSCs, demonstrating that dopamine-mediated suppression of cholinergic synaptic transmission is specifically through activation of Drosophila D1-like receptors. Biophysical analysis of miniature EPSCs indicated that cholinergic suppression by activation of D1-like receptors is presynaptic in origin. Dopamine modulation of cholinergic transmission is not mediated through the cAMP/protein kinase A signaling pathway as cholinergic suppression by dopamine occurred in the presence of the protein kinase A inhibitor H-89. In addition, an adenylate cyclase activator, forskolin, led to an increase, not a decrease, of cholinergic EPSC frequency. Finally, we showed that activation of D1-like receptors decreased the frequency of action potentials in cultured Drosophila neurons by inhibiting excitatory cholinergic transmission. All our data demonstrated that activation of D1-like receptors in Drosophila neurons negatively modulates excitatory cholinergic synaptic transmission and thus inhibits neuronal excitability. [source]

Dopamine modulation of excitatory currents in the striatum is dictated by the expression of D1 or D2 receptors and modified by endocannabinoids

Dopamine transporter knock-out mice are hypersensitive to 3-nitropropionic acid-induced striatal damage

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2002
Pierre-O.
Abstract Evidence suggests that dopamine is involved in the modulation of striatal excitotoxic processes. To further investigate this issue, we studied the effects of systemic ,low-dose' (total dose, 340 mg/kg in 7 days) 3-nitropropionic acid (3-NP) intoxication in dopamine transporter knock-out mice (DAT,/,) compared to wildtype (DAT+/+) mice. Systemic ,low-dose' 3-NP induced a significant impairment in a rotarod task only in DAT,/, mice. Histopathology also demonstrated a significant reduction of the striatal volume (,7%, P < 0.05), neuronal density (,12.5%, P < 0.001) and absolute number estimates of striatal neurons (,11.5%, P < 0.001) in DAT,/, compared to DAT+/+ mice, with increased glial activation, independent of the degree of succinate dehydrogenase inhibition. These findings strengthen the hypothesis for dopamine modulation of excitotoxicity within the nigrostriatal system. [source]