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Joaquim A. Ribeiro - One of the best experts on this subject based on the ideXlab platform.
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dopamine galanin Receptor heteromers modulate cholinergic neurotransmission in the rat ventral hippocampus
The Journal of Neuroscience, 2011Co-Authors: Estefania Moreno, César Quiroz, Carme Lluis, Carla Ferrada, Sandeep Kumar Barodia, Nadine Kabbani, Peter J Mccormick, Enric I. Canela, Rafael Franco, Joaquim A. RibeiroAbstract:Previous studies have shown that dopamine and galanin modulate cholinergic transmission in the hippocampus, but little is known about the mechanisms involved and their possible interactions. By using resonance energy transfer techniques in transfected mammalian cells, we demonstrated the existence of heteromers between the dopamine D1-Like Receptors (D1 and D5) and galanin Gal1, but not Gal2 Receptors. Within the D1–Gal1 and D5–Gal1 Receptor heteromers, dopamine Receptor activation potentiated and dopamine Receptor blockade counteracted MAPK activation induced by stimulation of Gal1 Receptors, whereas Gal1 Receptor activation or blockade did not modify D1-Like Receptor-mediated MAPK activation. Ability of a D1-Like Receptor antagonist to block galanin-induced MAPK activation (cross-antagonism) was used as a “biochemical fingerprint” of D1-Like–Gal1 Receptor heteromers, allowing their identification in the rat ventral hippocampus. The functional role of D1-Like–Gal Receptor heteromers was demonstrated in synaptosomes from rat ventral hippocampus, where galanin facilitated acetylcholine release, but only with costimulation of D1-Like Receptors. Electrophysiological experiments in rat ventral hippocampal slices showed that these Receptor interactions modulate hippocampal synaptic transmission. Thus, a D1-Like Receptor agonist that was ineffective when administered alone turned an inhibitory effect of galanin into an excitatory effect, an interaction that required cholinergic neurotransmission. Altogether, our results strongly suggest that D1-Like–Gal1 Receptor heteromers act as processors that integrate signals of two different neurotransmitters, dopamine and galanin, to modulate hippocampal cholinergic neurotransmission.
Estefania Moreno - One of the best experts on this subject based on the ideXlab platform.
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dopamine galanin Receptor heteromers modulate cholinergic neurotransmission in the rat ventral hippocampus
The Journal of Neuroscience, 2011Co-Authors: Estefania Moreno, César Quiroz, Carme Lluis, Carla Ferrada, Sandeep Kumar Barodia, Nadine Kabbani, Peter J Mccormick, Enric I. Canela, Rafael Franco, Joaquim A. RibeiroAbstract:Previous studies have shown that dopamine and galanin modulate cholinergic transmission in the hippocampus, but little is known about the mechanisms involved and their possible interactions. By using resonance energy transfer techniques in transfected mammalian cells, we demonstrated the existence of heteromers between the dopamine D1-Like Receptors (D1 and D5) and galanin Gal1, but not Gal2 Receptors. Within the D1–Gal1 and D5–Gal1 Receptor heteromers, dopamine Receptor activation potentiated and dopamine Receptor blockade counteracted MAPK activation induced by stimulation of Gal1 Receptors, whereas Gal1 Receptor activation or blockade did not modify D1-Like Receptor-mediated MAPK activation. Ability of a D1-Like Receptor antagonist to block galanin-induced MAPK activation (cross-antagonism) was used as a “biochemical fingerprint” of D1-Like–Gal1 Receptor heteromers, allowing their identification in the rat ventral hippocampus. The functional role of D1-Like–Gal Receptor heteromers was demonstrated in synaptosomes from rat ventral hippocampus, where galanin facilitated acetylcholine release, but only with costimulation of D1-Like Receptors. Electrophysiological experiments in rat ventral hippocampal slices showed that these Receptor interactions modulate hippocampal synaptic transmission. Thus, a D1-Like Receptor agonist that was ineffective when administered alone turned an inhibitory effect of galanin into an excitatory effect, an interaction that required cholinergic neurotransmission. Altogether, our results strongly suggest that D1-Like–Gal1 Receptor heteromers act as processors that integrate signals of two different neurotransmitters, dopamine and galanin, to modulate hippocampal cholinergic neurotransmission.
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Dopamine–Galanin Receptor Heteromers Modulate Cholinergic Neurotransmission in the Rat Ventral Hippocampus
The Journal of Neuroscience, 2011Co-Authors: Estefania Moreno, César Quiroz, Carla Ferrada, Sandeep Kumar Barodia, Nadine Kabbani, Peter J Mccormick, Enric I. Canela, Carme LluisAbstract:Previous studies have shown that dopamine and galanin modulate cholinergic transmission in the hippocampus, but little is known about the mechanisms involved and their possible interactions. By using resonance energy transfer techniques in transfected mammalian cells, we demonstrated the existence of heteromers between the dopamine D1-Like Receptors (D1 and D5) and galanin Gal1, but not Gal2 Receptors. Within the D1–Gal1 and D5–Gal1 Receptor heteromers, dopamine Receptor activation potentiated and dopamine Receptor blockade counteracted MAPK activation induced by stimulation of Gal1 Receptors, whereas Gal1 Receptor activation or blockade did not modify D1-Like Receptor-mediated MAPK activation. Ability of a D1-Like Receptor antagonist to block galanin-induced MAPK activation (cross-antagonism) was used as a “biochemical fingerprint” of D1-Like–Gal1 Receptor heteromers, allowing their identification in the rat ventral hippocampus. The functional role of D1-Like–Gal Receptor heteromers was demonstrated in synaptosomes from rat ventral hippocampus, where galanin facilitated acetylcholine release, but only with costimulation of D1-Like Receptors. Electrophysiological experiments in rat ventral hippocampal slices showed that these Receptor interactions modulate hippocampal synaptic transmission. Thus, a D1-Like Receptor agonist that was ineffective when administered alone turned an inhibitory effect of galanin into an excitatory effect, an interaction that required cholinergic neurotransmission. Altogether, our results strongly suggest that D1-Like–Gal1 Receptor heteromers act as processors that integrate signals of two different neurotransmitters, dopamine and galanin, to modulate hippocampal cholinergic neurotransmission.
Carme Lluis - One of the best experts on this subject based on the ideXlab platform.
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dopamine galanin Receptor heteromers modulate cholinergic neurotransmission in the rat ventral hippocampus
The Journal of Neuroscience, 2011Co-Authors: Estefania Moreno, César Quiroz, Carme Lluis, Carla Ferrada, Sandeep Kumar Barodia, Nadine Kabbani, Peter J Mccormick, Enric I. Canela, Rafael Franco, Joaquim A. RibeiroAbstract:Previous studies have shown that dopamine and galanin modulate cholinergic transmission in the hippocampus, but little is known about the mechanisms involved and their possible interactions. By using resonance energy transfer techniques in transfected mammalian cells, we demonstrated the existence of heteromers between the dopamine D1-Like Receptors (D1 and D5) and galanin Gal1, but not Gal2 Receptors. Within the D1–Gal1 and D5–Gal1 Receptor heteromers, dopamine Receptor activation potentiated and dopamine Receptor blockade counteracted MAPK activation induced by stimulation of Gal1 Receptors, whereas Gal1 Receptor activation or blockade did not modify D1-Like Receptor-mediated MAPK activation. Ability of a D1-Like Receptor antagonist to block galanin-induced MAPK activation (cross-antagonism) was used as a “biochemical fingerprint” of D1-Like–Gal1 Receptor heteromers, allowing their identification in the rat ventral hippocampus. The functional role of D1-Like–Gal Receptor heteromers was demonstrated in synaptosomes from rat ventral hippocampus, where galanin facilitated acetylcholine release, but only with costimulation of D1-Like Receptors. Electrophysiological experiments in rat ventral hippocampal slices showed that these Receptor interactions modulate hippocampal synaptic transmission. Thus, a D1-Like Receptor agonist that was ineffective when administered alone turned an inhibitory effect of galanin into an excitatory effect, an interaction that required cholinergic neurotransmission. Altogether, our results strongly suggest that D1-Like–Gal1 Receptor heteromers act as processors that integrate signals of two different neurotransmitters, dopamine and galanin, to modulate hippocampal cholinergic neurotransmission.
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Dopamine–Galanin Receptor Heteromers Modulate Cholinergic Neurotransmission in the Rat Ventral Hippocampus
The Journal of Neuroscience, 2011Co-Authors: Estefania Moreno, César Quiroz, Carla Ferrada, Sandeep Kumar Barodia, Nadine Kabbani, Peter J Mccormick, Enric I. Canela, Carme LluisAbstract:Previous studies have shown that dopamine and galanin modulate cholinergic transmission in the hippocampus, but little is known about the mechanisms involved and their possible interactions. By using resonance energy transfer techniques in transfected mammalian cells, we demonstrated the existence of heteromers between the dopamine D1-Like Receptors (D1 and D5) and galanin Gal1, but not Gal2 Receptors. Within the D1–Gal1 and D5–Gal1 Receptor heteromers, dopamine Receptor activation potentiated and dopamine Receptor blockade counteracted MAPK activation induced by stimulation of Gal1 Receptors, whereas Gal1 Receptor activation or blockade did not modify D1-Like Receptor-mediated MAPK activation. Ability of a D1-Like Receptor antagonist to block galanin-induced MAPK activation (cross-antagonism) was used as a “biochemical fingerprint” of D1-Like–Gal1 Receptor heteromers, allowing their identification in the rat ventral hippocampus. The functional role of D1-Like–Gal Receptor heteromers was demonstrated in synaptosomes from rat ventral hippocampus, where galanin facilitated acetylcholine release, but only with costimulation of D1-Like Receptors. Electrophysiological experiments in rat ventral hippocampal slices showed that these Receptor interactions modulate hippocampal synaptic transmission. Thus, a D1-Like Receptor agonist that was ineffective when administered alone turned an inhibitory effect of galanin into an excitatory effect, an interaction that required cholinergic neurotransmission. Altogether, our results strongly suggest that D1-Like–Gal1 Receptor heteromers act as processors that integrate signals of two different neurotransmitters, dopamine and galanin, to modulate hippocampal cholinergic neurotransmission.
Rita A. Fuchs - One of the best experts on this subject based on the ideXlab platform.
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Cocaine seeking and taking: role of hippocampal dopamine D1-Like Receptors.
The International Journal of Neuropsychopharmacology, 2014Co-Authors: Audrey M. Wells, Rita A. FuchsAbstract:Despite the well-documented involvement of dopamine D1-Like Receptor stimulation in cocaine-induced goal-directed behaviours, little is known about the specific contribution of D1-Like Receptor populations in the dorsal hippocampus (DH) to drug context-induced cocaine-seeking or drug-reinforced instrumental behaviours. To investigate this question, rats were trained to lever press for un-signalled cocaine infusions in a distinct context followed by extinction training in a different context. Cocaine-seeking behaviour (non-reinforced lever responding) was then assessed in the previously cocaine-paired and extinction contexts. SCH23390-induced D1-Like Receptor antagonism in the DH, but not the overlying trunk region of the somatosensory cortex, dose-dependently inhibited drug context-induced cocaine-seeking behaviour, without altering cocaine-reinforced instrumental responding, cocaine intake, food-reinforced instrumental responding, or general motor activity, relative to vehicle treatment. These findings suggest that D1-Like Receptor stimulation in the DH is critical for the incentive motivational effects and/or memory of cocaine-paired contextual stimuli that contribute to drug-seeking behaviour.
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contribution of a mesocorticolimbic subcircuit to drug context induced reinstatement of cocaine seeking behavior in rats
Neuropsychopharmacology, 2014Co-Authors: Heather C Lasseter, Audrey M. Wells, Amy A Arguello, Matthew A Hodges, Rita A. FuchsAbstract:Cocaine-seeking behavior triggered by drug-paired environmental context exposure is dependent on orbitofrontal cortex (OFC)–basolateral amygdala (BLA) interactions. Here, we present evidence supporting the hypothesis that dopaminergic input from the ventral tegmental area (VTA) to the OFC critically regulates these interactions. In experiment 1, we employed site-specific pharmacological manipulations to show that dopamine D1-Like Receptor stimulation in the OFC is required for drug context-induced reinstatement of cocaine-seeking behavior following extinction training in an alternate context. Intra-OFC pretreatment with the dopamine D1-Like Receptor antagonist, SCH23390, dose-dependently attenuated cocaine-seeking behavior in an anatomically selective manner, without altering motor performance. Furthermore, the effects of SCH23390 could be surmounted by co-administration of a sub-threshold dose of the D1-Like Receptor agonist, SKF81297. In experiment 2, we examined effects of D1-Like Receptor antagonism in the OFC on OFC-BLA interactions using a functional disconnection manipulation. Unilateral SCH23390 administration into the OFC plus GABA agonist-induced neural inactivation of the contralateral or ipsilateral BLA disrupted drug context-induced cocaine-seeking behavior relative to vehicle, while independent unilateral manipulations of these brain regions were without effect. Finally, in experiment 3, we used fluorescent retrograde tracers to demonstrate that the VTA, but not the substantia nigra, sends dense intra- and interhemispheric projections to the OFC, which in turn has reciprocal bi-hemispheric connections with the BLA. These findings support that dopaminergic input from the VTA, via dopamine D1-Like Receptor stimulation in the OFC, is required for OFC–BLA functional interactions. Thus, a VTA–OFC–BLA neural circuit promotes drug context-induced motivated behavior.
Mustafa F. Lokhandwala - One of the best experts on this subject based on the ideXlab platform.
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Potential Dopamine-1 Receptor Stimulation in Hypertension Management
Current Hypertension Reports, 2011Co-Authors: Mohammad Asghar, Seyed Khosrow Tayebati, Mustafa F. Lokhandwala, Tahir HussainAbstract:The role of dopamine Receptors in blood pressure regulation is well established. Genetic ablation of both dopamine D1-Like Receptor subtypes (D1, D5) and D2-like Receptor subtypes (D2, D3, D4) results in a hypertensive phenotype in mice. This review focuses on the dopamine D1-Like Receptor subtypes D1 and D5 (especially D1 Receptors), as they play a major role in regulating sodium homeostasis and blood pressure. Studies mostly describing the role of renal dopamine D1-Like Receptors are included, as the kidneys play a pivotal role in the maintenance of sodium homeostasis and the long-term regulation of blood pressure. We also attempt to describe the interaction between D1-Like Receptors and other proteins, especially angiotensin II type 1 and type 2 Receptors, which are involved in the maintenance of sodium homeostasis and blood pressure. Finally, we discuss a new concept of renal D1 Receptor regulation in hypertension that involves oxidative stress mechanisms.
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Tempol reduces oxidative stress and restores renal dopamine D1-Like Receptor- G protein coupling and function in hyperglycemic rats.
American Journal of Physiology-renal Physiology, 2006Co-Authors: Aditi Marwaha, Mustafa F. LokhandwalaAbstract:Dopamine via activation of renal D1-Like Receptors inhibits the activities of Na-K-ATPase and Na/H exchanger and subsequently increases sodium excretion. Decreased renal dopamine production and sod...
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Hydrogen peroxide causes uncoupling of dopamine D1-Like Receptors from G proteins via a mechanism involving protein kinase C and G-protein-coupled Receptor kinase 2.
Free Radical Biology and Medicine, 2005Co-Authors: Mohammad Asghar, Anees Ahmad Banday, Riham Zein Fardoun, Mustafa F. LokhandwalaAbstract:Abstract Dopamine, via activation of D1-Like Receptors, inhibits Na,K-ATPase and Na,H-exchanger in renal proximal tubules and promotes sodium excretion. This effect of dopamine is not seen in conditions associated with oxidative stress such as hypertension, diabetes, and aging due to uncoupling of D1-Like Receptors from G proteins. To identify the role of oxidative stress in uncoupling of the D1-Like Receptors, we utilized primary cultures from rat renal proximal tubules. Hydrogen peroxide (H2O2), an oxidant, treatment to the cell cultures increased the level of malondialdehyde, a marker of oxidative damage. Further, H2O2 decreased membranous D1-Like Receptor numbers and proteins, D1-Like agonist (SKF 38393)-mediated [35S]GTPγS binding and SKF 38393-mediated inhibition of Na,K-ATPase. Moreover, H2O2 treatment to the cultures caused membranous translocation of G-protein-coupled Receptor kinase 2 (GRK 2) and increased serine phosphorylation of D1A Receptors accompanied by an increase in protein kinase C (PKC) activity. Interestingly, PKC inhibitors blocked the H2O2-mediated stimulation of GRK 2 and serine phosphorylation of D1A Receptors. Further, GRK 2 antisense but not scrambled oligonucleotides attenuated the effect of H2O2 on membranous expression of GRK 2. Moreover, direct activation of PKC with phorbol ester (PMA) resulted in reduction of SKF 38393-mediated [35S]GTPγS binding. We conclude that H2O2 stimulates PKC leading to the activation of GRK 2, which causes serine phopshorylation of D1A Receptors and Receptor G-protein uncoupling in these cells, resulting in impairment in D1-Like Receptor function.
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Dopamine inhibits na,h-exchanger via D1-Like Receptor-mediated stimulation of protein kinase a in renal proximal tubules.
Clinical and Experimental Hypertension, 2000Co-Authors: Sucheta A. Beheray, Tahir Hussain, Mustafa F. LokhandwalaAbstract:Dopamine causes natriuresis and diuresis via activation of D1-Like Receptors located in the renal proximal tubules. It is reported that this response to dopamine results from the inhibition of Na,H-exchanger and Na,K-ATPase. Earlier studies have suggested a role of protein kinase A (PKA) in the inhibition of Na,H-exchanger, however, the effect of dopamine or the dopamine Receptor subtype responsible for the stimulation of PKA has not been reported. Present study was designed to examine the effect of dopamine and D1-Like Receptor agonist, SKF 38393, on the stimulation of PKA activity in rat renal proximal tubules. Dopamine and SKF 38393 (1 nM – 1 μM) caused stimulation of PKA activity, an effect which was antagonized by a D1-Like Receptor antagonist, SCH 23390 (10 μM). Stimulation of PKA activity was also seen with forskolin and di-butyryl cAMP. We also observed that dopamine and SKF 38393 inhibited Na,H-exchanger activity in the proximal tubules. This response was blocked by SCH 23390 and Rp-cAMPS triethy...
