The Experts below are selected from a list of 20346 Experts worldwide ranked by ideXlab platform
Allan C. Collins - One of the best experts on this subject based on the ideXlab platform.
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nicotinic agonists stimulate Acetylcholine Release from mouse interpeduncular nucleus a function mediated by a different nachr than dopamine Release from striatum
Journal of Neurochemistry, 2008Co-Authors: Sharon R Grady, Andrew M Reynolds, Natalie M. Meinerz, Michael J Mcintosh, Michael J. Marks, Jean-pierre Changeux, Marina R. Picciotto, Allan C. CollinsAbstract:Acetylcholine Release stimulated by nicotinic agonists was measured as radioactivity Released from perfused synaptosomes prepared from mouse interpeduncular nucleus (IPN) that had been loaded with [ 3 H]choline. Agonist-stimulated Release was dependent upon external calcium and over 90% of Released radioactivity was Acetylcholine. The Release process was characterized by dose response curves for 13 agonists and inhibition curves for six antagonists. a-Conotoxin MII did not inhibit this Release, while a-conotoxin AuIB inhibited 50% of agonist-stimulated Release. Comparison of this process with [ 3 H]dopamine Release from mouse striatal synaptosomes indicated that different forms of nicotinic Acetylcholine receptors (nAChRs) may mediate these processes. This was confirmed by assays using mice homozygous for the b2 subunit null mutation. The deletion of the b2 subunit had no effect on agonist-stimulated Acetylcholine Release, but abolished agonist-stimulated Release of dopamine from striatal synaptosomes. Mice heterozygous for the b2 subunit null mutation showed decreased dopamine Release evoked by L-nicotine with no apparent change in EC50 value, as well as similar decreases in both transient and persistent phases of Release with no changes in desensitization rates.
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nicotinic agonists stimulate Acetylcholine Release from mouse interpeduncular nucleus a function mediated by a different nachr than dopamine Release from striatum
Journal of Neurochemistry, 2008Co-Authors: Sharon R Grady, Andrew M Reynolds, Natalie M. Meinerz, Michael J Mcintosh, Michael J. Marks, Jean-pierre Changeux, Marina R. Picciotto, Allan C. CollinsAbstract:Acetylcholine Release stimulated by nicotinic agonists was measured as radioactivity Released from perfused synaptosomes prepared from mouse interpeduncular nucleus (IPN) that had been loaded with [ 3 H]choline. Agonist-stimulated Release was dependent upon external calcium and over 90% of Released radioactivity was Acetylcholine. The Release process was characterized by dose response curves for 13 agonists and inhibition curves for six antagonists. a-Conotoxin MII did not inhibit this Release, while a-conotoxin AuIB inhibited 50% of agonist-stimulated Release. Comparison of this process with [ 3 H]dopamine Release from mouse striatal synaptosomes indicated that different forms of nicotinic Acetylcholine receptors (nAChRs) may mediate these processes. This was confirmed by assays using mice homozygous for the b2 subunit null mutation. The deletion of the b2 subunit had no effect on agonist-stimulated Acetylcholine Release, but abolished agonist-stimulated Release of dopamine from striatal synaptosomes. Mice heterozygous for the b2 subunit null mutation showed decreased dopamine Release evoked by L-nicotine with no apparent change in EC50 value, as well as similar decreases in both transient and persistent phases of Release with no changes in desensitization rates.
Willy Mayo - One of the best experts on this subject based on the ideXlab platform.
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The neurosteroid pregnenolone sulfate infused into the medial septum nucleus increases hippocampal Acetylcholine and spatial memory in rats.
Brain Research, 2002Co-Authors: Muriel Darnaudéry, Marc Pallarès, Michel Le Moal, Pier Vincenzo Piazza, Willy MayoAbstract:The effects of an infusion of the neurosteroid pregnenolone sulfate into the medial septum on Acetylcholine Release in the hippocampus and on spatial memory were evaluated in two experiments. Results show that pregnenolone sulfate enhanced Acetylcholine Release by more than 50% of baseline and improved recognition memory of a familiar environment. Therefore, our results suggest that the septo-hippocampal pathway could be involved in the promnesic properties of this neurosteroid.
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The neurosteroid pregnenolone sulfate infused into the nucleus basalis increases both Acetylcholine Release in the frontal cortex or amygdala and spatial memory
Neuroscience, 1998Co-Authors: Marc Pallarès, Muriel Darnaudéry, Michel Le Moal, Willy MayoAbstract:Abstract The effects of an infusion (5 ng) of the neurosteroid pregnenolone sulfate into the nucleus basalis magnocellularis on Acetylcholine Release in the frontoparietal cortex and basolateral amygdala were evaluated during the 130 min post-injection in male Sprague–Dawley rats using in vivo microdialysis coupled “on line” with high performance liquid chromatography detection. One week later, the same animals were tested for spatial memory after another infusion of pregnenolone sulfate (5 ng) into the nucleus basalis. Results show that pregnenolone sulfate enhanced Acetylcholine Release by more than 50% of baseline concentrations in the two structures relative to a control injection. The duration of this effect was longer in cortex (130 min) than in amygdala (30 min). Furthermore, pregnenolone sulfate improved memory performance in a task based upon spatial recognition of a familiar environment. A significant positive correlation ( r =0.49) was found between the recognition score in the spatial memory test and the levels of Acetylcholine Release in the frontoparietal cortex but not in the basolateral amygdala. Therefore, our results suggest that the nucleus basalis magnocellularis-cortical pathway could be in part responsible for the promnesic effect of pregnenolone sulfate. This neurosteroid acts as a negative modulator of the GABA A receptor complex and positively modulates the N -methyl- d -aspartate receptor, possibly resulting in a global stimulatory effect on central cholinergic neurotransmission.
Ralph Lydic - One of the best experts on this subject based on the ideXlab platform.
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adenosine a1 receptors in mouse pontine reticular formation depress breathing increase anesthesia recovery time and decrease Acetylcholine Release
Anesthesiology, 2013Co-Authors: George C Gettys, Helen A Baghdoyan, Ed Kimlin, Ralph LydicAbstract:Background: Clinical and preclinical data demonstrate the analgesic actions of adenosine. Central administration of adenosine agonists, however, suppresses arousal and breathing by poorly understood mechanisms. This study tested the two-tailed hypothesis that adenosine A1 receptors in the pontine reticular formation (PRF) of C57BL/6J mice modulate breathing, behavioral arousal, and PRF Acetylcholine Release. Methods: Three sets of experiments used 51 mice. First, breathing was measured by plethysmography after PRF microinjection of the adenosine A1 receptor agonist N6-sulfophenyl adenosine (SPA) or saline. Second, mice were anesthetized with isoflurane and the time to recovery of righting response (RoRR) was quantified after a PRF microinjection of SPA or saline. Third, Acetylcholine Release in the PRF was measured before and during microdialysis delivery of SPA, the adenosine A1 receptor antagonist 1, 3-dipropyl-8-cyclopentylxanthine, or SPA and 1, 3-dipropyl-8-cyclopentylxanthine. Results: First, SPA significantly decreased respiratory rate (−18%), tidal volume (−12%), and minute ventilation (−16%). Second, SPA concentration accounted for 76% of the variance in RoRR. Third, SPA concentration accounted for a significant amount of the variance in Acetylcholine Release (52%), RoRR (98%), and breathing rate (86%). 1, 3-dipropyl-8-cyclopentylxanthine alone caused a concentration-dependent increase in Acetylcholine, a decrease in RoRR, and a decrease in breathing rate. Coadministration of SPA and 1, 3-dipropyl-8-cyclopentylxanthine blocked the SPA-induced decrease in Acetylcholine and increase in RoRR. Conclusions: Endogenous adenosine acting at adenosine A1 receptors in the PRF modulates breathing, behavioral arousal, and Acetylcholine Release. The results support the interpretation that an adenosinergic-cholinergic interaction within the PRF comprises one neurochemical mechanism underlying the wakefulness stimulus for breathing.
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dialysis delivery of an adenosine a1 receptor agonist to the pontine reticular formation decreases Acetylcholine Release and increases anesthesia recovery time
Anesthesiology, 2003Co-Authors: Diana Tanase, Helen A Baghdoyan, Ralph LydicAbstract:Background : Adenosine modulates cell excitability, Acetylcholine Release, nociception, and sleep. Pontine cholinergic neurotransmission contributes to the generation and maintenance of electroencephalographic and behavioral arousal. Adenosine A 1 receptors inhibit arousal-promoting, pontine cholinergic neurons, and adenosine enhances sleep. No previous studies have determined whether pontine adenosine also modulates recovery from anesthesia. Therefore, the current study tested the hypotheses that dialysis delivery of the adenosine A 1 receptor agonist N 6 -p-sulfophenyladenosine (SPA) into the pontine reticular formation would decrease Acetylcholine Release and increase the time needed for recovery from halothane anesthesia. Methods : A microdialysis probe was positioned in the pontine reticular formation of halothane-anesthetized cats. Probes were perfused with Ringer's solution (control) followed by the adenosine A 1 receptor agonist SPA (0.088 or 8.8 mM). Dependent measures included Acetylcholine Release and a numeric assessment of recovery from anesthesia. An intensive, within-subjects design and analysis of variance evaluated SPA's main effect on Acetylcholine Release and anesthetic recovery. The adenosine A 1 receptor antagonist 8-cyclopentyl-1,3-dipropy-Ixanthine (DPCPX, 100 μM ) was coadministered with SPA to test for antagonist blocking of SPA's effects. Results: SPA significantly (P < 0.0001) decreased Acetylcholine Release in the pontine reticular formation and significantly (P < 0.0001) delayed recovery from anesthesia. Coadministration of SPA and DPCPX caused no decrease in Acetylcholine Release or delay in postanesthetic recovery. Dialysis delivery of SPA into the cerebellar cortex confirmed that the SPA effects were site-specific to the pontine reticular formation. Coclusion:The results provide a novel extension of the sleep-promoting effects of adenosine by showing that pontine delivery of an adenosine A 1 receptor agonist delays resumption of wakefulness following halothane anesthesia. This extension is consistent with a potentially larger relevance of the current findings for efforts to specify neurons and molecules causing physiologic and behavioral traits comprising anesthetic states. These data support the conclusion that adenosine A 1 receptors in medial regions of the pontine reticular formation, known to modulate sleep, also contribute to the generation and/or maintenance of halothane anesthesia.
Michel Le Moal - One of the best experts on this subject based on the ideXlab platform.
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The neurosteroid pregnenolone sulfate infused into the medial septum nucleus increases hippocampal Acetylcholine and spatial memory in rats.
Brain Research, 2002Co-Authors: Muriel Darnaudéry, Marc Pallarès, Michel Le Moal, Pier Vincenzo Piazza, Willy MayoAbstract:The effects of an infusion of the neurosteroid pregnenolone sulfate into the medial septum on Acetylcholine Release in the hippocampus and on spatial memory were evaluated in two experiments. Results show that pregnenolone sulfate enhanced Acetylcholine Release by more than 50% of baseline and improved recognition memory of a familiar environment. Therefore, our results suggest that the septo-hippocampal pathway could be involved in the promnesic properties of this neurosteroid.
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The neurosteroid pregnenolone sulfate infused into the nucleus basalis increases both Acetylcholine Release in the frontal cortex or amygdala and spatial memory
Neuroscience, 1998Co-Authors: Marc Pallarès, Muriel Darnaudéry, Michel Le Moal, Willy MayoAbstract:Abstract The effects of an infusion (5 ng) of the neurosteroid pregnenolone sulfate into the nucleus basalis magnocellularis on Acetylcholine Release in the frontoparietal cortex and basolateral amygdala were evaluated during the 130 min post-injection in male Sprague–Dawley rats using in vivo microdialysis coupled “on line” with high performance liquid chromatography detection. One week later, the same animals were tested for spatial memory after another infusion of pregnenolone sulfate (5 ng) into the nucleus basalis. Results show that pregnenolone sulfate enhanced Acetylcholine Release by more than 50% of baseline concentrations in the two structures relative to a control injection. The duration of this effect was longer in cortex (130 min) than in amygdala (30 min). Furthermore, pregnenolone sulfate improved memory performance in a task based upon spatial recognition of a familiar environment. A significant positive correlation ( r =0.49) was found between the recognition score in the spatial memory test and the levels of Acetylcholine Release in the frontoparietal cortex but not in the basolateral amygdala. Therefore, our results suggest that the nucleus basalis magnocellularis-cortical pathway could be in part responsible for the promnesic effect of pregnenolone sulfate. This neurosteroid acts as a negative modulator of the GABA A receptor complex and positively modulates the N -methyl- d -aspartate receptor, possibly resulting in a global stimulatory effect on central cholinergic neurotransmission.
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Corticotropin-Releasing Factor Administered Centrally, but Not Peripherally, Stimulates Hippocampal Acetylcholine Release
Journal of Neurochemistry, 1998Co-Authors: Jamie Day, Michel Le Moal, Muriel Koehl, Stéfania MaccariAbstract:In addition to corticotropin-releasing factor's well-known role in mediating hormonal and behavioral responses to stress, this peptide also reportedly affects arousal and cognition, processes that classically have been associated with forebrain cholinergic systems. Corticotropin-releasing factor stimulation of cholinergic neurons might thus provide a mechanism for this peptide's cognitive effects. To examine this possibility, the present experiments characterize the effect of corticotropin-releasing factor on cholinergic neurotransmission, using in vivo microdialysis to measure hippocampal Acetylcholine Release. Corticotropin-releasing factor (0.5-5.0 microg/rat intracerebroventricularly) was found to increase dialysate concentrations of Acetylcholine in a dose-dependent manner in comparison with a control injection, the ovine peptide having a greater effect than the same dose of the human/rat peptide. This effect was found to be centrally mediated, independent of the peripheral effects of an exogenous corticotropin-releasing factor injection; subcutaneous injections of the peptide increased plasma concentrations of corticosterone, the adrenal hormone ultimately secreted in the rat's stress response, to the same level as did the central injections, without affecting hippocampal Acetylcholine Release. These results demonstrate that corticotropin-releasing factor, acting centrally, regulates hippocampal cholinergic activity, and suggest that corticotropin-releasing factor/Acetylcholine interactions may underlie some of the previously identified roles of these neurotransmitters in arousal, cognition, and stress.
Sharon R Grady - One of the best experts on this subject based on the ideXlab platform.
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nicotinic agonists stimulate Acetylcholine Release from mouse interpeduncular nucleus a function mediated by a different nachr than dopamine Release from striatum
Journal of Neurochemistry, 2008Co-Authors: Sharon R Grady, Andrew M Reynolds, Natalie M. Meinerz, Michael J Mcintosh, Michael J. Marks, Jean-pierre Changeux, Marina R. Picciotto, Allan C. CollinsAbstract:Acetylcholine Release stimulated by nicotinic agonists was measured as radioactivity Released from perfused synaptosomes prepared from mouse interpeduncular nucleus (IPN) that had been loaded with [ 3 H]choline. Agonist-stimulated Release was dependent upon external calcium and over 90% of Released radioactivity was Acetylcholine. The Release process was characterized by dose response curves for 13 agonists and inhibition curves for six antagonists. a-Conotoxin MII did not inhibit this Release, while a-conotoxin AuIB inhibited 50% of agonist-stimulated Release. Comparison of this process with [ 3 H]dopamine Release from mouse striatal synaptosomes indicated that different forms of nicotinic Acetylcholine receptors (nAChRs) may mediate these processes. This was confirmed by assays using mice homozygous for the b2 subunit null mutation. The deletion of the b2 subunit had no effect on agonist-stimulated Acetylcholine Release, but abolished agonist-stimulated Release of dopamine from striatal synaptosomes. Mice heterozygous for the b2 subunit null mutation showed decreased dopamine Release evoked by L-nicotine with no apparent change in EC50 value, as well as similar decreases in both transient and persistent phases of Release with no changes in desensitization rates.
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nicotinic agonists stimulate Acetylcholine Release from mouse interpeduncular nucleus a function mediated by a different nachr than dopamine Release from striatum
Journal of Neurochemistry, 2008Co-Authors: Sharon R Grady, Andrew M Reynolds, Natalie M. Meinerz, Michael J Mcintosh, Michael J. Marks, Jean-pierre Changeux, Marina R. Picciotto, Allan C. CollinsAbstract:Acetylcholine Release stimulated by nicotinic agonists was measured as radioactivity Released from perfused synaptosomes prepared from mouse interpeduncular nucleus (IPN) that had been loaded with [ 3 H]choline. Agonist-stimulated Release was dependent upon external calcium and over 90% of Released radioactivity was Acetylcholine. The Release process was characterized by dose response curves for 13 agonists and inhibition curves for six antagonists. a-Conotoxin MII did not inhibit this Release, while a-conotoxin AuIB inhibited 50% of agonist-stimulated Release. Comparison of this process with [ 3 H]dopamine Release from mouse striatal synaptosomes indicated that different forms of nicotinic Acetylcholine receptors (nAChRs) may mediate these processes. This was confirmed by assays using mice homozygous for the b2 subunit null mutation. The deletion of the b2 subunit had no effect on agonist-stimulated Acetylcholine Release, but abolished agonist-stimulated Release of dopamine from striatal synaptosomes. Mice heterozygous for the b2 subunit null mutation showed decreased dopamine Release evoked by L-nicotine with no apparent change in EC50 value, as well as similar decreases in both transient and persistent phases of Release with no changes in desensitization rates.
