The Experts below are selected from a list of 117 Experts worldwide ranked by ideXlab platform
Debora C Hipolide - One of the best experts on this subject based on the ideXlab platform.
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ampa receptors mediate Passive Avoidance deficits induced by sleep deprivation
Behavioural Brain Research, 2013Co-Authors: Francisco Paulino Dubiela, Claudio M Queiroz, Karin M Moreira, Jose N Nobrega, Luciane V Sita, Sergio Tufik, Debora C HipolideAbstract:The present study addressed the effects of sleep deprivation (SD) on AMPA receptor (AMPAR) binding in brain regions associated with learning and memory, and investigated whether treatment with drugs acting on AMPAR could prevent Passive Avoidance deficits in sleep deprived animals. [(3)H]AMPA binding and GluR1 in situ hybridization signals were quantified in different brain regions of male Wistar rats either immediately after 96 h of sleep deprivation or after 24h of sleep recovery following 96 h of sleep deprivation. Another group of animals were sleep deprived and then treated with either the AMPAR potentiator, aniracetam (25, 50 and 100mg/kg, acute administration) or the AMPAR antagonist GYKI-52466 (5 and 10mg/kg, acute and chronic administration) before Passive Avoidance training. Task performance was evaluated 2h and 24h after training. A significant reduction in [(3)H]AMPA binding was found in the hippocampal formation of SD animals, while no alterations were observed in GluR1 mRNA levels. The highest dose of aniracetam (100mg/kg) reverted SD-induced impairment of Passive Avoidance performance in both retention tests, whereas GYKI-52466 treatment had no effect. Pharmacological enhancement of AMPAR function may revert hippocampal-dependent learning impairments produced after SD. We argue that such effects might be associated with reduced AMPAR binding in the hippocampus of sleep deprived animals.
Paavo Riekkinen - One of the best experts on this subject based on the ideXlab platform.
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5-HT1A and muscarinic acetylcholine receptors jointly regulate Passive Avoidance behavior.
European journal of pharmacology, 1994Co-Authors: Paavo RiekkinenAbstract:Abstract The present study was designed to investigate the effects of combined stimulation of 5-HT 1A or 5-HT 2 receptors and blockade of muscarinic acetycholine receptors on Passive Avoidance behavior. Administration of 8- hydroxy -2-(di- n -propylamino)tetralin (8-OH-DPAT), a 5-HT 1A receptor agonist, and 1-(2,5-dimethoxyl-4-iodophenyl)-2-aminopropane (DOI), a 5-HT 2 receptor agonist, impaired Passive Avoidance acquisition (pre-training injections) and consolidation (post-training injections) performance. Ketanserin, a 5-HT 2 receptor antagonist, blocked the performance-impairing effect of DOI on Passive Avoidance consolidation. Interestingly, 5-HT receptor agonists may effect Passive Avoidance consolidation only during the immediate post-training period, as Passive Avoidance testing performance was not modulated by 8-OH-DPAT or DOI injected 30 min after the training trial. Furthermore, Passive Avoidance retention (pre-testing injections) performance was impaired only by the highest dose of 8-OH-DPAT, and DOI had no effect on Passive Avoidance retention. Next, the effects of combined 5-HT and acetylcholine receptor manipulations on Passive Avoidance behavior were studied. The effects on Passive Avoidance behavior of a combination of subthreshold doses of scopolamine, a muscarinic acetylcholine receptor antagonist, and 8-OH-DPAT were compared to those of a single high dose of scopolamine. A combination of small doses of scopolamine and 8-OH-DPAT impaired acquisition and consolidation of Passive Avoidance performance, but a single high dose of scopolamine impaired only acquisition performance. The small dose of 8-OH-DPAT also aggravated medial septal lesion-induced Passive Avoidance acquisition and consolidation failure. The combination of small doses of scopolamine and DOI had no effect on Passive Avoidance behavior. Peripherally acting scopolamine methylbromide alone or in combination with 8-OH-DPAT had no effect on Passive Avoidance performance. Motor activity in a swimming pool was altered by single and combined drug treatments; high doses of 8-OH-DPAT and scopolamine, and the combination of small doses of 8-OH-DPAT + scopolamine increased speed of swimming. Medial septum-lesioning also increased speed of swimming but the speed was not increased further by 8-OH-DPAT. The present data suggest that behavioral defect caused by hypostimulation of muscarinic acetylcholine receptors is aggravated by concurrent 5-HT 1A receptor stimulation.
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Cholinergic drugs regulate Passive Avoidance performance via the amygdala.
The Journal of pharmacology and experimental therapeutics, 1993Co-Authors: Paavo Riekkinen, M Riekkinen, J SirviöAbstract:The present study was designed to elucidate the role of the amygdala as a site of action of muscarinic and nicotinic receptor active drugs in modulating Avoidance (Passive Avoidance) and spatial navigation (water maze) performance. Quisqualic acid lesioning of the nucleus basalis decreased choline acetyltransferase activity in the amygdala and dorsolateral frontal cortex, but not in the hippocampus. Single or combined amygdala and nucleus basalis lesions did not impair water maze navigation. Combined amygdala and nucleus basalis lesioning did not impair Passive Avoidance performance any more severely than did either of the lesions alone. Scopolamine (a muscarinic antagonist) and mecamylamine (a nicotinic antagonist) induced a dose-dependent impairment of both Passive Avoidance and water maze performance. The effects of the cholinergic antagonists on Passive Avoidance performance were smaller in amygdala-lesioned rats than in the controls. Amygdala lesions did not modulate the effect of the cholinergic antagonists in impairing water-maze performance. Nicotine, a nicotinic agonist, and arecoline, a muscarinic agonist, restored Passive Avoidance performance in nucleus basalis-lesioned but not in nucleus basalis+amygdala-lesioned rats. Nicotine and arecoline did not improve water maze navigation in nucleus basalis-lesioned or nucleus basalis+amygdala-lesioned rats. The present results suggest that the nucleus basalis cholinergic projection may modulate Passive Avoidance performance via amygdaloid muscarinic and nicotinic receptors.
M Riekkinen - One of the best experts on this subject based on the ideXlab platform.
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Effects of scopolamine infusions into the anterior and posterior cingulate on Passive Avoidance and water maze navigation.
Brain research, 1995Co-Authors: P Riekkinen, J Kuitunen, M RiekkinenAbstract:We examined the role of anterior and posterior cingulate cortical muscarinic receptors in water maze spatial learning and Passive Avoidance. Pretraining and posttraining trial scopolamine (a mixed a muscarinic acetylcholine antagonist) infusions into the anterior cingulate cortex dose dependently (3 no effect; 10 and 30 micrograms impaired) impaired Passive Avoidance performance. Pretesting infusion into the anterior cingulate had no effect on Passive Avoidance. Scopolamine infusion into the anterior cingulate did not impair spatial navigation. On the contrary, scopolamine (3 micrograms no effect, 10 and 30 micrograms impaired) infusions into the posterior cingulate before daily training trials impaired water maze navigation to a hidden platform, but did not affect navigation to a visible escape platform or Passive Avoidance. Posttraining and pretesting infusion into the posterior cingulate did not impair WM spatial navigation. The present results indicate that muscarinic acetylcholine receptor antagonist may modulate Passive Avoidance performance via cholinergic receptors located in anterior cingulate cortex and the ability to develop a spatial navigation strategy via muscarinic receptors located in posterior cingulate.
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Cholinergic drugs regulate Passive Avoidance performance via the amygdala.
The Journal of pharmacology and experimental therapeutics, 1993Co-Authors: Paavo Riekkinen, M Riekkinen, J SirviöAbstract:The present study was designed to elucidate the role of the amygdala as a site of action of muscarinic and nicotinic receptor active drugs in modulating Avoidance (Passive Avoidance) and spatial navigation (water maze) performance. Quisqualic acid lesioning of the nucleus basalis decreased choline acetyltransferase activity in the amygdala and dorsolateral frontal cortex, but not in the hippocampus. Single or combined amygdala and nucleus basalis lesions did not impair water maze navigation. Combined amygdala and nucleus basalis lesioning did not impair Passive Avoidance performance any more severely than did either of the lesions alone. Scopolamine (a muscarinic antagonist) and mecamylamine (a nicotinic antagonist) induced a dose-dependent impairment of both Passive Avoidance and water maze performance. The effects of the cholinergic antagonists on Passive Avoidance performance were smaller in amygdala-lesioned rats than in the controls. Amygdala lesions did not modulate the effect of the cholinergic antagonists in impairing water-maze performance. Nicotine, a nicotinic agonist, and arecoline, a muscarinic agonist, restored Passive Avoidance performance in nucleus basalis-lesioned but not in nucleus basalis+amygdala-lesioned rats. Nicotine and arecoline did not improve water maze navigation in nucleus basalis-lesioned or nucleus basalis+amygdala-lesioned rats. The present results suggest that the nucleus basalis cholinergic projection may modulate Passive Avoidance performance via amygdaloid muscarinic and nicotinic receptors.
Francisco Paulino Dubiela - One of the best experts on this subject based on the ideXlab platform.
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ampa receptors mediate Passive Avoidance deficits induced by sleep deprivation
Behavioural Brain Research, 2013Co-Authors: Francisco Paulino Dubiela, Claudio M Queiroz, Karin M Moreira, Jose N Nobrega, Luciane V Sita, Sergio Tufik, Debora C HipolideAbstract:The present study addressed the effects of sleep deprivation (SD) on AMPA receptor (AMPAR) binding in brain regions associated with learning and memory, and investigated whether treatment with drugs acting on AMPAR could prevent Passive Avoidance deficits in sleep deprived animals. [(3)H]AMPA binding and GluR1 in situ hybridization signals were quantified in different brain regions of male Wistar rats either immediately after 96 h of sleep deprivation or after 24h of sleep recovery following 96 h of sleep deprivation. Another group of animals were sleep deprived and then treated with either the AMPAR potentiator, aniracetam (25, 50 and 100mg/kg, acute administration) or the AMPAR antagonist GYKI-52466 (5 and 10mg/kg, acute and chronic administration) before Passive Avoidance training. Task performance was evaluated 2h and 24h after training. A significant reduction in [(3)H]AMPA binding was found in the hippocampal formation of SD animals, while no alterations were observed in GluR1 mRNA levels. The highest dose of aniracetam (100mg/kg) reverted SD-induced impairment of Passive Avoidance performance in both retention tests, whereas GYKI-52466 treatment had no effect. Pharmacological enhancement of AMPAR function may revert hippocampal-dependent learning impairments produced after SD. We argue that such effects might be associated with reduced AMPAR binding in the hippocampus of sleep deprived animals.
Sergio Tufik - One of the best experts on this subject based on the ideXlab platform.
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ampa receptors mediate Passive Avoidance deficits induced by sleep deprivation
Behavioural Brain Research, 2013Co-Authors: Francisco Paulino Dubiela, Claudio M Queiroz, Karin M Moreira, Jose N Nobrega, Luciane V Sita, Sergio Tufik, Debora C HipolideAbstract:The present study addressed the effects of sleep deprivation (SD) on AMPA receptor (AMPAR) binding in brain regions associated with learning and memory, and investigated whether treatment with drugs acting on AMPAR could prevent Passive Avoidance deficits in sleep deprived animals. [(3)H]AMPA binding and GluR1 in situ hybridization signals were quantified in different brain regions of male Wistar rats either immediately after 96 h of sleep deprivation or after 24h of sleep recovery following 96 h of sleep deprivation. Another group of animals were sleep deprived and then treated with either the AMPAR potentiator, aniracetam (25, 50 and 100mg/kg, acute administration) or the AMPAR antagonist GYKI-52466 (5 and 10mg/kg, acute and chronic administration) before Passive Avoidance training. Task performance was evaluated 2h and 24h after training. A significant reduction in [(3)H]AMPA binding was found in the hippocampal formation of SD animals, while no alterations were observed in GluR1 mRNA levels. The highest dose of aniracetam (100mg/kg) reverted SD-induced impairment of Passive Avoidance performance in both retention tests, whereas GYKI-52466 treatment had no effect. Pharmacological enhancement of AMPAR function may revert hippocampal-dependent learning impairments produced after SD. We argue that such effects might be associated with reduced AMPAR binding in the hippocampus of sleep deprived animals.
