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Magda Giordano - One of the best experts on this subject based on the ideXlab platform.
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Changes in Sleep–Waking Cycle after striatal excitotoxic lesions
Behavioural brain research, 2002Co-Authors: Juan Mena-segovia, Oscar Prospéro-garcía, León Cintra, Magda GiordanoAbstract:Abstract Huntington's disease (HD) patients show severe diurnal choreic movements, while during slow-wave Sleep (SWS) abnormal movements subside. Sleep disturbances in HD, including irregular delta activity and decreases in SWS, have also been reported. Striatal excitotoxic lesions have been shown to induce increased nocturnal spontaneous locomotor activity in rodents. In order to characterize the changes in circadian activity and Sleep patterns and their correlation with motor activity after striatal excitotoxic lesions, Sprague–Dawley rats were implanted and lesioned; their locomotor and EEG activities were recorded for either 4 or 24 h during baseline or 7 and 30 days post-lesion. Locomotor activity increased significantly at 7 days post-lesion during the dark phase of the light–dark Cycle. In contrast, total time spent in wakefulness (W) increased at 30 days post-lesion during the light phase of the Cycle. This increase was at the expense of SWS duration. No disruption of the circadian curves was observed. Increases in the number of W-bouts and decreases in the duration of SWS-bouts were also observed. These results suggest the possible participation of the striatum in the regulation of the Sleep–Waking Cycle, independent of locomotor activity. The increase in W could be due to loss of inhibition of target structures involved in regulation of the Sleep–Waking Cycle.
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changes in Sleep Waking Cycle after striatal excitotoxic lesions
Behavioural Brain Research, 2002Co-Authors: Juan Menasegovia, Oscar Prosperogarcia, León Cintra, Magda GiordanoAbstract:Abstract Huntington's disease (HD) patients show severe diurnal choreic movements, while during slow-wave Sleep (SWS) abnormal movements subside. Sleep disturbances in HD, including irregular delta activity and decreases in SWS, have also been reported. Striatal excitotoxic lesions have been shown to induce increased nocturnal spontaneous locomotor activity in rodents. In order to characterize the changes in circadian activity and Sleep patterns and their correlation with motor activity after striatal excitotoxic lesions, Sprague–Dawley rats were implanted and lesioned; their locomotor and EEG activities were recorded for either 4 or 24 h during baseline or 7 and 30 days post-lesion. Locomotor activity increased significantly at 7 days post-lesion during the dark phase of the light–dark Cycle. In contrast, total time spent in wakefulness (W) increased at 30 days post-lesion during the light phase of the Cycle. This increase was at the expense of SWS duration. No disruption of the circadian curves was observed. Increases in the number of W-bouts and decreases in the duration of SWS-bouts were also observed. These results suggest the possible participation of the striatum in the regulation of the Sleep–Waking Cycle, independent of locomotor activity. The increase in W could be due to loss of inhibition of target structures involved in regulation of the Sleep–Waking Cycle.
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Research report Changes in Sleep/Waking Cycle after striatal excitotoxic lesions
2002Co-Authors: Juan Mena-segovia, Magda GiordanoAbstract:Huntington’s disease (HD) patients show severe diurnal choreic movements, while during slow-wave Sleep (SWS) abnormal movements subside. Sleep disturbances in HD, including irregular delta activity and decreases in SWS, have also been reported. Striatal excitotoxic lesions have been shown to induce increased nocturnal spontaneous locomotor activity in rodents. In order to characterize the changes in circadian activity and Sleep patterns and their correlation with motor activity after striatal excitotoxic lesions, Sprague/Dawley rats were implanted and lesioned; their locomotor and EEG activities were recorded for either 4 or 24 h during baseline or 7 and 30 days post-lesion. Locomotor activity increased significantly at 7 days post-lesion during the dark phase of the light/dark Cycle. In contrast, total time spent in wakefulness (W) increased at 30 days post-lesion during the light phase of the Cycle. This increase was at the expense of SWS duration. No disruption of the circadian curves was observed. Increases in the number of W-bouts and decreases in the duration of SWS-bouts were also observed. These results suggest the possible participation of the striatum in the regulation of the Sleep/Waking Cycle, independent of locomotor activity. The increase in W could be due to loss of inhibition of target structures involved in regulation of the Sleep/Waking Cycle. # 2002 Elsevier Science B.V. All rights reserved.
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research report changes in Sleep Waking Cycle after striatal excitotoxic lesions
2002Co-Authors: Juan Menasegovia, Magda GiordanoAbstract:Huntington’s disease (HD) patients show severe diurnal choreic movements, while during slow-wave Sleep (SWS) abnormal movements subside. Sleep disturbances in HD, including irregular delta activity and decreases in SWS, have also been reported. Striatal excitotoxic lesions have been shown to induce increased nocturnal spontaneous locomotor activity in rodents. In order to characterize the changes in circadian activity and Sleep patterns and their correlation with motor activity after striatal excitotoxic lesions, Sprague/Dawley rats were implanted and lesioned; their locomotor and EEG activities were recorded for either 4 or 24 h during baseline or 7 and 30 days post-lesion. Locomotor activity increased significantly at 7 days post-lesion during the dark phase of the light/dark Cycle. In contrast, total time spent in wakefulness (W) increased at 30 days post-lesion during the light phase of the Cycle. This increase was at the expense of SWS duration. No disruption of the circadian curves was observed. Increases in the number of W-bouts and decreases in the duration of SWS-bouts were also observed. These results suggest the possible participation of the striatum in the regulation of the Sleep/Waking Cycle, independent of locomotor activity. The increase in W could be due to loss of inhibition of target structures involved in regulation of the Sleep/Waking Cycle. # 2002 Elsevier Science B.V. All rights reserved.
Claude Gottesmann - One of the best experts on this subject based on the ideXlab platform.
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influence of a gabab receptor antagonist on the Sleep Waking Cycle in the rat
Brain Research, 1997Co-Authors: P. Gauthier, Gabriel Gandolfo, Christian Arnaud, Claude GottesmannAbstract:Abstract The influence of CGP 35348 (a GABAB receptor antagonist) on the Sleep–Waking Cycle was studied in rats. The animals were injected i.p. at the beginning of the light period and the data expressed by 2-h periods and total duration (6 h). At 100 mg/kg, slow-wave Sleep (SWS) was decreased during the 6-h recording with a peculiar decrease during the first 2 h. SWS was subdivided into three stages: slow-waves; spindles occurring as SWS deepens; and intermediate stage appearing prior to paradoxical Sleep (PS). Only the slow-wave stage and intermediate stage were decreased. Waking was increased during the 6-h recording. It was subdivided into Waking with hippocampal theta rhythm (psychomotor active Waking) and Waking without theta activity (quiet Waking). Both were increased during the first 2 h. However, quiet Waking was increased throughout the recording duration. At 300 mg/kg, SWS was decreased during the three 2-h periods. This decrease was principally related to a decrease of the slow-wave stage. PS was increased over the 6-h recording with a marked increase during the second 2-h period. Consequently, under the influence of the GABAB receptor antagonist, the SWS was decreased at the expense of behavioral stages with cortical low-voltage activity (Waking and PS). GABAergic neurons are present in the mesopontine structures responsible for these two stages. We can conclude that endogenous GABA acting at the GABAB receptor level participates in the regulation of Waking and PS.
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Influence of a GABAB receptor antagonist on the Sleep–Waking Cycle in the rat
Brain Research, 1997Co-Authors: P. Gauthier, Gabriel Gandolfo, Christian Arnaud, Claude GottesmannAbstract:Abstract The influence of CGP 35348 (a GABAB receptor antagonist) on the Sleep–Waking Cycle was studied in rats. The animals were injected i.p. at the beginning of the light period and the data expressed by 2-h periods and total duration (6 h). At 100 mg/kg, slow-wave Sleep (SWS) was decreased during the 6-h recording with a peculiar decrease during the first 2 h. SWS was subdivided into three stages: slow-waves; spindles occurring as SWS deepens; and intermediate stage appearing prior to paradoxical Sleep (PS). Only the slow-wave stage and intermediate stage were decreased. Waking was increased during the 6-h recording. It was subdivided into Waking with hippocampal theta rhythm (psychomotor active Waking) and Waking without theta activity (quiet Waking). Both were increased during the first 2 h. However, quiet Waking was increased throughout the recording duration. At 300 mg/kg, SWS was decreased during the three 2-h periods. This decrease was principally related to a decrease of the slow-wave stage. PS was increased over the 6-h recording with a marked increase during the second 2-h period. Consequently, under the influence of the GABAB receptor antagonist, the SWS was decreased at the expense of behavioral stages with cortical low-voltage activity (Waking and PS). GABAergic neurons are present in the mesopontine structures responsible for these two stages. We can conclude that endogenous GABA acting at the GABAB receptor level participates in the regulation of Waking and PS.
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Sleep-Waking Cycle in chronic rat preparations with brain stem transected at the caudopontine level
Brain research bulletin, 1995Co-Authors: Claude Gottesmann, Gabriel Gandolfo, Zernicki BAbstract:Abstract The brain stem of rats was transacted at the middle of the nucleus retiarlaris pontla caudalis The preparations were maintained 2–9 days, and their EEG activity and behavior were studied. Maintained EEG activity and EEG arousal to visual and olfactory stimull Indicated the presence of Sleep-Waking Cycle. Three stages were identified. Two of them corresponded to Waking with hippocampal theta rhythm and to slow wave Sleep in intact rats. The third stage (absent in intact rate) was characterized by slow waves and spindles of low amplitude in the cortex and low frequency theta rhythm, and it was considered as “drowsiness”. Waking without theta rhythm, paradoxical Sleep, and its forerunner Intermediate stage were never found. Paroxystic-like EEG episodes were frequently observed. Thus, although present, the Sleep-Waking Cycle is severely Impaired in the caudopontlrn rats. The Impairment is similar to that found previously In rate transacted at the Intercollicular or pretri-geminal level. The preparations were able to crawl abortively and to swallow liquid. Their respiratory rhythm was normal, but the heart rate increased. Thus, the caudal part of the preparations showed remarkable ability in controlling motor and vegetative functions.
León Cintra - One of the best experts on this subject based on the ideXlab platform.
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Changes in Sleep–Waking Cycle after striatal excitotoxic lesions
Behavioural brain research, 2002Co-Authors: Juan Mena-segovia, Oscar Prospéro-garcía, León Cintra, Magda GiordanoAbstract:Abstract Huntington's disease (HD) patients show severe diurnal choreic movements, while during slow-wave Sleep (SWS) abnormal movements subside. Sleep disturbances in HD, including irregular delta activity and decreases in SWS, have also been reported. Striatal excitotoxic lesions have been shown to induce increased nocturnal spontaneous locomotor activity in rodents. In order to characterize the changes in circadian activity and Sleep patterns and their correlation with motor activity after striatal excitotoxic lesions, Sprague–Dawley rats were implanted and lesioned; their locomotor and EEG activities were recorded for either 4 or 24 h during baseline or 7 and 30 days post-lesion. Locomotor activity increased significantly at 7 days post-lesion during the dark phase of the light–dark Cycle. In contrast, total time spent in wakefulness (W) increased at 30 days post-lesion during the light phase of the Cycle. This increase was at the expense of SWS duration. No disruption of the circadian curves was observed. Increases in the number of W-bouts and decreases in the duration of SWS-bouts were also observed. These results suggest the possible participation of the striatum in the regulation of the Sleep–Waking Cycle, independent of locomotor activity. The increase in W could be due to loss of inhibition of target structures involved in regulation of the Sleep–Waking Cycle.
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changes in Sleep Waking Cycle after striatal excitotoxic lesions
Behavioural Brain Research, 2002Co-Authors: Juan Menasegovia, Oscar Prosperogarcia, León Cintra, Magda GiordanoAbstract:Abstract Huntington's disease (HD) patients show severe diurnal choreic movements, while during slow-wave Sleep (SWS) abnormal movements subside. Sleep disturbances in HD, including irregular delta activity and decreases in SWS, have also been reported. Striatal excitotoxic lesions have been shown to induce increased nocturnal spontaneous locomotor activity in rodents. In order to characterize the changes in circadian activity and Sleep patterns and their correlation with motor activity after striatal excitotoxic lesions, Sprague–Dawley rats were implanted and lesioned; their locomotor and EEG activities were recorded for either 4 or 24 h during baseline or 7 and 30 days post-lesion. Locomotor activity increased significantly at 7 days post-lesion during the dark phase of the light–dark Cycle. In contrast, total time spent in wakefulness (W) increased at 30 days post-lesion during the light phase of the Cycle. This increase was at the expense of SWS duration. No disruption of the circadian curves was observed. Increases in the number of W-bouts and decreases in the duration of SWS-bouts were also observed. These results suggest the possible participation of the striatum in the regulation of the Sleep–Waking Cycle, independent of locomotor activity. The increase in W could be due to loss of inhibition of target structures involved in regulation of the Sleep–Waking Cycle.
Oscar Prospéro-garcía - One of the best experts on this subject based on the ideXlab platform.
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Entopeduncular nucleus endocannabinoid system modulates Sleep-Waking Cycle and mood in rats.
Pharmacology biochemistry and behavior, 2013Co-Authors: Mónica Méndez-díaz, Alejandra E. Ruiz-contreras, Seraid Caynas-rojas, Vianney Arteaga Santacruz, Raúl Aguilar-roblero, Oscar Prospéro-garcíaAbstract:Abstract Since the pioneering work of Gadea-Ciria (Gadea-Ciria M, Stadler H, Lloyd KG, Bartholini G. Acetylcholine release within the cat striatum during the Sleep–wakefulness Cycle. Nature 1973; 243:518–519) indicating pointing to the involvement of acetylcholine and basal ganglia in Sleep regulation; extensive literature has suggested that this brain complex participates in the control of the Sleep–Waking Cycle (SWC). On the other hand, it has been demonstrated that the endocannabinoid system (eCBS) is prominently involved in the regulation of the SWC, mood and its related disorders. Since cannabinoid receptor 1 (CB1R) is highly expressed in basal ganglia, in particular in the entopeduncular nucleus (EP), we believe that it is important to know what the role of the EP CB1R is on SWC, depression, and anxiety. To provide insight into the role of the EP CB1R in the regulation of wakefulness (W), non-rapid eye movement Sleep (NREMs) and rapid eye movement Sleep (REMs), rats were recorded for 24 h immediately after a single intra-EP administration of N-arachidonoylethanolamine (AEA) or 1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-(1-piperidyl)pyrazole-3-carboxamide (AM251; CB1 inverse agonist). Likewise, the effect of these drugs on anxiety and depression was tested by means of the elevated plus maze (EPM) and forced swim test (FST), respectively. Results demonstrate that AEA increases NREMs expression, while AM251 increases W and decreases both NREMs and REMs. In addition, administration of AM251 decreases the time rats spent in the open arms and increases immobility time in the FST. It seems that activation of the CB1R in the EP is important to induce Sleep, while its blockade promotes W, as well as anxiety and depression, somewhat resembling insomnia in humans. These results suggest that the EP CB1R is modulating Sleep and mood.
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Activation of PAR1 in the lateral hypothalamus of rats enhances food intake and REMS through CB1R.
Neuroreport, 2012Co-Authors: Marcel Pérez-morales, Ilia Alvarado-capuleño, Ana M. López-colomé, Mónica Méndez-díaz, Alejandra E. Ruiz-contreras, Oscar Prospéro-garcíaAbstract:: The activation of protease-activated receptor 1 (PAR1) in cultured rat hippocampal neurons triggers synaptic retrograde signaling through the endocannabinoid 2-arachidonoylglycerol, thereby activating the cannabinoid receptor 1 (CB1R). CB1R is a metabotropic receptor activated by marihuana and endocannabinoids that suppresses neurotransmitter release. Also, activation of the CB1R increases rapid eye movement Sleep (REMS) and food intake. The lateral hypothalamus is a crucial structure to modulate both feeding and Waking. To evaluate the effect of PAR1 stimulation in the lateral hypothalamus on food intake and on the Sleep-Waking Cycle, we implanted rats with electrodes, for recording Sleep, and cannulae, to administer S1820, a selective PAR1 agonist peptide, bilaterally into the lateral hypothalamus. To determine whether the effects induced by PAR1 stimulation were mediated by CB1R activation, we administered AM251, a CB1R inverse agonist, to block S1820 effects. Our results show that the stimulation of PAR1 into the lateral hypothalamus increases both food intake and REMS and such effects were prevented by AM251, indicating that PAR1 modulates both food intake and the Sleep-Waking Cycle, in the lateral hypothalamus, through CB1R activation. This study shows novel behavioral changes induced by PAR1 activation and further supports the notion that endocannabinoids are food intake and REMS promoters.
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Oleoylethanolamide affects food intake and Sleep–Waking Cycle through a hypothalamic modulation
Pharmacological research, 2010Co-Authors: Edgar Soria-gómez, Khalil Guzmán, O. Pech-rueda, Corinne J. Montes-rodriguez, M. Cisneros, Oscar Prospéro-garcíaAbstract:Oleoylethanolamide (OEA) is an endogenous molecule related to endocannabinoids (eCBs) that induces satiety. It binds to the peroxisome-proliferator-activated receptor alpha (PPAR alpha). PPAR alpha is involved in feeding regulation and it has been proposed to play a role in Sleep modulation. The objective of the present work is to show if this molecule modifies the Sleep-Waking Cycle through central mechanisms. We have found that the peripheral administration of OEA reduces food intake and increases Waking with a concomitant reduction of rapid eye movement Sleep. Additionally, this treatment produces deactivation of the lateral hypothalamus, as inferred from the c-Fos expression evaluation. Finally, intra-lateral hypothalamus injection of OEA has mirrored the effects induced by this molecule when it is peripherally administered. In conclusion, we show for the very first time that OEA can modify the Sleep-Waking Cycle and food intake, apparently mediated by the lateral hypothalamus.
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Changes in Sleep–Waking Cycle after striatal excitotoxic lesions
Behavioural brain research, 2002Co-Authors: Juan Mena-segovia, Oscar Prospéro-garcía, León Cintra, Magda GiordanoAbstract:Abstract Huntington's disease (HD) patients show severe diurnal choreic movements, while during slow-wave Sleep (SWS) abnormal movements subside. Sleep disturbances in HD, including irregular delta activity and decreases in SWS, have also been reported. Striatal excitotoxic lesions have been shown to induce increased nocturnal spontaneous locomotor activity in rodents. In order to characterize the changes in circadian activity and Sleep patterns and their correlation with motor activity after striatal excitotoxic lesions, Sprague–Dawley rats were implanted and lesioned; their locomotor and EEG activities were recorded for either 4 or 24 h during baseline or 7 and 30 days post-lesion. Locomotor activity increased significantly at 7 days post-lesion during the dark phase of the light–dark Cycle. In contrast, total time spent in wakefulness (W) increased at 30 days post-lesion during the light phase of the Cycle. This increase was at the expense of SWS duration. No disruption of the circadian curves was observed. Increases in the number of W-bouts and decreases in the duration of SWS-bouts were also observed. These results suggest the possible participation of the striatum in the regulation of the Sleep–Waking Cycle, independent of locomotor activity. The increase in W could be due to loss of inhibition of target structures involved in regulation of the Sleep–Waking Cycle.
Juan Mena-segovia - One of the best experts on this subject based on the ideXlab platform.
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Changes in Sleep–Waking Cycle after striatal excitotoxic lesions
Behavioural brain research, 2002Co-Authors: Juan Mena-segovia, Oscar Prospéro-garcía, León Cintra, Magda GiordanoAbstract:Abstract Huntington's disease (HD) patients show severe diurnal choreic movements, while during slow-wave Sleep (SWS) abnormal movements subside. Sleep disturbances in HD, including irregular delta activity and decreases in SWS, have also been reported. Striatal excitotoxic lesions have been shown to induce increased nocturnal spontaneous locomotor activity in rodents. In order to characterize the changes in circadian activity and Sleep patterns and their correlation with motor activity after striatal excitotoxic lesions, Sprague–Dawley rats were implanted and lesioned; their locomotor and EEG activities were recorded for either 4 or 24 h during baseline or 7 and 30 days post-lesion. Locomotor activity increased significantly at 7 days post-lesion during the dark phase of the light–dark Cycle. In contrast, total time spent in wakefulness (W) increased at 30 days post-lesion during the light phase of the Cycle. This increase was at the expense of SWS duration. No disruption of the circadian curves was observed. Increases in the number of W-bouts and decreases in the duration of SWS-bouts were also observed. These results suggest the possible participation of the striatum in the regulation of the Sleep–Waking Cycle, independent of locomotor activity. The increase in W could be due to loss of inhibition of target structures involved in regulation of the Sleep–Waking Cycle.
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Research report Changes in Sleep/Waking Cycle after striatal excitotoxic lesions
2002Co-Authors: Juan Mena-segovia, Magda GiordanoAbstract:Huntington’s disease (HD) patients show severe diurnal choreic movements, while during slow-wave Sleep (SWS) abnormal movements subside. Sleep disturbances in HD, including irregular delta activity and decreases in SWS, have also been reported. Striatal excitotoxic lesions have been shown to induce increased nocturnal spontaneous locomotor activity in rodents. In order to characterize the changes in circadian activity and Sleep patterns and their correlation with motor activity after striatal excitotoxic lesions, Sprague/Dawley rats were implanted and lesioned; their locomotor and EEG activities were recorded for either 4 or 24 h during baseline or 7 and 30 days post-lesion. Locomotor activity increased significantly at 7 days post-lesion during the dark phase of the light/dark Cycle. In contrast, total time spent in wakefulness (W) increased at 30 days post-lesion during the light phase of the Cycle. This increase was at the expense of SWS duration. No disruption of the circadian curves was observed. Increases in the number of W-bouts and decreases in the duration of SWS-bouts were also observed. These results suggest the possible participation of the striatum in the regulation of the Sleep/Waking Cycle, independent of locomotor activity. The increase in W could be due to loss of inhibition of target structures involved in regulation of the Sleep/Waking Cycle. # 2002 Elsevier Science B.V. All rights reserved.