The Experts below are selected from a list of 66 Experts worldwide ranked by ideXlab platform
T N Fedorova - One of the best experts on this subject based on the ideXlab platform.
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intracerebroventricular injection of ouabain causes mania like behavior in mice through d2 receptor activation
Scientific Reports, 2019Co-Authors: A V Lopachev, Anna B Volnova, Anna Evdokimenko, Denis Abaimov, Yulia Timoshina, Rogneda B Kazanskaya, O M Lopacheva, Alex L Deal, Evgeny A Budygin, T N FedorovaAbstract:Intracerebroventricular (ICV) administration of ouabain, an inhibitor of the Na, K-ATPase, is an approach used to study the physiological functions of the Na, K-ATPase and cardiotonic steroids in the central nervous system, known to cause mania-like hyperactivity in rats. We describe a mouse model of ouabain-induced mania-like behavior. ICV administration of 0.5 µl of 50 µM (25 pmol, 14.6 ng) ouabain into each Lateral Brain Ventricle results in increased locomotor activity, stereotypical behavior, and decreased anxiety level an hour at minimum. Fast-scan cyclic voltammetry showed that administration of 50 µM ouabain causes a drastic drop in dopamine uptake rate, confirmed by elevated concentrations of dopamine metabolites detected in the striatum 1 h after administration. Ouabain administration also caused activation of Akt, deactivation of GSK3β and activation of ERK1/2 in the striatum of ouabain-treated mice. All of the abovementioned effects are attenuated by haloperidol (70 µg/kg intraperitoneally). Observed effects were not associated with neurotoxicity, since no dystrophic neuron changes in Brain structures were demonstrated by histological analysis. This newly developed mouse model of ouabain-induced mania-like behavior could provide a perspective tool for studying the interactions between the Na,K-ATPase and the dopaminergic system.
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intracerebroventricular injection of ouabain causes mania like behavior in mice through d2 receptor activation
Scientific Reports, 2019Co-Authors: A V Lopachev, Anna B Volnova, Anna Evdokimenko, Denis Abaimov, Yulia Timoshina, Rogneda B Kazanskaya, O M Lopacheva, Alex L Deal, Evgeny A Budygin, T N FedorovaAbstract:Intracerebroventricular (ICV) administration of ouabain, an inhibitor of the Na, K-ATPase, is an approach used to study the physiological functions of the Na, K-ATPase and cardiotonic steroids in the central nervous system, known to cause mania-like hyperactivity in rats. We describe a mouse model of ouabain-induced mania-like behavior. ICV administration of 0.5 µl of 50 µM (25 pmol, 14.6 ng) ouabain into each Lateral Brain Ventricle results in increased locomotor activity, stereotypical behavior, and decreased anxiety level an hour at minimum. Fast-scan cyclic voltammetry showed that administration of 50 µM ouabain causes a drastic drop in dopamine uptake rate, confirmed by elevated concentrations of dopamine metabolites detected in the striatum 1 h after administration. Ouabain administration also caused activation of Akt, deactivation of GSK3β and activation of ERK1/2 in the striatum of ouabain-treated mice. All of the abovementioned effects are attenuated by haloperidol (70 µg/kg intraperitoneally). Observed effects were not associated with neurotoxicity, since no dystrophic neuron changes in Brain structures were demonstrated by histological analysis. This newly developed mouse model of ouabain-induced mania-like behavior could provide a perspective tool for studying the interactions between the Na,K-ATPase and the dopaminergic system.
A V Lopachev - One of the best experts on this subject based on the ideXlab platform.
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intracerebroventricular injection of ouabain causes mania like behavior in mice through d2 receptor activation
Scientific Reports, 2019Co-Authors: A V Lopachev, Anna B Volnova, Anna Evdokimenko, Denis Abaimov, Yulia Timoshina, Rogneda B Kazanskaya, O M Lopacheva, Alex L Deal, Evgeny A Budygin, T N FedorovaAbstract:Intracerebroventricular (ICV) administration of ouabain, an inhibitor of the Na, K-ATPase, is an approach used to study the physiological functions of the Na, K-ATPase and cardiotonic steroids in the central nervous system, known to cause mania-like hyperactivity in rats. We describe a mouse model of ouabain-induced mania-like behavior. ICV administration of 0.5 µl of 50 µM (25 pmol, 14.6 ng) ouabain into each Lateral Brain Ventricle results in increased locomotor activity, stereotypical behavior, and decreased anxiety level an hour at minimum. Fast-scan cyclic voltammetry showed that administration of 50 µM ouabain causes a drastic drop in dopamine uptake rate, confirmed by elevated concentrations of dopamine metabolites detected in the striatum 1 h after administration. Ouabain administration also caused activation of Akt, deactivation of GSK3β and activation of ERK1/2 in the striatum of ouabain-treated mice. All of the abovementioned effects are attenuated by haloperidol (70 µg/kg intraperitoneally). Observed effects were not associated with neurotoxicity, since no dystrophic neuron changes in Brain structures were demonstrated by histological analysis. This newly developed mouse model of ouabain-induced mania-like behavior could provide a perspective tool for studying the interactions between the Na,K-ATPase and the dopaminergic system.
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intracerebroventricular injection of ouabain causes mania like behavior in mice through d2 receptor activation
Scientific Reports, 2019Co-Authors: A V Lopachev, Anna B Volnova, Anna Evdokimenko, Denis Abaimov, Yulia Timoshina, Rogneda B Kazanskaya, O M Lopacheva, Alex L Deal, Evgeny A Budygin, T N FedorovaAbstract:Intracerebroventricular (ICV) administration of ouabain, an inhibitor of the Na, K-ATPase, is an approach used to study the physiological functions of the Na, K-ATPase and cardiotonic steroids in the central nervous system, known to cause mania-like hyperactivity in rats. We describe a mouse model of ouabain-induced mania-like behavior. ICV administration of 0.5 µl of 50 µM (25 pmol, 14.6 ng) ouabain into each Lateral Brain Ventricle results in increased locomotor activity, stereotypical behavior, and decreased anxiety level an hour at minimum. Fast-scan cyclic voltammetry showed that administration of 50 µM ouabain causes a drastic drop in dopamine uptake rate, confirmed by elevated concentrations of dopamine metabolites detected in the striatum 1 h after administration. Ouabain administration also caused activation of Akt, deactivation of GSK3β and activation of ERK1/2 in the striatum of ouabain-treated mice. All of the abovementioned effects are attenuated by haloperidol (70 µg/kg intraperitoneally). Observed effects were not associated with neurotoxicity, since no dystrophic neuron changes in Brain structures were demonstrated by histological analysis. This newly developed mouse model of ouabain-induced mania-like behavior could provide a perspective tool for studying the interactions between the Na,K-ATPase and the dopaminergic system.
Andrew V. Schally - One of the best experts on this subject based on the ideXlab platform.
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effects of the lhrh antagonist cetrorelix on affective and cognitive functions in rats
Regulatory Peptides, 2010Co-Authors: Gyula Telegdy, Agnes Adamik, Masaru Tanaka, Andrew V. SchallyAbstract:Abstract The decapeptide LHRH antagonist, Cetrorelix, inhibits gonadotropin and sex-steroid secretion. Cetrorelix is used for IVF-ET procedures and for the treatment of benign prostatic hyperplasia, endometriosis and leiomyomas. However little is known about the effects of Cetrorelix on Brain functions. Previously we have tested Cetrorelix in mice on the impairment of the consolidation of a passive avoidance behavior caused by beta-amyloid 25–35, anxiolytic action in the plus-maze, antidepressive action in a forced swimming test, tail suspension and open-field behavior following its administration into the Lateral Brain Ventricle. In the present study we repeated and extended the experiments in rats in order to determine whether there are species differences in the action of Cetrorelix between mice and rats. The effects of Cetrorelix evaluated included the methods used in mice without tail suspension test and extended by measuring core temperature. Cetrorelix fully blocked the impairment of the consolidation of passive avoidance learning when given icv 30 min following administration of beta-amyloid 25–35. If beta-amyloid 25–35 and Cetrorelix were given simultaneously, Cetrorelix was ineffective. Cetrorelix elicited slight anxiogenic and stronger anxiolytic action in the plus-maze, depending on the dose used. In the forced swimming tests, Cetrorelix showed antidepressive-like action. In open-field behavior tests Cetrorelix displayed a U-type action on locomotion with 0.5 and 2 µg increasing locomotion, and increase rearing but and had no effect on grooming at 0.5–2 µg. Cetrorelix had no action on core temperature. Our findings demonstrate that Cetrorelix is able to correct the impairment of the memory consolidation caused by beta-amyloid 25–35. Cetrorelix elicits anxiolytic and antidepressive action, slightly increases locomotion and rearing in open field, but it does not influence the core temperature. The results obtained in rats are similar to those reported previously by us in mice. Collectively our findings confirm the effects of Cetrorelix on Brain function in two species and suggest the possible merit of a clinical trial with Cetrorelix in patients with anxiety, depression and Alzheimer's disease.
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effects of the lhrh antagonist cetrorelix on the Brain function in mice
Neuropeptides, 2009Co-Authors: Gyula Telegdy, Masaru Tanaka, Andrew V. SchallyAbstract:The decapeptide Cetrorelix, an LHRH antagonist, inhibits gonadotropin and sex steroid secretion. Cetrorelix is used for IVF-ET procedures and for the treatment of patients with prostate carcinoma, benign prostatic hyperplasia, endometriosis, leiomyomas and, ovarian cancer. However little is known about the effects of Cetrorelix on the Brain function. In the present work the influence of Cetrorelix on different aspects of the Brain function was studied following its administration into the Lateral Brain Ventricle in mice. The effects tested included the impairment of the consolidation of a passive avoidance reflex caused by beta-amyloid 25-35, anxiolytic action in the plus-maze, antidepressive action in a forced swimming test and a tail suspension test and open-field behavior. In the passive avoidance test, beta-amyloid 25-35 administered immediately after the learning trial impaired the consolidation of passive avoidance learning. Cetrorelix fully blocked the impairment of the consolidation of passive avoidance learning when given icv 30 min following beta-amyloid 25-35 administration. If beta-amyloid 25-35 and Cetrorelix icv were given simultaneously, the Cetrorelix attenuated, but did not block the action of the beta-amyloid 25-35. Cetrorelix elicited anxiolytic action in the plus-maze, depending on the dose used. In the forced swimming and tail suspension tests, Cetrorelix demonstrated antidepressive-like action. Concerning open-field behavior, Cetrorelix displayed no action on locomotion, rearing or grooming. The results demonstrate that Cetrorelix affects Brain function: and is able to correct the impairment of the memory consolidation caused by beta-amyloid 25-35. Cetrorelix also elicits anxiolytic and antidepressive action, but it does not influence the open-field activity. Further experimental work with Cetrorelix is necessary, but the results imply the possible merit of a clinical trial with Cetrorelix in patients with anxiety, depression and Alzheimer's disease.
Agata R Plech - One of the best experts on this subject based on the ideXlab platform.
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The effect of gamma-aminobutyric acid injected into Lateral Brain Ventricle of rats after prenatal cadmium intoxication on flash visual evoked potentials (FVEP)
Klinika oczna, 2001Co-Authors: Ewa Herba, Dorota Pojda-wilczek, Stefan M Pojda, Ryszard Szkilnik, Agata R PlechAbstract:PURPOSE: To find out any influence of gamma-aminobutyric acid (GABA) injected into Lateral Brain Ventricle in newborn rats prenatally exposed to cadmium (Cd). METHOD: 18 white, Wistar, offspring rats were divided into 3 groups, each consisting of 6 rats (control, 5 ppm and 50 ppm of Cd in drinking water). Newborns were examined when they were 3-6 months old. FVEP were recorded before and after GABA injections. Two doses of GABA were used, 10 and 100 nmols. The statistic analysis with the test of t-Student was performed to estimate the amplitudes and latencies of the negative wave N1 and the next positive one P2. p < 0.05 was used to indicate significant difference. RESULTS: No significant changes in the latencies of peak N1 and P2 in the control and Cd 5 ppm groups (101-103%) after 10 nmols GABA were observed. However, the shortened (91-97%) of them was observed after both doses of GABA in Cd 50 ppm group. The mean value of amplitude of N1 in control rats increased to 127% after 10 nmols GABA and 142% after 100 nmols GABA. Moreover, the mean amplitude of P2 in this group increased to 108% and 146%, respectively. The high significant increase of the amplitudes of N1 (181-280%) and P2 (160-177%) waves were received after both doses of GABA in Cd groups. CONCLUSION: Cadmium increased the sensitivity of GABA-receptors in the OUN.
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The effect of dopamine injected into the Lateral Brain Ventricle on flash visual evoked potential (FVEP) after prenatal intoxication with cadmium
Klinika oczna, 2000Co-Authors: Ewa Herba, Dorota Pojda-wilczek, Stefan M Pojda, Agata R Plech, Ryszard SzkilnikAbstract:PURPOSE Earlier studies demonstrated that exposure, especially prenatal, of mammalians to cadmium (Cd) results in disorders of visual evoked potentials (FVEP). The purpose of this study is to find out any influence of cadmium intoxications on the effect of dopamine (DA) on FVEP. METHOD 18 Wistar albino rats in 3-6 months of age were divided into 3 groups: control (drinking tap water only), prenatal exposure of 5 ppm, and 50 ppm Cd. Flash visual evoked potentials (FVEP) were recorded before and after injections of dopamine (DA) 100 and 200 nmols into the Lateral Brain Ventricle. The amplitude and latency of N1 and P2 were statistically analysed by the test of t-Student. p < 0.05 was used to indicate significant difference. RESULTS There were no statistical differences of mean latency of P2 waves between initial records of FVEP and after both doses of DA in all observed groups. The amplitudes of both waves increased after DA injections compared to initial values in all groups. The differences were statistically significant. The mean latencies of N1 peak were prolonged after both DA doses (106-109%) compared to the initial records (100%) in the control group; however, there were no changes of it in the Cd-treated groups before and after DA injections. CONCLUSION Cadmium blocked the dopamine effect on the latencies of N1 and P2 of FVEP (because it prolonged them alone); however, cadmium increased the stimulative effect of dopamine on their amplitudes.
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The effect of prenatal exposure to cadmium on flash visual evoked potentials in rat offspring before and after injection of norepinephrine into the Lateral Brain Ventricle
Klinika oczna, 2000Co-Authors: Ewa Herba, Dorota Pojda-wilczek, Stefan M Pojda, Ryszard Brus, Agata R PlechAbstract:AIM It is known that norepinephrine (NE) in low doses increases the amplitude of flash visual evoked potential (FVEP). The purpose of this paper was to find out if cadmium (Cd) intoxication changes the NE effect on FVEP. MATERIAL AND METHODS 18 Wistar albino rats were divided into 3 groups: 6 received 5 ppm, next 6 received 50 ppm cadmium in drinking water since time of conception and during 21 days after delivery and 6 as a control group received tap water only. Newborns were examined when they were 3 to 6 months old. FVEP were recorded before and after injection of 10 microliters saline and then NE into the right Lateral Brain Ventricle. Two doses of NE 25 and 50 nmols were used. Amplitudes of the first deep negative wave (N1) and the next positive one (P2) were measured from isoelectric line to peaks. For statistic analysis the Student t-test was performed with statistical significance by p < 0.05. RESULTS The prolongation of N1 and P2 latencies of FVEP was observed in all groups after both doses of NE, the differences were statistically significant after doses of 25 nmols NE. The amplitude of N1 increased after NE in all groups, in the control one till 205-225% and 143-151% in Cd groups. The amplitude of P2 in control group was higher (109-113%) after NE compared to initial value (100%). Cadmium caused the decrease (of 56-90%) after both doses of NE. The differences of amplitudes were statistically significant. The prenatal treatment by cadmium caused the lower sensitivity of FVEP to NE.
Ewa Herba - One of the best experts on this subject based on the ideXlab platform.
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The effect of gamma-aminobutyric acid injected into Lateral Brain Ventricle of rats after prenatal cadmium intoxication on flash visual evoked potentials (FVEP)
Klinika oczna, 2001Co-Authors: Ewa Herba, Dorota Pojda-wilczek, Stefan M Pojda, Ryszard Szkilnik, Agata R PlechAbstract:PURPOSE: To find out any influence of gamma-aminobutyric acid (GABA) injected into Lateral Brain Ventricle in newborn rats prenatally exposed to cadmium (Cd). METHOD: 18 white, Wistar, offspring rats were divided into 3 groups, each consisting of 6 rats (control, 5 ppm and 50 ppm of Cd in drinking water). Newborns were examined when they were 3-6 months old. FVEP were recorded before and after GABA injections. Two doses of GABA were used, 10 and 100 nmols. The statistic analysis with the test of t-Student was performed to estimate the amplitudes and latencies of the negative wave N1 and the next positive one P2. p < 0.05 was used to indicate significant difference. RESULTS: No significant changes in the latencies of peak N1 and P2 in the control and Cd 5 ppm groups (101-103%) after 10 nmols GABA were observed. However, the shortened (91-97%) of them was observed after both doses of GABA in Cd 50 ppm group. The mean value of amplitude of N1 in control rats increased to 127% after 10 nmols GABA and 142% after 100 nmols GABA. Moreover, the mean amplitude of P2 in this group increased to 108% and 146%, respectively. The high significant increase of the amplitudes of N1 (181-280%) and P2 (160-177%) waves were received after both doses of GABA in Cd groups. CONCLUSION: Cadmium increased the sensitivity of GABA-receptors in the OUN.
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The effect of dopamine injected into the Lateral Brain Ventricle on flash visual evoked potential (FVEP) after prenatal intoxication with cadmium
Klinika oczna, 2000Co-Authors: Ewa Herba, Dorota Pojda-wilczek, Stefan M Pojda, Agata R Plech, Ryszard SzkilnikAbstract:PURPOSE Earlier studies demonstrated that exposure, especially prenatal, of mammalians to cadmium (Cd) results in disorders of visual evoked potentials (FVEP). The purpose of this study is to find out any influence of cadmium intoxications on the effect of dopamine (DA) on FVEP. METHOD 18 Wistar albino rats in 3-6 months of age were divided into 3 groups: control (drinking tap water only), prenatal exposure of 5 ppm, and 50 ppm Cd. Flash visual evoked potentials (FVEP) were recorded before and after injections of dopamine (DA) 100 and 200 nmols into the Lateral Brain Ventricle. The amplitude and latency of N1 and P2 were statistically analysed by the test of t-Student. p < 0.05 was used to indicate significant difference. RESULTS There were no statistical differences of mean latency of P2 waves between initial records of FVEP and after both doses of DA in all observed groups. The amplitudes of both waves increased after DA injections compared to initial values in all groups. The differences were statistically significant. The mean latencies of N1 peak were prolonged after both DA doses (106-109%) compared to the initial records (100%) in the control group; however, there were no changes of it in the Cd-treated groups before and after DA injections. CONCLUSION Cadmium blocked the dopamine effect on the latencies of N1 and P2 of FVEP (because it prolonged them alone); however, cadmium increased the stimulative effect of dopamine on their amplitudes.
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The effect of prenatal exposure to cadmium on flash visual evoked potentials in rat offspring before and after injection of norepinephrine into the Lateral Brain Ventricle
Klinika oczna, 2000Co-Authors: Ewa Herba, Dorota Pojda-wilczek, Stefan M Pojda, Ryszard Brus, Agata R PlechAbstract:AIM It is known that norepinephrine (NE) in low doses increases the amplitude of flash visual evoked potential (FVEP). The purpose of this paper was to find out if cadmium (Cd) intoxication changes the NE effect on FVEP. MATERIAL AND METHODS 18 Wistar albino rats were divided into 3 groups: 6 received 5 ppm, next 6 received 50 ppm cadmium in drinking water since time of conception and during 21 days after delivery and 6 as a control group received tap water only. Newborns were examined when they were 3 to 6 months old. FVEP were recorded before and after injection of 10 microliters saline and then NE into the right Lateral Brain Ventricle. Two doses of NE 25 and 50 nmols were used. Amplitudes of the first deep negative wave (N1) and the next positive one (P2) were measured from isoelectric line to peaks. For statistic analysis the Student t-test was performed with statistical significance by p < 0.05. RESULTS The prolongation of N1 and P2 latencies of FVEP was observed in all groups after both doses of NE, the differences were statistically significant after doses of 25 nmols NE. The amplitude of N1 increased after NE in all groups, in the control one till 205-225% and 143-151% in Cd groups. The amplitude of P2 in control group was higher (109-113%) after NE compared to initial value (100%). Cadmium caused the decrease (of 56-90%) after both doses of NE. The differences of amplitudes were statistically significant. The prenatal treatment by cadmium caused the lower sensitivity of FVEP to NE.
