The Experts below are selected from a list of 2046 Experts worldwide ranked by ideXlab platform
Lechoslaw Turski - One of the best experts on this subject based on the ideXlab platform.
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long term effects of pilocarpine in rats structural damage of the brain triggers kindling and spontaneous recurrent seizures
Epilepsia, 1991Co-Authors: Esper A Cavalheiro, Joao Pereira Leite, Zuner A Bortolotto, Waldemar A Turski, Chrysanthy Ikonomidou, Lechoslaw TurskiAbstract:Structural damage of the human brain (perinatal damage, cerebral trauma, head injury, cerebrovascular and degenerative diseases, intracranial tumor, metabolic diseases, toxins, drug-induced seizures) may lead to chronic epilepsy in survivors. Epidemiologic analyses show that a considerable time-delay occurs between the exposure of the brain to injury and the appearance of seizures. Such seizures are usually partial or mixed, may develop at any age, and are difficult to treat. In rats subjected to structural damage of the brain induced by sustained convulsions triggered by systemic administration of the Cholinergic Agent pilocarpine, spontaneous seizures may develop after a mean latency of 14-15 days. The mean frequency of spontaneous recurrent convulsions remains constant for several months. Evolution of these convulsions proceeds through several electrographic and behavioral stages resembling kindling. Kindling may be otherwise induced in rodents by repeated systemic administration of convulsants or by repeated electrical stimulation of sensitive brain regions. These observations demonstrate that structural damage of the brain may lead to spontaneously recurrent convulsions (chronic epilepsy) in rats and that kindling may be involved in the evolution of such a condition. This finding suggests that kindling mechanisms underlie the development of epileptic foci from structural brain lesions. Such mechanisms may be involved in the etiology of some forms of epilepsy in humans.
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long term effects of pilocarpine in rats structural damage of the brain triggers kindling and spontaneous recurrent seizures
Epilepsia, 1991Co-Authors: Esper A Cavalheiro, Joao Pereira Leite, Zuner A Bortolotto, Waldemar A Turski, Chrysanthy Ikonomidou, Lechoslaw TurskiAbstract:Summary: Structural damage of the human brain (perinatal damage, cerebral trauma, head injury, cerebrovascular and degenerative diseases, intracranial tumor, metabolic diseases, toxins, drug-induced seizures) may lead to chronic epilepsy in survivors. Epidemiologic analyses show that a considerable time-delay occurs between the exposure of the brain to injury and the appearance of seizures. Such seizures are usually partial or mixed, may develop at any age, and are difficult to treat. In rats subjected to structural damage of the brain induced by sustained convulsions triggered by systemic administration of the Cholinergic Agent pilocarpine, spontaneous seizures may develop after a mean latency of 14–15 days. The mean frequency of spontaneous recurrent convulsions remains constant for several months. Evolution of these convulsions proceeds through several electrographic and behavioral stages resembling kindling. Kindling may be otherwise induced in rodents by repeated systemic administration of convulsants or by repeated electrical stimulation of sensitive brain regions. These observations demonstrate that structural damage of the brain may lead to spontaneously recurrent convulsions (chronic epilepsy) in rats and that kindling may be involved in the evolution of such a condition. This finding suggests that kindling mechanisms underlie the development of epileptic foci from structural brain lesions. Such mechanisms may be involved in the etiology of some forms of epilepsy in humans. RESUME Des lesions structurelles du cerveau humain (apres souffrance perinatale, traumatisme cerebral, maladies cerebro-vasculaires ou degeneratives, tumeurs intracrâniennes, maladies metaboliques, induction par substances toxiques ou par medicaments) peut entrainer une epilepsie chronique chez les survivals. Les analyses epidemiologiques montrent qu'il y a un long delai entre ľexposition du cerveau a la cause de la lesion e ľapparition des crises. De telles crises sont generalement partielles ou mixtes, peuvent survenir a n'importe quel âge, et sont de traitement difficile. Chez des rats, soumis a une lesion structurelle du cerveau induite par des convulsions prolongaees apres administration systemique de pilocarpine, des crises spontanees peuvent survenir apres une latence moyenne de 14 a 15 jours. La frequence moyenne des convulsions recidivant spontanement reste constante pendant quelques mois. ľevolution de ces convulsions traverse plusieurs stades electrographiques et comportementaux qui ressemblent a ceux observes dans le kindling. Le kindling peut etre induit chez les rongeurs par ľadministration systemique repetee de produits convulsivants ou par une stimulation electrique repetee de regions sensibles du cerveau. Ces observations demontrent qu'une lesion structurelle du cerveau peut provoquer chez le rat des convulsions recidivant de facon spontanee, c'est-a-dire une epilepsie chronique et que le kindling peut etre un mgeanisme d'un tel etat. Ces donnees suggerent qu'un mecanisme de kindling soustend le developpement de foyers epileptiques a partir de lesions cerebrales structurelles. De tels mecanismes peuvent etre impliques dans ľeliologie de certaines formes d'epilepsie humaine.
Esper A Cavalheiro - One of the best experts on this subject based on the ideXlab platform.
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long term effects of pilocarpine in rats structural damage of the brain triggers kindling and spontaneous recurrent seizures
Epilepsia, 1991Co-Authors: Esper A Cavalheiro, Joao Pereira Leite, Zuner A Bortolotto, Waldemar A Turski, Chrysanthy Ikonomidou, Lechoslaw TurskiAbstract:Structural damage of the human brain (perinatal damage, cerebral trauma, head injury, cerebrovascular and degenerative diseases, intracranial tumor, metabolic diseases, toxins, drug-induced seizures) may lead to chronic epilepsy in survivors. Epidemiologic analyses show that a considerable time-delay occurs between the exposure of the brain to injury and the appearance of seizures. Such seizures are usually partial or mixed, may develop at any age, and are difficult to treat. In rats subjected to structural damage of the brain induced by sustained convulsions triggered by systemic administration of the Cholinergic Agent pilocarpine, spontaneous seizures may develop after a mean latency of 14-15 days. The mean frequency of spontaneous recurrent convulsions remains constant for several months. Evolution of these convulsions proceeds through several electrographic and behavioral stages resembling kindling. Kindling may be otherwise induced in rodents by repeated systemic administration of convulsants or by repeated electrical stimulation of sensitive brain regions. These observations demonstrate that structural damage of the brain may lead to spontaneously recurrent convulsions (chronic epilepsy) in rats and that kindling may be involved in the evolution of such a condition. This finding suggests that kindling mechanisms underlie the development of epileptic foci from structural brain lesions. Such mechanisms may be involved in the etiology of some forms of epilepsy in humans.
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long term effects of pilocarpine in rats structural damage of the brain triggers kindling and spontaneous recurrent seizures
Epilepsia, 1991Co-Authors: Esper A Cavalheiro, Joao Pereira Leite, Zuner A Bortolotto, Waldemar A Turski, Chrysanthy Ikonomidou, Lechoslaw TurskiAbstract:Summary: Structural damage of the human brain (perinatal damage, cerebral trauma, head injury, cerebrovascular and degenerative diseases, intracranial tumor, metabolic diseases, toxins, drug-induced seizures) may lead to chronic epilepsy in survivors. Epidemiologic analyses show that a considerable time-delay occurs between the exposure of the brain to injury and the appearance of seizures. Such seizures are usually partial or mixed, may develop at any age, and are difficult to treat. In rats subjected to structural damage of the brain induced by sustained convulsions triggered by systemic administration of the Cholinergic Agent pilocarpine, spontaneous seizures may develop after a mean latency of 14–15 days. The mean frequency of spontaneous recurrent convulsions remains constant for several months. Evolution of these convulsions proceeds through several electrographic and behavioral stages resembling kindling. Kindling may be otherwise induced in rodents by repeated systemic administration of convulsants or by repeated electrical stimulation of sensitive brain regions. These observations demonstrate that structural damage of the brain may lead to spontaneously recurrent convulsions (chronic epilepsy) in rats and that kindling may be involved in the evolution of such a condition. This finding suggests that kindling mechanisms underlie the development of epileptic foci from structural brain lesions. Such mechanisms may be involved in the etiology of some forms of epilepsy in humans. RESUME Des lesions structurelles du cerveau humain (apres souffrance perinatale, traumatisme cerebral, maladies cerebro-vasculaires ou degeneratives, tumeurs intracrâniennes, maladies metaboliques, induction par substances toxiques ou par medicaments) peut entrainer une epilepsie chronique chez les survivals. Les analyses epidemiologiques montrent qu'il y a un long delai entre ľexposition du cerveau a la cause de la lesion e ľapparition des crises. De telles crises sont generalement partielles ou mixtes, peuvent survenir a n'importe quel âge, et sont de traitement difficile. Chez des rats, soumis a une lesion structurelle du cerveau induite par des convulsions prolongaees apres administration systemique de pilocarpine, des crises spontanees peuvent survenir apres une latence moyenne de 14 a 15 jours. La frequence moyenne des convulsions recidivant spontanement reste constante pendant quelques mois. ľevolution de ces convulsions traverse plusieurs stades electrographiques et comportementaux qui ressemblent a ceux observes dans le kindling. Le kindling peut etre induit chez les rongeurs par ľadministration systemique repetee de produits convulsivants ou par une stimulation electrique repetee de regions sensibles du cerveau. Ces observations demontrent qu'une lesion structurelle du cerveau peut provoquer chez le rat des convulsions recidivant de facon spontanee, c'est-a-dire une epilepsie chronique et que le kindling peut etre un mgeanisme d'un tel etat. Ces donnees suggerent qu'un mecanisme de kindling soustend le developpement de foyers epileptiques a partir de lesions cerebrales structurelles. De tels mecanismes peuvent etre impliques dans ľeliologie de certaines formes d'epilepsie humaine.
Xu-feng Huang - One of the best experts on this subject based on the ideXlab platform.
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galantamine improves cognition hippocampal inflammation and synaptic plasticity impairments induced by lipopolysaccharide in mice
Journal of Neuroinflammation, 2018Co-Authors: Yi Liu, Yuyun Zhang, Xian Zheng, Tongyong Fang, Xia Yang, Xuan Luo, Anlei Guo, Kelly A. Newell, Xu-feng HuangAbstract:Neuroinflammation plays an important role in the onset and progression of neurodegenerative diseases such as Alzheimer’s disease. Lipopolysaccharide (LPS, endotoxin) levels are higher in the brains of Alzheimer’s disease patients and are associated with neuroinflammation and cognitive decline, while neural Cholinergic signaling controls inflammation. This study aimed to examine the efficacy of galantamine, a clinically approved Cholinergic Agent, in alleviating LPS-induced neuroinflammation and cognitive decline as well as the associated mechanism. Mice were treated with galantamine (4 mg/kg, intraperitoneal injection) for 14 days prior to LPS exposure (intracerebroventricular injection). Cognitive tests were performed, including the Morris water maze and step-through tests. mRNA expression of the microglial marker (CD11b), astrocytic marker (GFAP), and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) were examined in the hippocampus by quantitative RT-PCR. The inflammatory signaling molecule, nuclear factor-kappa B (NF-κB p65), and synapse-associated proteins (synaptophysin, SYN, and postsynaptic density protein 95, PSD-95) were examined in the hippocampus by western blotting. Furthermore, NF-κB p65 levels in microglial cells and hippocampal neurons were examined in response to LPS and galantamine. Galantamine treatment prevented LPS-induced deficits in spatial learning and memory as well as memory acquisition of the passive avoidance response. Galantamine decreased the expression of microglia and astrocyte markers (CD11b and GFAP), pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), and NF-κB p65 in the hippocampus of LPS-exposed mice. Furthermore, galantamine ameliorated LPS-induced loss of synapse-associated proteins (SYN and PSD-95) in the hippocampus. In the in vitro study, LPS increased NF-κB p65 levels in microglia (BV-2 cells); the supernatant of LPS-stimulated microglia (Mi-sup), but not LPS, decreased the viability of hippocampal neuronal cells (HT-22 cells) and increased NF-κB p65 levels as well as expression of pro-inflammatory cytokines (IL-1β, IL-6) in HT-22 cells. Importantly, galantamine reduced the inflammatory response not only in the BV-2 microglia cell line, but also in the HT-22 hippocampal neuronal cell line. These findings indicate that galantamine could be a promising treatment to improve endotoxin-induced cognitive decline and neuroinflammation in neurodegenerative diseases.
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Galantamine improves cognition, hippocampal inflammation, and synaptic plasticity impairments induced by lipopolysaccharide in mice
BMC, 2018Co-Authors: Yi Liu, Yuyun Zhang, Xian Zheng, Tongyong Fang, Xia Yang, Xuan Luo, Anlei Guo, Kelly A. Newell, Xu-feng HuangAbstract:Abstract Background Neuroinflammation plays an important role in the onset and progression of neurodegenerative diseases such as Alzheimer’s disease. Lipopolysaccharide (LPS, endotoxin) levels are higher in the brains of Alzheimer’s disease patients and are associated with neuroinflammation and cognitive decline, while neural Cholinergic signaling controls inflammation. This study aimed to examine the efficacy of galantamine, a clinically approved Cholinergic Agent, in alleviating LPS-induced neuroinflammation and cognitive decline as well as the associated mechanism. Methods Mice were treated with galantamine (4 mg/kg, intraperitoneal injection) for 14 days prior to LPS exposure (intracerebroventricular injection). Cognitive tests were performed, including the Morris water maze and step-through tests. mRNA expression of the microglial marker (CD11b), astrocytic marker (GFAP), and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) were examined in the hippocampus by quantitative RT-PCR. The inflammatory signaling molecule, nuclear factor-kappa B (NF-κB p65), and synapse-associated proteins (synaptophysin, SYN, and postsynaptic density protein 95, PSD-95) were examined in the hippocampus by western blotting. Furthermore, NF-κB p65 levels in microglial cells and hippocampal neurons were examined in response to LPS and galantamine. Results Galantamine treatment prevented LPS-induced deficits in spatial learning and memory as well as memory acquisition of the passive avoidance response. Galantamine decreased the expression of microglia and astrocyte markers (CD11b and GFAP), pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), and NF-κB p65 in the hippocampus of LPS-exposed mice. Furthermore, galantamine ameliorated LPS-induced loss of synapse-associated proteins (SYN and PSD-95) in the hippocampus. In the in vitro study, LPS increased NF-κB p65 levels in microglia (BV-2 cells); the supernatant of LPS-stimulated microglia (Mi-sup), but not LPS, decreased the viability of hippocampal neuronal cells (HT-22 cells) and increased NF-κB p65 levels as well as expression of pro-inflammatory cytokines (IL-1β, IL-6) in HT-22 cells. Importantly, galantamine reduced the inflammatory response not only in the BV-2 microglia cell line, but also in the HT-22 hippocampal neuronal cell line. Conclusions These findings indicate that galantamine could be a promising treatment to improve endotoxin-induced cognitive decline and neuroinflammation in neurodegenerative diseases
Chrysanthy Ikonomidou - One of the best experts on this subject based on the ideXlab platform.
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long term effects of pilocarpine in rats structural damage of the brain triggers kindling and spontaneous recurrent seizures
Epilepsia, 1991Co-Authors: Esper A Cavalheiro, Joao Pereira Leite, Zuner A Bortolotto, Waldemar A Turski, Chrysanthy Ikonomidou, Lechoslaw TurskiAbstract:Structural damage of the human brain (perinatal damage, cerebral trauma, head injury, cerebrovascular and degenerative diseases, intracranial tumor, metabolic diseases, toxins, drug-induced seizures) may lead to chronic epilepsy in survivors. Epidemiologic analyses show that a considerable time-delay occurs between the exposure of the brain to injury and the appearance of seizures. Such seizures are usually partial or mixed, may develop at any age, and are difficult to treat. In rats subjected to structural damage of the brain induced by sustained convulsions triggered by systemic administration of the Cholinergic Agent pilocarpine, spontaneous seizures may develop after a mean latency of 14-15 days. The mean frequency of spontaneous recurrent convulsions remains constant for several months. Evolution of these convulsions proceeds through several electrographic and behavioral stages resembling kindling. Kindling may be otherwise induced in rodents by repeated systemic administration of convulsants or by repeated electrical stimulation of sensitive brain regions. These observations demonstrate that structural damage of the brain may lead to spontaneously recurrent convulsions (chronic epilepsy) in rats and that kindling may be involved in the evolution of such a condition. This finding suggests that kindling mechanisms underlie the development of epileptic foci from structural brain lesions. Such mechanisms may be involved in the etiology of some forms of epilepsy in humans.
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long term effects of pilocarpine in rats structural damage of the brain triggers kindling and spontaneous recurrent seizures
Epilepsia, 1991Co-Authors: Esper A Cavalheiro, Joao Pereira Leite, Zuner A Bortolotto, Waldemar A Turski, Chrysanthy Ikonomidou, Lechoslaw TurskiAbstract:Summary: Structural damage of the human brain (perinatal damage, cerebral trauma, head injury, cerebrovascular and degenerative diseases, intracranial tumor, metabolic diseases, toxins, drug-induced seizures) may lead to chronic epilepsy in survivors. Epidemiologic analyses show that a considerable time-delay occurs between the exposure of the brain to injury and the appearance of seizures. Such seizures are usually partial or mixed, may develop at any age, and are difficult to treat. In rats subjected to structural damage of the brain induced by sustained convulsions triggered by systemic administration of the Cholinergic Agent pilocarpine, spontaneous seizures may develop after a mean latency of 14–15 days. The mean frequency of spontaneous recurrent convulsions remains constant for several months. Evolution of these convulsions proceeds through several electrographic and behavioral stages resembling kindling. Kindling may be otherwise induced in rodents by repeated systemic administration of convulsants or by repeated electrical stimulation of sensitive brain regions. These observations demonstrate that structural damage of the brain may lead to spontaneously recurrent convulsions (chronic epilepsy) in rats and that kindling may be involved in the evolution of such a condition. This finding suggests that kindling mechanisms underlie the development of epileptic foci from structural brain lesions. Such mechanisms may be involved in the etiology of some forms of epilepsy in humans. RESUME Des lesions structurelles du cerveau humain (apres souffrance perinatale, traumatisme cerebral, maladies cerebro-vasculaires ou degeneratives, tumeurs intracrâniennes, maladies metaboliques, induction par substances toxiques ou par medicaments) peut entrainer une epilepsie chronique chez les survivals. Les analyses epidemiologiques montrent qu'il y a un long delai entre ľexposition du cerveau a la cause de la lesion e ľapparition des crises. De telles crises sont generalement partielles ou mixtes, peuvent survenir a n'importe quel âge, et sont de traitement difficile. Chez des rats, soumis a une lesion structurelle du cerveau induite par des convulsions prolongaees apres administration systemique de pilocarpine, des crises spontanees peuvent survenir apres une latence moyenne de 14 a 15 jours. La frequence moyenne des convulsions recidivant spontanement reste constante pendant quelques mois. ľevolution de ces convulsions traverse plusieurs stades electrographiques et comportementaux qui ressemblent a ceux observes dans le kindling. Le kindling peut etre induit chez les rongeurs par ľadministration systemique repetee de produits convulsivants ou par une stimulation electrique repetee de regions sensibles du cerveau. Ces observations demontrent qu'une lesion structurelle du cerveau peut provoquer chez le rat des convulsions recidivant de facon spontanee, c'est-a-dire une epilepsie chronique et que le kindling peut etre un mgeanisme d'un tel etat. Ces donnees suggerent qu'un mecanisme de kindling soustend le developpement de foyers epileptiques a partir de lesions cerebrales structurelles. De tels mecanismes peuvent etre impliques dans ľeliologie de certaines formes d'epilepsie humaine.
Waldemar A Turski - One of the best experts on this subject based on the ideXlab platform.
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long term effects of pilocarpine in rats structural damage of the brain triggers kindling and spontaneous recurrent seizures
Epilepsia, 1991Co-Authors: Esper A Cavalheiro, Joao Pereira Leite, Zuner A Bortolotto, Waldemar A Turski, Chrysanthy Ikonomidou, Lechoslaw TurskiAbstract:Structural damage of the human brain (perinatal damage, cerebral trauma, head injury, cerebrovascular and degenerative diseases, intracranial tumor, metabolic diseases, toxins, drug-induced seizures) may lead to chronic epilepsy in survivors. Epidemiologic analyses show that a considerable time-delay occurs between the exposure of the brain to injury and the appearance of seizures. Such seizures are usually partial or mixed, may develop at any age, and are difficult to treat. In rats subjected to structural damage of the brain induced by sustained convulsions triggered by systemic administration of the Cholinergic Agent pilocarpine, spontaneous seizures may develop after a mean latency of 14-15 days. The mean frequency of spontaneous recurrent convulsions remains constant for several months. Evolution of these convulsions proceeds through several electrographic and behavioral stages resembling kindling. Kindling may be otherwise induced in rodents by repeated systemic administration of convulsants or by repeated electrical stimulation of sensitive brain regions. These observations demonstrate that structural damage of the brain may lead to spontaneously recurrent convulsions (chronic epilepsy) in rats and that kindling may be involved in the evolution of such a condition. This finding suggests that kindling mechanisms underlie the development of epileptic foci from structural brain lesions. Such mechanisms may be involved in the etiology of some forms of epilepsy in humans.
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long term effects of pilocarpine in rats structural damage of the brain triggers kindling and spontaneous recurrent seizures
Epilepsia, 1991Co-Authors: Esper A Cavalheiro, Joao Pereira Leite, Zuner A Bortolotto, Waldemar A Turski, Chrysanthy Ikonomidou, Lechoslaw TurskiAbstract:Summary: Structural damage of the human brain (perinatal damage, cerebral trauma, head injury, cerebrovascular and degenerative diseases, intracranial tumor, metabolic diseases, toxins, drug-induced seizures) may lead to chronic epilepsy in survivors. Epidemiologic analyses show that a considerable time-delay occurs between the exposure of the brain to injury and the appearance of seizures. Such seizures are usually partial or mixed, may develop at any age, and are difficult to treat. In rats subjected to structural damage of the brain induced by sustained convulsions triggered by systemic administration of the Cholinergic Agent pilocarpine, spontaneous seizures may develop after a mean latency of 14–15 days. The mean frequency of spontaneous recurrent convulsions remains constant for several months. Evolution of these convulsions proceeds through several electrographic and behavioral stages resembling kindling. Kindling may be otherwise induced in rodents by repeated systemic administration of convulsants or by repeated electrical stimulation of sensitive brain regions. These observations demonstrate that structural damage of the brain may lead to spontaneously recurrent convulsions (chronic epilepsy) in rats and that kindling may be involved in the evolution of such a condition. This finding suggests that kindling mechanisms underlie the development of epileptic foci from structural brain lesions. Such mechanisms may be involved in the etiology of some forms of epilepsy in humans. RESUME Des lesions structurelles du cerveau humain (apres souffrance perinatale, traumatisme cerebral, maladies cerebro-vasculaires ou degeneratives, tumeurs intracrâniennes, maladies metaboliques, induction par substances toxiques ou par medicaments) peut entrainer une epilepsie chronique chez les survivals. Les analyses epidemiologiques montrent qu'il y a un long delai entre ľexposition du cerveau a la cause de la lesion e ľapparition des crises. De telles crises sont generalement partielles ou mixtes, peuvent survenir a n'importe quel âge, et sont de traitement difficile. Chez des rats, soumis a une lesion structurelle du cerveau induite par des convulsions prolongaees apres administration systemique de pilocarpine, des crises spontanees peuvent survenir apres une latence moyenne de 14 a 15 jours. La frequence moyenne des convulsions recidivant spontanement reste constante pendant quelques mois. ľevolution de ces convulsions traverse plusieurs stades electrographiques et comportementaux qui ressemblent a ceux observes dans le kindling. Le kindling peut etre induit chez les rongeurs par ľadministration systemique repetee de produits convulsivants ou par une stimulation electrique repetee de regions sensibles du cerveau. Ces observations demontrent qu'une lesion structurelle du cerveau peut provoquer chez le rat des convulsions recidivant de facon spontanee, c'est-a-dire une epilepsie chronique et que le kindling peut etre un mgeanisme d'un tel etat. Ces donnees suggerent qu'un mecanisme de kindling soustend le developpement de foyers epileptiques a partir de lesions cerebrales structurelles. De tels mecanismes peuvent etre impliques dans ľeliologie de certaines formes d'epilepsie humaine.