The Experts below are selected from a list of 261 Experts worldwide ranked by ideXlab platform

Peter Paul De Deyn - One of the best experts on this subject based on the ideXlab platform.

  • pentylenetetrazole induced Seizure Susceptibility in the tau58 4 transgenic mouse model of tauopathy
    Neuroscience, 2020
    Co-Authors: Jan Van Erum, Femke Valkenburg, Debby Van Dam, Peter Paul De Deyn
    Abstract:

    In several tauopathies such as Alzheimer's disease (AD), an increased incidence of Seizures is observed. Tau, one of the major proteins implicated in AD pathology, is an important regulator of neural network excitability and might participate in the underlying epileptic cascade. However, the mechanisms underlying this relationship are not fully elucidated. We aim to investigate this mechanism by analyzing Seizure Susceptibility to the convulsant pentylenetetrazole (PTZ) in a novel rodent tauopathy model. A single dose of PTZ was systemically injected in Tau58/4 transgenic mice. To investigate whether young and aged heterozygous (HET) mice exhibit a higher Susceptibility to Seizures in comparison with wild-type (WT) littermates, video electroencephalography (EEG) in combination with behavioral scoring according to a modified Racine scale was used. The employment of different dosage groups enabled us to characterize the dose range reliably inducing Seizures. Here, we report an increased Seizure Susceptibility in young but not in old HET Tau58/4 mice. Young HET animals displayed more severe Seizures and had a reduced latency to the first Seizure compared to WTs. Also, age-related differences in Susceptibility could be demonstrated for both genotypes. Identification and targeting of secondary diseases such as epilepsy, which aggravate dementia and lead to earlier institutionalization, is key. This study finds that tau pathology itself is sufficient to alter Seizure Susceptibility in a rodent model, indicating that the disease process is crucial in the emergence of epilepsy in patients with tauopathy.

  • Pentylenetetrazole-induced Seizure Susceptibility in the Tau58/4 Transgenic Mouse Model of Tauopathy
    Neuroscience, 2019
    Co-Authors: Jan Van Erum, Femke Valkenburg, Debby Van Dam, Peter Paul De Deyn
    Abstract:

    In several tauopathies such as Alzheimer's disease (AD), an increased incidence of Seizures is observed. Tau, one of the major proteins implicated in AD pathology, is an important regulator of neural network excitability and might participate in the underlying epileptic cascade. However, the mechanisms underlying this relationship are not fully elucidated. We aim to investigate this mechanism by analyzing Seizure Susceptibility to the convulsant pentylenetetrazole (PTZ) in a novel rodent tauopathy model. A single dose of PTZ was systemically injected in Tau58/4 transgenic mice. To investigate whether young and aged heterozygous (HET) mice exhibit a higher Susceptibility to Seizures in comparison with wild-type (WT) littermates, video electroencephalography (EEG) in combination with behavioral scoring according to a modified Racine scale was used. The employment of different dosage groups enabled us to characterize the dose range reliably inducing Seizures. Here, we report an increased Seizure Susceptibility in young but not in old HET Tau58/4 mice. Young HET animals displayed more severe Seizures and had a reduced latency to the first Seizure compared to WTs. Also, age-related differences in Susceptibility could be demonstrated for both genotypes. Identification and targeting of secondary diseases such as epilepsy, which aggravate dementia and lead to earlier institutionalization, is key. This study finds that tau pathology itself is sufficient to alter Seizure Susceptibility in a rodent model, indicating that the disease process is crucial in the emergence of epilepsy in patients with tauopathy.

Quentin J. Pittman - One of the best experts on this subject based on the ideXlab platform.

  • Prenatal transport stress, postnatal maternal behavior, and offspring sex differentially affect Seizure Susceptibility in young rats
    Epilepsy & behavior : E&B, 2013
    Co-Authors: Chikako Moriyama, Michael A. Galic, Quentin J. Pittman, Richelle Mychasiuk, Tara S. Perrot, R. William Currie, Michael J. Esser
    Abstract:

    Epilepsy is a heterogeneous and chronic neurological condition of undefined etiology in the majority of cases. Similarly, the pathogenesis of the unprovoked Seizures that lead to epilepsy is not known. We are interested in the factors that modify inherent Seizure Susceptibility, with a particular focus on those occurring during the prenatal and early postnatal periods. Female Sprague-Dawley rats were bred in-house or transported during pregnancy at one of two gestational days (G9 or G16). The effects of transport stress, maternal behavior, and offspring sex were then examined in terms of how they were related to provoked Seizure Susceptibility to kainic acid (KA) or a model of febrile convulsions (FCs) on postnatal day 14 (P14). We also examined the pattern of neuronal activation in the hippocampus and amygdala as indicated by the density of FosB protein immunoreactivity (FosB-ir). Results demonstrated only a small and inconsistent effect of transport alone, suggesting that the groups differed slightly prior to experimental manipulations. However, the influence of maternal behaviors such as licking and grooming (LG), arched back nursing (ABN), and dam-off time (DO) exerted a much stronger effect on the offspring. Dams designated as high LG gave birth to smaller litters, had pups that weighed less, had greater Seizure Susceptibility and severity, and had more FosB-ir neurons predominantly in the ventral hippocampus and the medial subnucleus of the amygdala (MeA). We also found a sex-dependent effect such that P14 males were smaller than their female littermates and had a greater Seizure Susceptibility and severity. Taken together, these results suggest an impact of prenatal and postnatal factors, as well as sex, on Seizure Susceptibility in young animals.

  • Contributions of peripheral inflammation to Seizure Susceptibility: cytokines and brain excitability.
    Epilepsy research, 2009
    Co-Authors: Kiarash Riazi, Michael A. Galic, Quentin J. Pittman
    Abstract:

    Inflammation is an important factor in the pathophysiology of Seizure generation and epileptogenesis. While the role of CNS inflammation is well acknowledged as an important factor in Seizure pathophysiology, less is known about the role of peripheral inflammation. Systemic inflammation induces a mirror inflammatory response in the brain that might have transient or long-term effects on Seizure Susceptibility. The focus of our laboratory research is the study of the interaction of systemic inflammatory events with neuronal excitability and Seizure Susceptibility. In this paper we provide a review of our findings and discuss possible mechanisms.

  • Postnatal Inflammation Increases Seizure Susceptibility in Adult Rats
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008
    Co-Authors: Michael A. Galic, Kiarash Riazi, James G. Heida, Abdeslam Mouihate, Neil M. Fournier, Sarah J. Spencer, Lisa E. Kalynchuk, G. Campbell Teskey, Quentin J. Pittman
    Abstract:

    There are critical postnatal periods during which even subtle interventions can have long-lasting effects on adult physiology. We asked whether an immune challenge during early postnatal development can alter neuronal excitability and Seizure Susceptibility in adults. Postnatal day 14 (P14) male Sprague Dawley rats were injected with the bacterial endotoxin lipopolysaccharide (LPS), and control animals received sterile saline. Three weeks later, extracellular recordings from hippocampal slices revealed enhanced field EPSP slopes after Schaffer collateral stimulation and increased epileptiform burst-firing activity in CA1 after 4-aminopyridine application. Six to 8 weeks after postnatal LPS injection, Seizure Susceptibility was assessed in response to lithium–pilocarpine, kainic acid, and pentylenetetrazol. Rats treated with LPS showed significantly greater adult Seizure Susceptibility to all convulsants, as well as increased cytokine release and enhanced neuronal degeneration within the hippocampus after limbic Seizures. These persistent increases in Seizure Susceptibility occurred only when LPS was given during a critical postnatal period (P7 and P14) and not before (P1) or after (P20). This early effect of LPS on adult Seizures was blocked by concurrent intracerebroventricular administration of a tumor necrosis factor α (TNFα) antibody and mimicked by intracerebroventricular injection of rat recombinant TNFα. Postnatal LPS injection did not result in permanent changes in microglial (Iba1) activity or hippocampal cytokine [IL-1β (interleukin-1β) and TNFα] levels, but caused a slight increase in astrocyte (GFAP) numbers. These novel results indicate that a single LPS injection during a critical postnatal period causes a long-lasting increase in Seizure Susceptibility that is strongly dependent on TNFα.

  • Postnatal inflammation increases Seizure Susceptibility in adult rats
    Neuroscience, 2008
    Co-Authors: Michael A. Galic, Kiarash Riazi, James G. Heida, Abdeslam Mouihate, Neil M. Fournier, Sarah J. Spencer, Lisa E. Kalynchuk, G. Campbell Teskey, Quentin J. Pittman
    Abstract:

    There are critical postnatal periods during which even subtle interventions can have long-lasting effects on adult physiology. We asked whether an immune challenge during early postnatal development can alter neuronal excitability and Seizure Susceptibility in adults. Postnatal day 14 (P14) male Sprague Dawley rats were injected with the bacterial endotoxin lipopolysaccharide (LPS), and control animals received sterile saline. Three weeks later, extracellular recordings from hippocampal slices revealed enhanced field EPSP slopes after Schaffer collateral stimulation and increased epileptiform burst-firing activity in CA1 after 4-aminopyridine application. Six to 8 weeks after postnatal LPS injection, Seizure Susceptibility was assessed in response to lithium-pilocarpine, kainic acid, and pentylenetetrazol

Debby Van Dam - One of the best experts on this subject based on the ideXlab platform.

  • pentylenetetrazole induced Seizure Susceptibility in the tau58 4 transgenic mouse model of tauopathy
    Neuroscience, 2020
    Co-Authors: Jan Van Erum, Femke Valkenburg, Debby Van Dam, Peter Paul De Deyn
    Abstract:

    In several tauopathies such as Alzheimer's disease (AD), an increased incidence of Seizures is observed. Tau, one of the major proteins implicated in AD pathology, is an important regulator of neural network excitability and might participate in the underlying epileptic cascade. However, the mechanisms underlying this relationship are not fully elucidated. We aim to investigate this mechanism by analyzing Seizure Susceptibility to the convulsant pentylenetetrazole (PTZ) in a novel rodent tauopathy model. A single dose of PTZ was systemically injected in Tau58/4 transgenic mice. To investigate whether young and aged heterozygous (HET) mice exhibit a higher Susceptibility to Seizures in comparison with wild-type (WT) littermates, video electroencephalography (EEG) in combination with behavioral scoring according to a modified Racine scale was used. The employment of different dosage groups enabled us to characterize the dose range reliably inducing Seizures. Here, we report an increased Seizure Susceptibility in young but not in old HET Tau58/4 mice. Young HET animals displayed more severe Seizures and had a reduced latency to the first Seizure compared to WTs. Also, age-related differences in Susceptibility could be demonstrated for both genotypes. Identification and targeting of secondary diseases such as epilepsy, which aggravate dementia and lead to earlier institutionalization, is key. This study finds that tau pathology itself is sufficient to alter Seizure Susceptibility in a rodent model, indicating that the disease process is crucial in the emergence of epilepsy in patients with tauopathy.

  • Pentylenetetrazole-induced Seizure Susceptibility in the Tau58/4 Transgenic Mouse Model of Tauopathy
    Neuroscience, 2019
    Co-Authors: Jan Van Erum, Femke Valkenburg, Debby Van Dam, Peter Paul De Deyn
    Abstract:

    In several tauopathies such as Alzheimer's disease (AD), an increased incidence of Seizures is observed. Tau, one of the major proteins implicated in AD pathology, is an important regulator of neural network excitability and might participate in the underlying epileptic cascade. However, the mechanisms underlying this relationship are not fully elucidated. We aim to investigate this mechanism by analyzing Seizure Susceptibility to the convulsant pentylenetetrazole (PTZ) in a novel rodent tauopathy model. A single dose of PTZ was systemically injected in Tau58/4 transgenic mice. To investigate whether young and aged heterozygous (HET) mice exhibit a higher Susceptibility to Seizures in comparison with wild-type (WT) littermates, video electroencephalography (EEG) in combination with behavioral scoring according to a modified Racine scale was used. The employment of different dosage groups enabled us to characterize the dose range reliably inducing Seizures. Here, we report an increased Seizure Susceptibility in young but not in old HET Tau58/4 mice. Young HET animals displayed more severe Seizures and had a reduced latency to the first Seizure compared to WTs. Also, age-related differences in Susceptibility could be demonstrated for both genotypes. Identification and targeting of secondary diseases such as epilepsy, which aggravate dementia and lead to earlier institutionalization, is key. This study finds that tau pathology itself is sufficient to alter Seizure Susceptibility in a rodent model, indicating that the disease process is crucial in the emergence of epilepsy in patients with tauopathy.

Jan Van Erum - One of the best experts on this subject based on the ideXlab platform.

  • pentylenetetrazole induced Seizure Susceptibility in the tau58 4 transgenic mouse model of tauopathy
    Neuroscience, 2020
    Co-Authors: Jan Van Erum, Femke Valkenburg, Debby Van Dam, Peter Paul De Deyn
    Abstract:

    In several tauopathies such as Alzheimer's disease (AD), an increased incidence of Seizures is observed. Tau, one of the major proteins implicated in AD pathology, is an important regulator of neural network excitability and might participate in the underlying epileptic cascade. However, the mechanisms underlying this relationship are not fully elucidated. We aim to investigate this mechanism by analyzing Seizure Susceptibility to the convulsant pentylenetetrazole (PTZ) in a novel rodent tauopathy model. A single dose of PTZ was systemically injected in Tau58/4 transgenic mice. To investigate whether young and aged heterozygous (HET) mice exhibit a higher Susceptibility to Seizures in comparison with wild-type (WT) littermates, video electroencephalography (EEG) in combination with behavioral scoring according to a modified Racine scale was used. The employment of different dosage groups enabled us to characterize the dose range reliably inducing Seizures. Here, we report an increased Seizure Susceptibility in young but not in old HET Tau58/4 mice. Young HET animals displayed more severe Seizures and had a reduced latency to the first Seizure compared to WTs. Also, age-related differences in Susceptibility could be demonstrated for both genotypes. Identification and targeting of secondary diseases such as epilepsy, which aggravate dementia and lead to earlier institutionalization, is key. This study finds that tau pathology itself is sufficient to alter Seizure Susceptibility in a rodent model, indicating that the disease process is crucial in the emergence of epilepsy in patients with tauopathy.

  • Pentylenetetrazole-induced Seizure Susceptibility in the Tau58/4 Transgenic Mouse Model of Tauopathy
    Neuroscience, 2019
    Co-Authors: Jan Van Erum, Femke Valkenburg, Debby Van Dam, Peter Paul De Deyn
    Abstract:

    In several tauopathies such as Alzheimer's disease (AD), an increased incidence of Seizures is observed. Tau, one of the major proteins implicated in AD pathology, is an important regulator of neural network excitability and might participate in the underlying epileptic cascade. However, the mechanisms underlying this relationship are not fully elucidated. We aim to investigate this mechanism by analyzing Seizure Susceptibility to the convulsant pentylenetetrazole (PTZ) in a novel rodent tauopathy model. A single dose of PTZ was systemically injected in Tau58/4 transgenic mice. To investigate whether young and aged heterozygous (HET) mice exhibit a higher Susceptibility to Seizures in comparison with wild-type (WT) littermates, video electroencephalography (EEG) in combination with behavioral scoring according to a modified Racine scale was used. The employment of different dosage groups enabled us to characterize the dose range reliably inducing Seizures. Here, we report an increased Seizure Susceptibility in young but not in old HET Tau58/4 mice. Young HET animals displayed more severe Seizures and had a reduced latency to the first Seizure compared to WTs. Also, age-related differences in Susceptibility could be demonstrated for both genotypes. Identification and targeting of secondary diseases such as epilepsy, which aggravate dementia and lead to earlier institutionalization, is key. This study finds that tau pathology itself is sufficient to alter Seizure Susceptibility in a rodent model, indicating that the disease process is crucial in the emergence of epilepsy in patients with tauopathy.

Jamie Maguire - One of the best experts on this subject based on the ideXlab platform.