The Experts below are selected from a list of 20262 Experts worldwide ranked by ideXlab platform

Lynne A Fieber - One of the best experts on this subject based on the ideXlab platform.

  • habituation in the tail withdrawal reflex circuit is impaired during aging in aplysia californica
    Frontiers in Aging Neuroscience, 2016
    Co-Authors: Andrew T Kempsell, Lynne A Fieber
    Abstract:

    The relevance of putative contributors to Age-Related Memory Loss are poorly understood. The tail withdrawal circuit of the sea hare, a straightforward neural model, was used to investigate the aging characteristics of rudimentary learning. The simplicity of this neuronal circuit permits attribution of declines in the function of specific neurons to aging declines. Memory was impaired in advanced age animals compared to their performance at the peak of sexual maturity, with habituation training failing to attenuate the tail withdrawal response or to reduce tail motoneuron excitability, as occurred in peak maturity siblings. Baseline motoneuron excitability of aged animals was significantly lower, perhaps contributing to a smaller scope for attenuation. Conduction velocity in afferent fibers to tail sensory neurons (SN) decreased during aging. The findings suggest that Age-Related changes in tail sensory and motor neurons result in deterioration of a simple form of learning in Aplysia.

  • aging in sensory and motor neurons results in learning failure in aplysia californica
    PLOS ONE, 2015
    Co-Authors: Andrew T Kempsell, Lynne A Fieber
    Abstract:

    The physiological and molecular mechanisms of Age-Related Memory Loss are complicated by the complexity of vertebrate nervous systems. This study takes advantage of a simple neural model to investigate nervous system aging, focusing on changes in learning and Memory in the form of behavioral sensitization in vivo and synaptic facilitation in vitro. The effect of aging on the tail withdrawal reflex (TWR) was studied in Aplysia californica at maturity and late in the annual lifecycle. We found that short-term sensitization in TWR was absent in aged Aplysia. This implied that the neuronal machinery governing nonassociative learning was compromised during aging. Synaptic plasticity in the form of short-term facilitation between tail sensory and motor neurons decreased during aging whether the sensitizing stimulus was tail shock or the heterosynaptic modulator serotonin (5-HT). Together, these results suggest that the cellular mechanisms governing behavioral sensitization are compromised during aging, thereby nearly eliminating sensitization in aged Aplysia.

  • Aging in sensory and motor neurons results in learning failure in Aplysia californica
    2015
    Co-Authors: Andrew T Kempsell, Lynne A Fieber
    Abstract:

    The physiological and molecular mechanisms of Age-Related Memory Loss are complicated by the complexity of vertebrate nervous systems. This study takes advantage of a simple neural model to investigate nervous system aging, focusing on changes in learning and Memory in the form of behavioral sensitization in vivo and synaptic facilitation in vitro. The effect of aging on the tail withdrawal reflex (TWR) was studied in Aplysia californica at maturity and late in the annual lifecycle. We found that short-term sensitization in TWR was absent in aged Aplysia. This implied that the neuronal machinery governing nonassociative learning was compromised during aging. Synaptic plasticity in the form of short-term facilitation between tail sensory and motor neurons decreased during aging whether the sensitizing stimulus was tail shock or the heterosynaptic modulator serotonin (5-HT). Together, these results suggest that the cellular mechanisms governing behavioral sensitization are compromised during aging, thereby nearly eliminating sensitization in aged Aplysia.   The first file contains data for behavioral experiments investigating Memory for sensitization in the tail withdrawal reflex as a function of aging. The second file contains data for electrophysiological experiments described in the paper. The data is organized according to the figures in the paper. Each tab is labeled with the appropriate figure that corresponds to the data.

Andrew T Kempsell - One of the best experts on this subject based on the ideXlab platform.

  • habituation in the tail withdrawal reflex circuit is impaired during aging in aplysia californica
    Frontiers in Aging Neuroscience, 2016
    Co-Authors: Andrew T Kempsell, Lynne A Fieber
    Abstract:

    The relevance of putative contributors to Age-Related Memory Loss are poorly understood. The tail withdrawal circuit of the sea hare, a straightforward neural model, was used to investigate the aging characteristics of rudimentary learning. The simplicity of this neuronal circuit permits attribution of declines in the function of specific neurons to aging declines. Memory was impaired in advanced age animals compared to their performance at the peak of sexual maturity, with habituation training failing to attenuate the tail withdrawal response or to reduce tail motoneuron excitability, as occurred in peak maturity siblings. Baseline motoneuron excitability of aged animals was significantly lower, perhaps contributing to a smaller scope for attenuation. Conduction velocity in afferent fibers to tail sensory neurons (SN) decreased during aging. The findings suggest that Age-Related changes in tail sensory and motor neurons result in deterioration of a simple form of learning in Aplysia.

  • aging in sensory and motor neurons results in learning failure in aplysia californica
    PLOS ONE, 2015
    Co-Authors: Andrew T Kempsell, Lynne A Fieber
    Abstract:

    The physiological and molecular mechanisms of Age-Related Memory Loss are complicated by the complexity of vertebrate nervous systems. This study takes advantage of a simple neural model to investigate nervous system aging, focusing on changes in learning and Memory in the form of behavioral sensitization in vivo and synaptic facilitation in vitro. The effect of aging on the tail withdrawal reflex (TWR) was studied in Aplysia californica at maturity and late in the annual lifecycle. We found that short-term sensitization in TWR was absent in aged Aplysia. This implied that the neuronal machinery governing nonassociative learning was compromised during aging. Synaptic plasticity in the form of short-term facilitation between tail sensory and motor neurons decreased during aging whether the sensitizing stimulus was tail shock or the heterosynaptic modulator serotonin (5-HT). Together, these results suggest that the cellular mechanisms governing behavioral sensitization are compromised during aging, thereby nearly eliminating sensitization in aged Aplysia.

  • Aging in sensory and motor neurons results in learning failure in Aplysia californica
    2015
    Co-Authors: Andrew T Kempsell, Lynne A Fieber
    Abstract:

    The physiological and molecular mechanisms of Age-Related Memory Loss are complicated by the complexity of vertebrate nervous systems. This study takes advantage of a simple neural model to investigate nervous system aging, focusing on changes in learning and Memory in the form of behavioral sensitization in vivo and synaptic facilitation in vitro. The effect of aging on the tail withdrawal reflex (TWR) was studied in Aplysia californica at maturity and late in the annual lifecycle. We found that short-term sensitization in TWR was absent in aged Aplysia. This implied that the neuronal machinery governing nonassociative learning was compromised during aging. Synaptic plasticity in the form of short-term facilitation between tail sensory and motor neurons decreased during aging whether the sensitizing stimulus was tail shock or the heterosynaptic modulator serotonin (5-HT). Together, these results suggest that the cellular mechanisms governing behavioral sensitization are compromised during aging, thereby nearly eliminating sensitization in aged Aplysia.   The first file contains data for behavioral experiments investigating Memory for sensitization in the tail withdrawal reflex as a function of aging. The second file contains data for electrophysiological experiments described in the paper. The data is organized according to the figures in the paper. Each tab is labeled with the appropriate figure that corresponds to the data.

David S. Olton - One of the best experts on this subject based on the ideXlab platform.

  • activation of the medial septal area attenuates ltp of the lateral perforant path and enhances heterosynaptic ltd of the medial perforant path in aged rats
    Brain Research, 1993
    Co-Authors: Kevin Pang, Megan J Williams, David S. Olton
    Abstract:

    Age-Related Memory impairments may be due to dysfunction of the septohippocampal system. The medial septal area (MSA) provides the major cholinergic projection to the hippocampus and is critical for Memory. Knowledge of the neurobiological mechanisms by which the cholinergic system can attenuate Age-Related Memory Loss can facilitate the development of effective cognitive enhancers. At present, one of the best neurobiological models of Memory formation is long-term potentiation/long-term depression (LTP/LTD). In previous studies, intraseptal infusion of the muscarinic agonist oxotremorine, which excites MSA neurons, improved Memory in aged rats. The present study examined LTP and LTD in aged Fisher 344 rats following intraseptal infusion of oxotremorine. LTP and LTD were assessed using the slope of the EPSP recorded from the hilar region of the dentate gyrus. Induction of LTP was blocked in the lateral perforant path, but not in the medial perforant path, following intraseptal infusions of oxotremorine. The generation and amplitude of heterosynaptic LTD was enhanced in the medial perforant path, but not in the lateral perforant path. The results provide evidence that pharmacological activation of the MSA can modulate LTP and LTD in the hippocampus of aged rats. The implications of these results with respect to Memory and synaptic plasticity in the hippocampus are discussed.

Gary W Small - One of the best experts on this subject based on the ideXlab platform.

  • cognitive and cerebral metabolic effects of celecoxib versus placebo in people with age related Memory Loss randomized controlled study
    American Journal of Geriatric Psychiatry, 2008
    Co-Authors: Gary W Small, Prabha Siddarth, Daniel H S Silverman, Linda M Ercoli, Karen J Miller, Helen Lavretsky, Susan Y Bookheimer, S C Huang, Jorge R Barrio
    Abstract:

    Objective Because anti-inflammatory drugs may delay cognitive decline and influence brain metabolism in normal aging, the authors determined the effects of the cyclooxygenase-2 inhibitor, celecoxib, on cognitive performance and regional cerebral glucose metabolism in nondemented volunteers with mild Age-Related Memory decline. Design Randomized, double-blind, placebo-controlled, parallel group trial with 18-months of exposure to study medication. Setting University research institute. Participants Eighty-eight subjects, aged 40–81 years (mean: 58.7, SD: 8.9 years) with mild self-reported Memory complaints but normal Memory performance scores were recruited from community physician referrals, media coverage, and advertising. Forty subjects completed the study. Interventions Daily celecoxib dose of 200 or 400 mg, or placebo. Main Outcome Measures Standardized neuropsychological test battery and statistical parametric mapping (SPM) of FDG-PET scans performed during mental rest. Results Measures of cognition showed significant between-group differences in executive functioning (F [1, 30] = 5.06, p=0.03) and language/semantic Memory ( F [1, 31] = 6.19, p=0.02), favoring the celecoxib group compared with the placebo group. Concomitantly, FDG-PET scans demonstrated bilateral metabolic increases in prefrontal cortex in the celecoxib group in the vicinity of Brodmann's areas 9 and 10, but not in the placebo group. SPM analyses of the PET data pooled by treatment arm corresponded to a 6% increase in activity over pretreatment levels (p Conclusions These results suggest that daily celecoxib use may improve cognitive performance and increase regional brain metabolism in people with age-associated Memory decline.

Eric R Kandel - One of the best experts on this subject based on the ideXlab platform.

  • rbap48 protein is a critical component of gpr158 ocn signaling and ameliorates age related Memory Loss
    Cell Reports, 2018
    Co-Authors: Stylianos Kosmidis, Alexandros Polyzos, Lucas R Harvey, Mary Youssef, Christine A Denny, Alex Dranovsky, Eric R Kandel
    Abstract:

    Precisely deciphering the molecular mechanisms of Age-Related Memory Loss is crucial to create appropriate therapeutic interventions. We have previously shown that the histone-binding protein RbAp48/Rbbp4 is a molecular determinant of Age-Related Memory Loss. By exploring how this protein regulates the genomic landscape of the hippocampal circuit, we find that RbAp48 controls the expression of BDNF and GPR158 proteins, both critical components of osteocalcin (OCN) signaling in the mouse hippocampus. We show that inhibition of RbAp48 in the hippocampal formation inhibits OCN's beneficial functions in cognition and causes deficits in discrimination Memory. In turn, disruption of OCN/GPR158 signaling leads to the downregulation of RbAp48 protein, mimicking the discrimination Memory deficits observed in the aged hippocampus. We also show that activation of the OCN/GPR158 pathway increases the expression of RbAp48 in the aged dentate gyrus and rescues Age-Related Memory Loss.

  • age related defects in spatial Memory are correlated with defects in the late phase of hippocampal long term potentiation in vitro and are attenuated by drugs that enhance the camp signaling pathway
    Proceedings of the National Academy of Sciences of the United States of America, 1999
    Co-Authors: Mary Elizabeth Bach, Mark Barad, Min Zhuo, Yun Fei Lu, Robert Shih, Isabelle M Mansuy, Robert D Hawkins, Eric R Kandel
    Abstract:

    To study the physiological and molecular mechanisms of Age-Related Memory Loss, we assessed spatial Memory in C57BL/B6 mice from different age cohorts and then measured in vitro the late phase of hippocampal long-term potentiation (L-LTP). Most young mice acquired the spatial task, whereas only a minority of aged mice did. Aged mice not only made significantly more errors but also exhibited greater individual differences. Slices from the hippocampus of aged mice exhibited significantly reduced L-LTP, and this was significantly and negatively correlated with errors in Memory. Because L-LTP depends on cAMP activation, we examined whether drugs that enhanced cAMP would attenuate the L-LTP and Memory defects. Both dopamine D1/D5 receptor agonists, which are positively coupled to adenylyl cyclase, and a cAMP phosphodiesterase inhibitor ameliorated the physiological as well as the Memory defects, consistent with the idea that a cAMP–protein kinase A-dependent signaling pathway is defective in Age-Related spatial Memory Loss.