Age-dependent glutamate induction of synaptic plasticity in cultured hippocampal neurons

Sapoznik, Sivan; Ivenshitz, Miriam; Segal, Menahem

doi:10.1101/lm.351706

Cited by 12 publications

(14 citation statements)

References 32 publications

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“…[77][78][79][80][81][82][83][84][85][86] Excessive activation of glutamate receptors has been shown to result in excitotoxicity with irreversible disruption of ion homeostasis and cell death. 87 This is in line with many studies reporting that excitotoxic mechanisms contribute to alterations in neuroplasticity 88 and memory. 89 Thus, our results may suggest that homeostatic mechanisms that keep cortical excitability within a normal physiological range are impaired in CI.…”

Section: Discussionsupporting

confidence: 83%

Increased Use-Dependent Plasticity in Chronic Insomnia

Salas¹,

Galea

Gamaldo

et al. 2014

Sleep

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This study provides the first evidence that patients with chronic insomnia have an increased plasticity response to physical exercise, possibly due to larger activation of glutamatergic mechanisms. This suggests a heightened state of neuroplasticity, which may reflect a form of maladaptive plasticity, similar to what has been described in dystonia patients and chronic phantom pain after amputation. These results could lead to development of novel treatments for chronic insomnia.

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Section: Discussionsupporting

confidence: 83%

Increased Use-Dependent Plasticity in Chronic Insomnia

Salas¹,

Galea

Gamaldo

et al. 2014

Sleep

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“…The mechanism of this progressive decline cannot be fully explained with our data, as there are a number of biologic and environmental changes associated with age including decreasing synaptic plasticity and cortical volume with increasing age. [41][42][43] A greater degree of disability 5 years postinjury among older patients may be explained by an increased number of actual and perceived health problems as compared to younger patients. A recent investigation noted patients older than 55 years of age report more problems with headaches, body temperature changes, communication difficulties, sleeping problems, and back and neck pains than age matched controls.…”

Section: Discussionmentioning

confidence: 99%

Impact of Age on Long-Term Recovery From Traumatic Brain Injury

Plata

Hart

Hammond³

et al. 2008

Archives of Physical Medicine and Rehabilitation

196

117

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Objective-To determine whether older persons are at increased risk for progressive functional decline after traumatic brain injury (TBI). Design-Longitudinal cohort study. Setting-Traumatic Brain Injury Model Systems (TBIMS) rehabilitation centers.Participants-Subjects enrolled in the TBIMS national dataset. Interventions-Not applicable.Main Outcome Measures-Disability Rating Scale (DRS), FIM instrument cognitive items, and the Glasgow Outcome Scale-Extended.Results-Participants were separated into 3 age tertiles: youngest (16-26y), intermediate (27-39y), and oldest (≥40y). DRS scores were comparable across age groups at admission to a rehabilitation center. The oldest group was slightly more disabled at discharge from rehabilitation despite having less severe acute injury severity than the younger groups. While DRS scores for the 2 younger groups improved significantly from year 1 to year 5, the greatest magnitude of improvement in disability was seen among the youngest group. Additionally, after dividing patients into groups according to whether their DRS scores improved (13%), declined (10%), or remained stable (77%) over time, the likelihood of decline was found to be greater for the 2 older groups than for the youngest group. A multiple regression model demonstrated that age has a significant negative influence on DRS score 5 years post-TBI after accounting for the effects of covariates.Conclusions-This study supported our primary hypothesis that older patients show greater decline over the first 5 years after TBI than younger patients. Additionally, the greatest amount of improvement in disability was observed among the youngest group of survivors. These results suggest TBI survivors, especially older patients, may be candidates for neuroprotective therapies after TBI.Reprint requests to Ramon Diaz-Arrastia, MD, PhD, 5323 Harry Hines Blvd, Dallas, TX 75390-9036, e-mail: ramon.diazarrastia@utsouthwestern.edu. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated. The resulting injuries range from mild disability to longterm disabilities or death. 3 It has been observed that particular subpopulations recover differently from similar injuries. One characteristic felt to have an impact on the degree of recovery is age: in general, the older the patient the worse the outcome. 7-12 Issues of TBI and aging are important to study because of the large and growing number of older people who are affected by TBI, which has a bimodal age distribution peaking in late adolescence/early adulthood and again after age 70. 3 NIH Public AccessTBI may interact negatively with aging in at least 2 ways: (1) recovery after TBI is more limited for older than younger survivors; and (2) older individuals who have suffered a TBI are at higher risk for progressive cognitive decline. First, advanced age at the time of injury may result in less complete recovery comp...

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“…The initial expansion was dependent on activation of NMDA receptors in the spine head while a long-lasting expansion was dependent on activation of kinases (566). Later studies reported that the change in spine volume was smaller than in the original report [Yang et al,40% (566); Lai et al, 40% (267)] and may develop over a longer time period [20 min (267, 583) or longer (442)]. Regardless of the magnitude of the immediate effects, the ability of spines to change their volume over a short time is impressive indeed.…”

Section: B Spine Expansionmentioning

confidence: 92%

Dendritic Spines: The Locus of Structural and Functional Plasticity

Sala

Segal

2014

Physiological Reviews

Self Cite

413

376

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The introduction of high-resolution time lapse imaging and molecular biological tools has changed dramatically the rate of progress towards the understanding of the complex structure-function relations in synapses of central spiny neurons. Standing issues, including the sequence of molecular and structural processes leading to formation, morphological change, and longevity of dendritic spines, as well as the functions of dendritic spines in neurological/psychiatric diseases are being addressed in a growing number of recent studies. There are still unsettled issues with respect to spine formation and plasticity: Are spines formed first, followed by synapse formation, or are synapses formed first, followed by emergence of a spine? What are the immediate and long-lasting changes in spine properties following exposure to plasticity-producing stimulation? Is spine volume/shape indicative of its function? These and other issues are addressed in this review, which highlights the complexity of molecular pathways involved in regulation of spine structure and function, and which contributes to the understanding of central synaptic interactions in health and disease.

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Age-dependent glutamate induction of synaptic plasticity in cultured hippocampal neurons

Cited by 12 publications

References 32 publications

Increased Use-Dependent Plasticity in Chronic Insomnia

Increased Use-Dependent Plasticity in Chronic Insomnia

Impact of Age on Long-Term Recovery From Traumatic Brain Injury

Dendritic Spines: The Locus of Structural and Functional Plasticity

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