Selective loss of hippocampal long-term potentiation, but not depression, following fluid percussion injury

D’Ambrosio, Raimondo; Maris, Donald O.; Grady, M. Sean; Winn, H. Richard; Janigro, Damir

doi:10.1016/s0006-8993(97)01412-1

Cited by 125 publications

(61 citation statements)

References 38 publications

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“…Earlier reports demonstrated that TBI results in a chronic inability of the CA1 hippocampal synapses to maintain synaptic plasticity (15)(16)(17)(18)(19). Similarly, the present results show that mice, failing to perform in the ORT, also display impaired LTP when recorded in hippocampal slices isolated 14 -16 d after injury.…”

Section: Discussionsupporting

confidence: 86%

D‐cycloserine improves functional recovery and reinstates long‐term potentiation (LTP) in a mouse model of closed head injury

Yaka¹,

Biegon

Grigoriadis³

et al. 2007

FASEB j.

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Traumatic brain injury triggers a massive glutamate efflux, activation of NMDA receptor channels, and cell death. Recently, we reported that NMDA receptors in mice are down-regulated from hours to days following closed head injury (CHI), and treatment with NMDA improved recovery of motor and cognitive functions up to 14 d post-injury. Here we show that a single injection of a low dose of D-cycloserine (DCS), a partial NMDA receptor agonist, in CHI mice 24 h post-injury, resulted in a faster and greater recovery of motor and memory functions as assessed by neurological severity score and object recognition tests, respectively. Moreover, DCS treatment of CHI mice led to a significant improvement of hippocampal long-term potentiation (LTP) in the CA1 region that was completely blunted in CHI control mice. However, DCS did not improve CHI-induced impairment in synaptic glutamate release measured by paired pulse facilitation (PPF) ratio in hippocampal CA1 region. Finally, CHI-induced reduction of brain-derived neurotrophic factor (BDNF) was fully restored following DCS treatment. Since DCS is in clinical use for other indications, the present study offers a novel approach to treat human brain injury.

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Section: Discussionsupporting

confidence: 86%

D‐cycloserine improves functional recovery and reinstates long‐term potentiation (LTP) in a mouse model of closed head injury

Yaka¹,

Biegon

Grigoriadis³

et al. 2007

FASEB j.

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“…In contrast to the DG’s hyperexcitable response to injury, area CA1 circuit activity becomes hypoexcitable. One week after FPI, CA1 has demonstrated a decreased net response to afferent fiber stimulation, accompanied by a higher threshold to initiate population spikes [84,109]. Therefore, the output of the CA1 circuit, mediated by the firing of CA1 pyramidal neurons, is diminished after injury.…”

Section: Pathophysiology Of Memory Impairment After Tbimentioning

confidence: 99%

Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury

Paternò

Folweiler

Cohen

2017

Curr Neurol Neurosci Rep

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Memory is fundamental to everyday life, and cognitive impairments resulting from traumatic brain injury (TBI) have devastating effects on TBI survivors. A contributing component to memory impairments caused by TBI are alterations in the neural circuits associated with memory function. In this review, we aim to bring together experimental findings that characterize behavioral memory deficits and the underlying pathophysiology of memory-involved circuits after TBI. While there is little doubt that TBI causes memory and cognitive dysfunction, it is difficult to conclude which memory phase i.e., encoding, maintenance or retrieval is specifically altered by TBI. This is most likely due to variation in behavioral protocols and experimental models. Additionally we review a selection of experimental treatments that hold translational potential to mitigate memory dysfunction following injury.

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“….1370 affects both hippocampal-dependent place learning, as well as hippocampal-independent cue learning (Bramlett et al, 1997). Electrophysiological studies have also found reduced hippocampal LTP in vivo in rats following TBI (D'Ambrosio et al, 1998;Miyazaki et al, 1992;Sanders et al, 2000). Some studies have documented that such deficits in rodents can persist even months after the initial injury, mirroring the long-term cognitive deficits seen after human TBI (Pierce et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Hippocampal Theta Dysfunction after Lateral Fluid Percussion Injury

Fedor

Berman

Muizelaar

et al. 2010

Journal of Neurotrauma

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Chronic memory deficits are a major cause of morbidity following traumatic brain injury (TBI). In the rat, the hippocampal theta rhythm is a well-studied correlate of memory function. This study sought to investigate disturbances in hippocampal theta rhythm following lateral fluid percussion injury in the rat. A total of 13 control rats and 12 TBI rats were used. Electrodes were implanted in bilateral hippocampi and an electroencephalogram (EEG) was recorded while the rats explored a new environment, and also while navigating a modified version of the Barnes maze. Theta power and peak theta frequency were significantly attenuated in the injured animals. Further, injured rats were less likely to develop a spatial strategy for Barnes maze navigation compared to control rats. In conclusion, rats sustaining lateral fluid percussion injury demonstrated deficits in hippocampal theta activity. These deficits may contribute to the underlying memory problems seen in chronic TBI.

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Selective loss of hippocampal long-term potentiation, but not depression, following fluid percussion injury

Cited by 125 publications

References 38 publications

D‐cycloserine improves functional recovery and reinstates long‐term potentiation (LTP) in a mouse model of closed head injury

D‐cycloserine improves functional recovery and reinstates long‐term potentiation (LTP) in a mouse model of closed head injury

Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury

Hippocampal Theta Dysfunction after Lateral Fluid Percussion Injury

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