Hyperexcitability of hippocampal CA1 neurons after fluid percussion injury of the rat cerebral cortex

Akasu, Takashi; Muraoka, Norihiro; Hasuo, Hiroshi

doi:10.1016/s0304-3940(02)00707-3

Cited by 32 publications

(20 citation statements)

References 13 publications

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“…Cytoarchitectual changes as demonstrated by selective hilar neuronal loss (Lowenstein et al, 1992;Toth et al, 1997;Santhakumar et al, 2000Santhakumar et al, , 2001 and mossy fiber sprouting (Santhakumar et al, 2001) have been shown and associated with dentate granule cell hyperexcitability, although some recent studies refute this hypothesis (Ratzliff et al, 2004). Larger, longer-lasting multiphasic field potential have been recorded from the hippocampus of animals after TBI compared to field potentials in controls (Santhakumar et al, 2000(Santhakumar et al, , 2001Akasu et al, 2002;Coulter et al, 2002). Decreased seizure threshold has also been demonstrated in other models of TBI.…”

Section: Traumatic Brain Injury-induced Spontaneous Recurrent Seizuresmentioning

confidence: 99%

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

DeLorenzo

Sun

Deshpande

2005

Pharmacology & Therapeutics

260

286

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Epilepsy is one of the most common neurological disorders. Although epilepsy can be idiopathic, it is estimated that up to 50% of all epilepsy cases are initiated by neurological insults and are called acquired epilepsy (AE). AE develops in 3 phases: (1) the injury (central nervous system [CNS] insult), (2) epileptogenesis (latency), and (3) the chronic epileptic (spontaneous recurrent seizure) phases. Status epilepticus (SE), stroke, and traumatic brain injury (TBI) are 3 major examples of common brain injuries that can lead to the development of AE. It is especially important to understand the molecular mechanisms that cause AE because it may lead to innovative strategies to prevent or cure this common condition. Recent studies have offered new insights into the cause of AE and indicate that injury-induced alterations in intracellular calcium concentration levels [Ca 2+ ] i and calcium homeostatic mechanisms play a role in the development and maintenance of AE. The injuries that cause AE are different, but they share a common molecular mechanism for producing brain damage -an increase in extracellular glutamate concentration that causes increased intracellular neuronal calcium, leading to neuronal injury and/or death. Neurons that survive the injury induced by glutamate and are exposed to increased [Ca 2+ ] i are the cellular substrates to develop epilepsy because dead cells do not seize. The neurons that survive injury sustain permanent long-term plasticity changes in [Ca 2+ ] i and calcium homeostatic mechanisms that are permanent and are a prominent feature of the epileptic phenotype. In the last several years, evidence has accumulated indicating that the prolonged alteration in neuronal calcium dynamics plays an important role in the induction and maintenance of the prolonged neuroplasticity changes underlying the epileptic phenotype. Understanding the role of calcium as a second messenger in the induction and maintenance of epilepsy may provide novel insights into therapeutic advances that will prevent and even cure AE.

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Section: Traumatic Brain Injury-induced Spontaneous Recurrent Seizuresmentioning

confidence: 99%

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

DeLorenzo

Sun

Deshpande

2005

Pharmacology & Therapeutics

260

286

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“…However, a previous study showed that the post-traumatic enhancement of excitatory synapses was not directly related to the disinhibition of GABAergic neurotransmission in the hippocampal CA1 area [21]. Further, FPI caused no considerable change in gross structure in the lateral hippocampal CA1 neurons lying 5 mm deep relative to the injured cerebral cortex [19,20,22]. Functional studies showed post-traumatic hyperactivity of excitatory synaptic transmission in DG neurons in FPI rats [29].…”

Section: Discussionmentioning

confidence: 98%

“…The optical response increased when the stimulus intensity was increased to 50 V. The effect of FPI on neuronal activity of the hippocampal CA1 area was also examined after a survival period of 1 week, during which the animal's behavior, including feeding and grooming, were normal. It was shown that blood obtained from the common carotid artery under pentobarbital anesthesia showed no evidence of significant cardiorespiratory compromise in FPI rats [19,20]. There was no significant difference in the weights of the sham-operated and FPI-treated rats before impact and 7 days later.…”

Section: Neuronal Activities In the Hippocampal Ca1 Area In Fpi Ratsmentioning

confidence: 94%

“…Lowering brain temperature produces behavioral protection after experimental TBI [17,18]. Recently, we showed a marked enhancement of neuronal excitability in the lateral hippocampus 1 week after administration of FPI to the cerebral cortex [19][20][21][22]. The aim of the present study was to examine whether very mild hypothermia (35°C) prevents the FPI-induced enhancement of excitatory synaptic transmission in the hippocampal CA1 area.…”

mentioning

confidence: 90%

“…Animals were maintained on a 12/12 (light-dark) cycle and given food ad libitum. FPI of the rat brain was induced by the methods described previously [4,5,[19][20][21]23]. Briefly, adult male Wistar rats (250-300 g) were anesthetized by intraperitoneal (i.p.)…”

Section: Surgical Operation and Fpimentioning

confidence: 99%

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Mild Hypothermia Prevents Post-Traumatic Hyperactivity of Excitatory Synapses in Rat Hippocampal CA1 Pyramidal Neurons

et al. 2009

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Structural and functional alterations of cerebellum following fluid percussion injury in rats

Liu

Park

et al. 2006

Exp Brain Res

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Cerebellum was shown to be vulnerable to traumatic brain injury (TBI) in experimental animals. However, the detailed pathological and functional changes within the cerebellum following TBI are not known. Using our established cerebellum fluid percussion injury (FPI) model, we characterized the temporal pattern and the nature of structural damage following FPI, as well as the functional changes of Purkinje cells in response to climbing fiber activation. Our results showed that 60% of Purkinje cells died within the first 24 h following moderate FPI. In contrast, clusters of densely stained shrunken granule cells were stained positive for terminal deoxynucleotidyl transferase-mediated UTP nick end labeling (TUNEL) in 1, 3 or 7 days following FPI animals. We also observed an accompanying structural damage to the cerebellar white matter tract. Disconnected axonal fibers appeared 1 day post-FPI, and loss of white matter fibers were visible 3 and 7 days post-FPI. Massive accumulation of beta-amyloid precursor protein (betaAPP) was found in the white matter tracts and molecular layer in the cerebellum of 1, 3 or 7 days FPI animals. Our functional study showed that the majority of Purkinje cells from 1 day and all cells from 3 to 7 days post-FPI had distorted membrane potential and synaptic responses to climbing fiber activation. These results suggested that there is a co-related structural and functional deterioration with a specific temporal pattern in the cerebellum following FPI. These observations provide a basis for future mechanistic investigations aiming to realize neuroprotection from cerebellar neuronal death and loss of cerebellar functionality.

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Hyperexcitability of hippocampal CA1 neurons after fluid percussion injury of the rat cerebral cortex

Cited by 32 publications

References 13 publications

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

Mild Hypothermia Prevents Post-Traumatic Hyperactivity of Excitatory Synapses in Rat Hippocampal CA1 Pyramidal Neurons

Structural and functional alterations of cerebellum following fluid percussion injury in rats

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