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

Ooba, Satomi; Hasuo, Hiroshi; Shigemori, Minoru; Yamashita, Shinichi; Akasu, Takashi

doi:10.2739/kurumemedj.56.49

Cited by 6 publications

(6 citation statements)

References 52 publications

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“…Hypothermia during and after a period of OGD reduced the release of glutamate [72]. In addition, fluid percussion injury (FPI) induces hyperactivity of the excitatory synapses in CA1 hippocampal pyramidal neurons, and mild hypothermia at 35°C maintained for 1–3 hours after 15 mins of FPI attenuates the excitatory damage to hippocampal neurons [73]. Taken together, these studies confim the neuroprotective effects of hypothermia via the blockade of excitotoxicity.…”

Section: Molecular Targets Of Hypothermiamentioning

confidence: 99%

Therapeutic Hypothermia as a Neuroprotective Strategy in Neonatal Hypoxic-Ischemic Brain Injury and Traumatic Brain Injury

Sinha²,

Pandya³

et al. 2012

CMM

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Evidence shows that artificially lowering body and brain temperature can significantly reduce the deleterious effects of brain injury in both newborns and adults. Although the benefits of therapeutic hypothermia have long been known and applied clinically, the underlying molecular mechanisms have yet to be elucidated. Hypoxic-ischemic brain injury and traumatic brain injury both trigger a series of biochemical and molecular events that cause additional brain insult. Induction of therapeutic hypothermia seems to ameliorate the molecular cascade that culminates in neuronal damage. Hypothermia attenuates the toxicity produced by the initial injury that would normally produce reactive oxygen species, neurotransmitters, inflammatory mediators, and apoptosis. Experiments have been performed on various depths and levels of hypothermia to explore neuroprotection. This review summarizes what is currently known about the beneficial effects of therapeutic hypothermia in experimental models of neonatal hypoxic-ischemic brain injury and traumatic brain injury, and explores the molecular mechanisms that could become the targets of novel therapies. In addition, this review summarizes the clinical implications of therapeutic hypothermia in newborn hypoxic-ischemic encephalopathy and adult traumatic brain injury.

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Section: Molecular Targets Of Hypothermiamentioning

confidence: 99%

Therapeutic Hypothermia as a Neuroprotective Strategy in Neonatal Hypoxic-Ischemic Brain Injury and Traumatic Brain Injury

Sinha²,

Pandya³

et al. 2012

CMM

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“…In the weeks and months after cortical impact, an epileptiform activity develops in adult (Hunt et al ., ) and in young animals (Nichols et al ., ). It has been repeatedly shown that a mechanical injury of adult rat brain results in hyperactivity of hippocampal neurons measured in slices (Akasu et al ., 2002; Ooba et al ., , ). Both optical response and number of APs activated by excitatory postsynaptic potential were significantly increased (Akasu et al ., 2002; Ooba et al ., ).…”

Section: Discussionmentioning

confidence: 99%

“…It has been repeatedly shown that a mechanical injury of adult rat brain results in hyperactivity of hippocampal neurons measured in slices (Akasu et al ., 2002; Ooba et al ., , ). Both optical response and number of APs activated by excitatory postsynaptic potential were significantly increased (Akasu et al ., 2002; Ooba et al ., ). Number of APs activated by a prolonged depolarizing pulse was not altered in an adult rat model of mechanical injury (Ooba et al ., ).…”

Section: Discussionmentioning

confidence: 99%

Fibrotic scar model and TGF‐β1 differently modulate action potential firing and voltage‐dependent ion currents in hippocampal neurons in primary culture

Ondacova

Moravcikova

Jurkovičová

et al. 2017

Eur J of Neuroscience

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Traumatic injury of the central nervous system is accompanied by various functional and morphological changes. Animal models of traumatic brain injury are commonly used to investigate changes in behaviour, morphology, in the expression of various proteins around the site of the injury, or the expression of diagnostically important biomarkers. Excitability of a single neuron at, or close to, the site of injury was rarely investigated. Several in vitro models were developed which allow such investigation. In the present work, we employed a fibrotic scar model according to Kimura-Kuroda and coauthors to analyse altered excitability of rat hippocampal neurons under the conditions mimicking traumatic brain injury. Hippocampal neurons from newborn rats were cultured either on a fibrotic scar model or in the presence of TGF-β1, a cytokine secreted at a brain injury site that may have both neuroprotective and neurodegenerative function. Fibrotic scar facilitated ability of neonatal hippocampal neurons to fire action potential series by increasing the density of voltage activated sodium and potassium currents. Chondroitin sulphate proteoglycans played substantial role in these effects, as proven by their full reversion after administration of Chondroitinase ABC. In contrast, TGF-β1 did not contribute to them. An application of TGF-β1 itself attenuated generation of action potentials, inhibited sodium current and potentiated potassium currents. Main alteration of electrophysiological parameters of neonatal hippocampal neurons caused by a fibrotic scar model is enhanced excitability. TGF-β1 may have predominantly neuroprotective role in injured rat hippocampus.

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“…While enhancement of excitatory synaptic activity and hyperactivity of CA1 neurons and regional CA1 increases in glucose metabolism have been observed immediately following moderate fluid percussive brain injury (Yoshino et al, 1992;Akasu et al, 2002;Ooba et al, 2009), this has not been studied directly in models of closed-head concussive injury (i.e. mTBI) and thus the mechanisms by which neurons in the CA1 region are susceptible to mTBI require further examination.…”

Section: Discussionmentioning

confidence: 99%

Neural Mechanisms Linking Mild Traumatic Brain Injury and Anxiety States in an Animal Model

Forster¹

2012

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

Cited by 6 publications

References 52 publications

Therapeutic Hypothermia as a Neuroprotective Strategy in Neonatal Hypoxic-Ischemic Brain Injury and Traumatic Brain Injury

Therapeutic Hypothermia as a Neuroprotective Strategy in Neonatal Hypoxic-Ischemic Brain Injury and Traumatic Brain Injury

Fibrotic scar model and TGF‐β1 differently modulate action potential firing and voltage‐dependent ion currents in hippocampal neurons in primary culture

Neural Mechanisms Linking Mild Traumatic Brain Injury and Anxiety States in an Animal Model

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