Hypoxia-induced hyperexcitability in vivo and in vitro in the immature hippocampus

Jensen, Frances E.; Wang, Carl

doi:10.1016/s0920-1211(96)00049-6

Cited by 62 publications

(43 citation statements)

References 59 publications

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“…The hippocampus is known to be involved in epileptiform activity. Its excitability threshold is very low, and even a trivial stimulus can evoke abnormal electrical discharge [21,22]. Consistent with other studies [23,24], the present study demonstrated that no detectable neuronal loss was observed in the hippocampus either immediately or 14 days after hypoxia-induced epileptic seizures in P 10 rats.…”

Section: Discussionsupporting

confidence: 92%

Downregulation of Hippocampal GABA after Hypoxia-Induced Seizures in Neonatal Rats

et al. 2011

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This study aims to determine the expression of Gamma-aminobutyric acid (GABA) following hypoxia in neonatal rats and explore how it may increase susceptibility to epilepsy later in life. A modified model of neonatal hypoxia-induced epileptic susceptibility was simulated by 17 min of hypoxia (5% O(2) and 95% N(2)) in postnatal day (P) 10 rats. Hippocampal glutamate decarboxylase (GAD) and parvalbumin (PV) during the development with or without hypoxia were examined using immunohistochemistry. No detectable neuronal loss was observed in the hippocampus either immediately or 14 days after hypoxia. During the development GAD- and PV-immunoreactivity increased substantially during P 11-13 and reached mature expression in the control rats, and decreased significantly at different time points except for a transient increase during P 11-13 in the hypoxic groups. Our study indicates that downregulation of hippocampal GABA after hypoxia-induced seizures in neonatal rats may contribute to higher epileptic susceptibility in later life.

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Section: Discussionsupporting

confidence: 92%

Downregulation of Hippocampal GABA after Hypoxia-Induced Seizures in Neonatal Rats

et al. 2011

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“…[55][56][57] Thus, Jensen and Wang 57 reported a bell-shaped developmental curve of the epileptogenic effect of anoxia in the in vivo studies; the rats aged P10 to P12, but not at younger or older ages, exhibited acute seizure activity during hypoxia. Although the epileptogenic action of anoxia in P10 to P12 rat hippocampal slices has not been reported, hypoxia induced more frequently ictal-like discharges at this age in slices perfused with Mg 2ϩ -free solution than in older rats.…”

Section: Discussionmentioning

confidence: 98%

Epileptogenic action of caffeine during anoxia in the neonatal rat hippocampus

et al. 1999

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Excessive maternal caffeine consumption can lead to fetal and neonatal pathology, but the underlying mechanisms have not been determined. Here, we report that low doses of caffeine generate seizures when applied in conjunction with brief anoxic episodes in the hippocampus of neonatal rats in vitro. In control conditions, brief (4–6 minutes) anoxic episodes reversibly depressed evoked synaptic responses and blocked the physiological pattern of network activity. In the presence of caffeine (50 μM), similar anoxic episodes generated ictal (29%) or interictal (33%) epileptiform activities often followed during reoxygenation by recurrent spontaneous seizure activity that persisted for several hours. These effects are likely mediated by a blockade of adenosine receptors by caffeine because (1) in control conditions, caffeine antagonized the inhibitory effect of selective A1 receptor agonist N6‐cyclopentyladenosine on excitatory synaptic responses, and (2) epileptogenic effects of caffeine were reproduced by selective A1 receptor antagonist 8‐cyclopentyl‐1,3‐dipropylxanthine and theophylline. Our findings suggest that endogenous adenosine released during anoxia acting via A1 receptors prevents seizures in the neonatal hippocampus and that the antagonism of these receptors by caffeine leads to epileptogenesis. This study suggests concerns about the safety of caffeine in the fetus and newborn. Ann Neurol 1999;46:95–102

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“…Rats (Long-Evans rats, Wistar rats and Sprague-Dawley rats) (Jensen et al, 1991(Jensen et al, , 1998Jensen and Wang, 1996;Moshe and Albala, 1985;Rakhade et al, 2008Rakhade et al, , 2011Wang et al, 2015) and mice (Leonard et al, 2013;Rakhade et al, 2012;Rubaj et al, 2003;Wais et al, 2009;Wang et al, 2013;Zanelli et al, 2014) are the most commonly used species, with a recent emerging use of other species, i.e., rabbits (Holtzman et al, 1999;Kekelidze et al, 2000), to study the molecular mechanisms in hypoxia-induced seizures in the immature brain. In rats, hypoxic seizures can only be induced during the critical developmental window, P6-12, which is a period of synaptic maturation and corresponds to the age-dependence of clinical hypoxia-associated neonatal seizures (Chiba, 1985;Jensen et al, 1991Jensen et al, , 1998Leonard et al, 2013;Owens et al, 1997;Rakhade and Jensen, 2009;Rakhade et al, 2011).…”

Section: Animalsmentioning

confidence: 99%

“…Q3 There are a number of hypoxia-induced seizure models that reproduce important clinical features of HIE in the neonatal http://dx.doi.org/10.1016/j.jneumeth.2015.09.023 0165-0270/© 2015 Published by Elsevier B.V. Holtzman et al (1999) and Kekelidze et al (2000) population by brief exposure of immature rats to graded global hypoxia (Jensen et al, 1991;Moshe and Albala, 1985) (Table 1). Such hypoxia-induced seizures usually occur in a specific age window and lead to both acute and long-term network hyperexcitability, spontaneous seizures and later in life cognitive deficits without acute neuronal death (Chen et al, 2006;Jensen et al, 1991Jensen et al, , 1998Jensen and Wang, 1996;Laroia et al, 1997;Moshe and Albala, 1985;Rakhade et al, 2011Rakhade et al, , 2008Rubaj et al, 2003;Sanchez et al, 2000Sanchez et al, , 2005Sanchez and Jensen, 2001;Sato et al, 1994;Sun et al, 2013;Wais et al, 2009;Yager and Ashwal, 2009;Yang et al, 2004;Zanelli et al, 2014). In this section, we will provide an overview of the animal species used in hypoxia-induced seizure study.…”

Section: Introductionmentioning

confidence: 99%