2002
DOI: 10.1016/s0304-3940(02)01154-0
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The role of Ca2+/calmodulin-dependent protein kinase II in mechanisms underlying neuronal hyperexcitability induced by repeated, brief exposure to hypoxia or high K+ in rat hippocampal slices

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Cited by 7 publications
(3 citation statements)
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“…CaMKII can be neatly suited to support the activity of bursting neurons connected via glutamatergic synapses. Of note, CA1 pyramidal neurons acquire an epileptic (repetitive) activity after brief exposures to high K + or hypoxia (Yechikhov et al 2002) that is dependent on Ca L channels and CaMKII. Ca L channels in preBötC neurons are potentiated after brief episodes of hypoxia due to activation of metabotropic glutamate receptors (Mironov & Richter, 1998) but the effects perhaps should be revisited to examine possible involvement of CaMKII that facilitates Ca L channels in the heart (Wu et al 2004).…”
Section: Discussionmentioning
confidence: 99%
“…CaMKII can be neatly suited to support the activity of bursting neurons connected via glutamatergic synapses. Of note, CA1 pyramidal neurons acquire an epileptic (repetitive) activity after brief exposures to high K + or hypoxia (Yechikhov et al 2002) that is dependent on Ca L channels and CaMKII. Ca L channels in preBötC neurons are potentiated after brief episodes of hypoxia due to activation of metabotropic glutamate receptors (Mironov & Richter, 1998) but the effects perhaps should be revisited to examine possible involvement of CaMKII that facilitates Ca L channels in the heart (Wu et al 2004).…”
Section: Discussionmentioning
confidence: 99%
“…To our knowledge, this is the first demonstration of L-VGCC enhancement by transient hypoxia in cortical neurons, which could contribute to post-hypoxic cortical hyperexcitability (Yechikhov et al, 2002), seizures or status epilepticus (Bladin et al, 2000; Krumholz et al, 1988). Increased intracellular Ca 2+ might activate calcium-dependent processes leading to necrotic or apoptotic cell death (Wasterlain et al, 1993), or alternatively, L-VGCC upregulation and calcium entry might facilitate post-hypoxic dephosphorylation and translocation of the Ca 2+ -dependent potassium channel Kv2.1, which suppresses neuronal excitability, and thus have a compensatory or protective effect (Misonou et al, 2005).…”
Section: Discussionmentioning
confidence: 84%
“…In order to investigate the possible mechanism of Q808, other electrophysiological experiments were performed. In an epileptiform model in which seizures were induced by high-K + [ 21 , 22 ], a high concentration of exogenous K + ions disturbs the balance of K + inside and outside the cell membrane, which closes outwardly rectifying potassium ion channels, leading to depolarization and enhanced excitability. In this experiment, Q808 significantly reduced the frequency of neuronal action potentials, which suggests that it may be increasing the concentration of K + ions or inactivating K + channels.…”
Section: Discussionmentioning
confidence: 99%