Research reportEffects of NMDA antagonists on picrotoxin-, low Mg2+- and low Ca2+-induced epileptogenesis and on evoked changes in extracellular Na+ and Ca2+ concentrations in rat hippocampal slices
References (64)
- et al.
Magnesium-free medium activates seizure-like events in the rat hippocampal slice
Brain Res.
(1986) - et al.
Selective inhibition of synaptic versus non-synaptic epileptogenesis by NMDA antagonists in the in vitro hippocampus
Epilepsy Res.
(1988) - et al.
Seizure-like discharges induced by lowering [Mg2+]0 in the human epileptogenic neocortex maintained in vitro
Brain Res.
(1987) - et al.
Genesis of epileptic interictal spikes. New knowledge of cortical feedback systems suggest neurophysiological explanation of brief paroxysms
Brain Res.
(1973) - et al.
Magnesium ions block an receptor-mediated component of synaptic transmission in rat hippocampus
Neurosci. Lett.
(1985) - et al.
Ketamine blocks an NMDA receptormediated component of synaptic transmission in rat hippocampus in a voltage-dependent manner
Neurosci. Lett.
(1988) - et al.
An receptor-independent excitatory action of partial reduction of extracellular [Mg2+]0 in CA1 region of rat hippocampal slices
Neurosci. Lett.
(1987) - et al.
Effects of anticonvulsants on spontaneous epileptiform activity which develops in the absence of chemical synaptic transmission in hippocampal slices
Brain Res.
(1985) - et al.
A selective antagonist depresses epileptiform activity in rat hippocampal slices
Neurosci. Lett.
(1985) - et al.
Ketamine and phencyclidine cause a voltage-dependent block of responses to l-aspartate acid
Neurosci. Lett.
(1985)
Epileptiform events induced by GABA-antagonists in entorhinal cortical cells are partly mediated by receptors
Brain Res.
The initiation and spread of epileptiform bursts in the in vitro hippocampal slice
Neuroscience
Effects of GABA on presumed presynaptic Ca2+ entry in hippocampal slices
Brain Res.
A comparison of the anticonvulsant potency of (±)-2-amino-phosphono-acid and (±)-2-amino-7-phosphonoheptanoic acid
Neuroscience
Epileptiform bursts elicited in CA3 hippocampal neurons by a variety of convulsants are not blocked by antagonists
Brain Res.
receptor-mediated increase in intracellular calcium is reduced by ketamine and phencyclidine
Eur. J. Pharmacol.
Inhibition of evoked sodium flux by MK-801
Brain Res.
Effects of ketamine and (+)-cyclazocine on 4-aminopyridine and ‘magnesium free’ epileptogenic activity in hippocampal slices of rats
Neuropharmacology
Synchronous epileptiform bursts without chemical transmission in CA2, CA3 and dentate areas of the hippocampus
Brain Res.
Epileptiform activity induced by lowering extracellular [Mg2+]0 in combined hippocampal-entorhinal cortex slices: modulation by receptors for norepinephrine and
Epilepsy Res.
N-Methylaspartate receptors mediate epileptiform activity evoked in some, but not all, conditions in rat neocortical slices
Neuroscience
Epileptiform activity in combined slices of the hippocampus, subiculum and entorhinal cortex during perfusion with low magnesium medium
Neurosci. Lett.
Ion-Selective Microelectrodes
Selective depression of excitatory amino acid induced depolarizations by magnesium ions in isolated spinal cord preparations
J. Physiol. (Lond.)
Mechanisms for low-calcium, high-magnesium-synchronous burst in the in vitro hippocampal slice
Anticonvulsant action of excitatory amino acid antagonists
Science
Stimulus-induced changes in extracellular Na+ and Cl− concentration in relation to changes in the size of the extracellular space
Exp. Brain Res.
Involvement of receptors in epileptiform bursting in the rat hippocampal slice
J. Physiol. (Lond.)
The role of calcium ions in tetanic and post-tetanic increase of miniature end-plate potential frequency
J. Physiol. (Lond.)
Mechanisms of neocortical epileptogenesis in vitro
J. Neurophysiol.
Low-calcium field burst discharges of CA1 pyramidal neurones in rat hippocampal slices
J. Physiol. (Lond.)
Picrotoxin induced epileptiform activity in hippocampus: role of endogenous versus synaptic factors
J. Neurophysiol.
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2021, Ecotoxicology and Environmental SafetyInfluence of tetramethylenedisulfotetramine on synchronous calcium oscillations at distinct developmental stages of hippocampal neuronal cultures
2017, NeuroToxicologyCitation Excerpt :TETS triggered Ca2+ responses that were normalized by NMDA receptor antagonist (Cao et al., 2012a). NMDA receptor antagonist also suppressed PTX-induced Ca2+ responses as well as the frequency and duration of the epileptiform discharges in the hippocampal slice preparation (Kohr and Heinemann, 1989). Blockade of NMDA receptors also normalized TETS, PTX or bicuculline-induced seizure (Czlonkowska et al., 2000; Shakarjian et al., 2015).
Astrocyte sodium signaling and neuro-metabolic coupling in the brain
2016, NeuroscienceCitation Excerpt :At the existing high extracellular baseline sodium concentration, the response characteristics of ion-selective microelectrodes are not favorable for the study of sodium signals evoked by minor or moderate levels of activity. With prolonged afferent stimulation or with induction of epileptiform discharges or spreading depression, however, this technique enabled detection of decreases in the extracellular sodium by up to about 15 mM (Dietzel et al., 1982; Zanotto and Heinemann, 1983; Hablitz and Heinemann, 1989; Kohr and Heinemann, 1989) Fig. 1A). Based on earlier studies in invertebrate preparations, it was long assumed that physiological activity is not accompanied by measurable changes in intracellular sodium concentrations (e.g., (Hodgkin and Huxley, 1952); many current text books).
Limbic networks and epileptiform synchronization: The view from the experimental side
2014, International Review of NeurobiologyCitation Excerpt :Intracellular recordings have shown that ictal discharges are associated with sustained depolarizations capped by sustained action potential firing (Fig. 4.3A). It has also been established that neuronal network synchronization during ictal activity depends on glutamatergic ionotropic neurotransmission (particularly that mediated by the NMDA receptor; Köhr & Heinemann, 1989; Löscher and Hönack, 1991; Traynelis & Dingledine, 1988) and on persistent Na+ currents that are fundamental to maintain the sustained action potential firing (Mantegazza, Curia, Biagini, Ragsdale, & Avoli, 2010). In line with this view, many of the most widely used antiepileptic drugs, including phenytoin, carbamazepine, lamotrigine, and, perhaps, topiramate, inhibit voltage-gated Na+ channels (Mantegazza et al., 2010).
The NMDA receptor complex as a therapeutic target in epilepsy: A review
2011, Epilepsy and BehaviorCitation Excerpt :Cunha et al. [178] demonstrated that post-status epilepticus rats exhibited extensive gliosis and cell loss in the hippocampal CA1, CA3 (70% cell loss for both areas) and dentate gyrus (60%) and that ketamine reduced cell loss in the hippocampus [178]. Other studies revealed that ketamine blocked epileptiform activity induced by alkalosis in rat neocortical slices [179], decreased 4-aminopyridine- or picrotoxin- or “magnesium free”-induced epileptogenic activity in hippocampal slices of rats [180,181], attenuated epileptogenic responses in a synaptic and a non-synaptic model of epileptogenesis in the CA1 region of the hippocampal slice [182], and had anticonvulsant effects on different patterns of epileptiform activity in rat temporal cortex slices [183]. Cortical epileptiform afterdischarges (spike-and-wave rhythms) induced by low-frequency stimulation of the sensorimotor cortex were dose-dependently shortened by ketamine [184].
Excitotoxic neonatal damage induced by monosodium glutamate reduces several GABAergic markers in the cerebral cortex and hippocampus in adulthood
2009, International Journal of Developmental Neuroscience