Effects of anticonvulsive drugs on pentylenetetrazol kindling and long-term potentiation in freely moving rats

Krug, Manfred; Becker, Axel; Grecksch, Gisela; Pfeiffer, Andreas F. H.; Matthies, Renate; Wagner, Maria

doi:10.1016/s0014-2999(98)00544-5

Cited by 16 publications

(11 citation statements)

References 44 publications

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“…Because the aim was to modulate inhibition during kindling progression, intraperitoneal administration of benzodiazepine (diazepam, Sigma, MO), which acts as a GABA (A) receptor ligand and facilitates inhibition, or vehicle ((2-Hydroxypropyl)-β-cyclodextrin, Sigma, MO) was injected at non-sedative doses that would not affect the locomotor activity (0.5-1 mg/kg) (Krug et al, 1998; Rosenberg et al, 1989) 30 minutes before the first stimulation on days 3 and 4 of the kindling acquisition (Fig. 1).…”

Section: Methodsmentioning

confidence: 99%

Different phases of afterdischarge during rapid kindling procedure in mice

2009

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SummaryThe basic mechanisms of hippocampal networks in epileptogenesis are not entirely understood. To help achieve a better understanding of these mechanisms, we studied the extra-cellular electricallyevoked responses in the hippocampi of mice during rapid kindling. Kindling protocol was achieved by stimulating the dorsal right hippocampus six times daily for four days using bipolar electrodes to produce sub-convulsive electrical discharges. Motor responses and analyzed electroencephalographic recordings showed progression from partial complex seizures to generalized seizures associated with different consecutive patterns within the afterdischarges. A spike-wave pattern appeared immediately after stimulation in combination with a poly-spike complex superimposed over the wave (AD1). AD1 was followed by a poly-spike complex (AD2), which was followed by a progressive modification of repetitive spikes (AD3). An ictal depression event was observed at the end of each AD3. Theta oscillations were observed at stage 1-2 of kindling, while beta/gamma oscillations appeared within AD2, associated with stage 4-5 from Racine's score. Benzodiazepine, a GABA (A) agonist (Diazepam) administered at non-sedative doses and only on days 3 and 4 of kindling, limited beta and gamma frequency bands and the progression of seizure severity, suggesting that the failure of GABA (A) agonism mediates the propagation or generalization of seizures. We conclude that different phases of afterdischarge occur during kindling and that high frequencies mediate generalization of seizures.

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Section: Methodsmentioning

confidence: 99%

Different phases of afterdischarge during rapid kindling procedure in mice

2009

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“…Collection of data from awake rats was advantageous because it allowed for assessment of LTP maintenance by monitoring responses over days and because anesthetics can interfere with physiological responses involved in synaptic plasticity (Krug et al, 1998) and can impair the maintenance phase of hippocampal LTP (Wei et al, 2002). Some of these data have been presented in abstract form (Dieguez and Barea-Rodriguez, 2002).…”

Section: Introductionmentioning

confidence: 99%

Aging impairs the late phase of long‐term potentiation at the medial perforant path‐CA3 synapse in awake rats

Dieguez

Barea-Rodrı́guez

2004

Synapse

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The effects of aging on long-term potentiation (LTP) in the dentate gyrus (DG) and CA1 are well documented, but LTP at the medial perforant path (MPP)-CA3 synapse of aged animals has remained unexplored. Because the MPP-DG and Schaffer-collateral-CA1 synapses account for only about 20% of total hippocampal synapses, global understanding of how aging affects hippocampal plasticity has remained limited. Much is known about LTP induction in the hippocampal formation, whereas the mechanisms that regulate LTP maintenance are less understood, especially during aging. We investigated the effects of aging on MPP-CA3 LTP induction and maintenance in awake rats. As is the case in the DG and CA1, high-frequency stimulation-induced LTP at the MPP-CA3 synapse is normal in aged rats. These data indicate that N-methyl-D-aspartate (NMDA) receptor-mediated processes are intact at the MPP-CA3 synapse in aged rats. In contrast, aging impaired the magnitude and duration of MPP-CA3 LTP over a period of days. Also, these data are consistent with reports that area CA3 is especially susceptible to age-related changes. Our data suggest that aging impairs mechanisms that regulate the late phase of MPP-CA3 LTP and contribute to a more global understanding of how aging affects hippocampal plasticity.

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“…Interestingly, the control animals subchronically treated with FP also showed a reduction in hippocampal CA3 neurones. In different kindling models an antiepileptic and protective effect was observed with MK-801, a non-competitive glutamate receptors (N-methyl-d-aspartic acid receptor, NMDA) antagonist (Minabe et al, 1992;Gilbert 1994;Gilbert and Burdette, 1996;Applegate et al, 1997;Yoshida et al, 1997;Krug et al, 1998) and there are abundant evidence that MK-801 could also induce neuronal damage in a dose-dependent manner (Peng et al, 2013). Interferences with the Akt1/GSK3␤ signaling pathway (Peng et al, 2013), adenosine A1 mediated neurotransmission (Okamura et al, 2004), oxidative stress and apoptotic changes (Ozyurt et al, 2007;Willis and Ray 2007) and other mechanisms contribute to MK-801 neurotoxicity.…”

Section: Discussionmentioning

confidence: 99%