Contradictory effects of GABA-B receptor agonists on cortical epileptic afterdischarges in immature rats

Mareš, Pavel; Tabashidze, Nana

doi:10.1016/j.brainresbull.2007.09.001

Cited by 18 publications

(6 citation statements)

References 29 publications

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“…Recently we demonstrated an important role of inhibition mediated by GABA-B receptors in cortical epileptic afterdischarges in immature rats (Mareš 2010). It is in agreement with our older finding that administration of an antagonist of GABA-B receptors CGP35348 results in marked prolongation of cortical afterdischarges in adult rats (Mareš et al 2007). Epileptic afterdischarges characterized by spike-and-wave rhythm in the EEG and clonic seizures are generated in the corticothalamic system (Pohl et al 1986).…”

supporting

confidence: 89%

“…This model offers two different epileptic phenomena to be evaluated -in addition to purely cortical interictal focal discharges a transition into ictal activity characterized by spike-and-wave rhythm in the EEG accompanied by clonic seizures. Both EEG and motor ictal phenomena are identical with those characteristic for the cortical epileptic afterdischarges (Mareš et al 2007). We hypothesized that antagonist of GABA-B receptors will augment epileptic activity also in a model of focal cortical seizures.…”

mentioning

confidence: 96%

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An Antagonist of GABA-B Receptors Potentiates Activity of Cortical Epileptic Foci

Mareš

Bernášková²,

Kubová³

2012

Physiol Res

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Cortical epileptic foci elicited by local application of bicuculline methiodide represent a model of interictal epileptic activity with a transition into ictal phases. We studied a role of GABA-B receptors in this model using GABA-B receptor antagonist CGP35348 in adult rats with implanted cortical electrodes and cannula. CGP35348 (100 or 200 mg/kg i.p.) did not affect interictal discharges but it augmented ictal activity. Latency to the first ictal episode was decreased by the lower dose of CGP35348, duration of episodes was increased by the higher dose. GABA-B receptor antagonist did not influence purely cortical epileptic phenomenon but it is proconvulsant in ictal activity generated with participation of subcortical structures.

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confidence: 89%

mentioning

confidence: 96%

An Antagonist of GABA-B Receptors Potentiates Activity of Cortical Epileptic Foci

Mareš

Bernášková²,

Kubová³

2012

Physiol Res

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“…[30] In humans, seizures have been reported both in overdose and withdrawal of oral baclofen. [31, 32] A series comparing 99 MS patients treated with intrathecal baclofen with a control group of 99 MS patients (46 of whom received oral baclofen as a symptomatic treatment) reported a significantly increased rate of epilepsy in association with the use of intrathecal baclofen (7% versus 1%).…”

Section: Relation Of Other Medications To Seizure Frequencymentioning

confidence: 99%

Seizures in Patients with Multiple Sclerosis

Kelley

Rodriguez

2009

CNS Drugs

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Seizures have been recognized to occur in multiple sclerosis since early descriptions of the disease. Various studies have attempted to determine the incidence and prevalence of seizures in multiple sclerosis; although they differ in the reported prevalence, seizures do appear to be more common in multiple sclerosis cohorts than in the general population.The pathological underpinning of seizures in multiple sclerosis remains indeterminate. Cortical and subcortical demyelination and inflammation may explain the increased frequency of seizures in multiple sclerosis, although this hypothetical correlation remains to be proven.Management of seizures in multiple sclerosis is similar to the management of seizures in other patients. Consideration of the underlying neurological deficits related to multiple sclerosis may be necessary, and dosages should be adjusted if increased sensitivity to antiepileptic side effects or interaction with other centrally-acting medications is suspected. The prognosis of epilepsy in patients with MS remains uncertain, with some studies suggesting a more favorable prognosis than others.

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“…Many reports suggest that elevated GABA concentrations exert both inhibitory and excitatory effects on neuronal firing [ 11 – 13 ]. Such contradictory scenario has also been reported in bath perfusion of a GABA B R agonist [ 14 , 15 ]. One potential mechanism is that elevation in ambient GABA concentration can reduce the inhibitory effect of GABAergic synapses on the connected excitatory neurons, resulting in an overall increase in excitability via the disinhibition of the neurons [ 12 , 14 ].…”

Section: Introductionmentioning

confidence: 84%

A Computational Model to Investigate GABA-Activated Astrocyte Modulation of Neuronal Excitation

Zhou

Sun

et al. 2020

Computational and Mathematical Methods in Medicine

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Gamma-aminobutyric acid (GABA) is critical for proper neural network function and can activate astrocytes to induce neuronal excitability; however, the mechanism by which astrocytes transform inhibitory signaling to excitatory enhancement remains unclear. Computational modeling can be a powerful tool to provide further understanding of how GABA-activated astrocytes modulate neuronal excitation. In the present study, we implemented a biophysical neuronal network model to investigate the effects of astrocytes on excitatory pre- and postsynaptic terminals following exposure to increasing concentrations of external GABA. The model completely describes the effects of GABA on astrocytes and excitatory presynaptic terminals within the framework of glutamatergic gliotransmission according to neurophysiological findings. Utilizing this model, our results show that astrocytes can rapidly respond to incoming GABA by inducing Ca2+ oscillations and subsequent gliotransmitter glutamate release. Elevation in GABA concentrations not only naturally decreases neuronal spikes but also enhances astrocytic glutamate release, which leads to an increase in astrocyte-mediated presynaptic release and postsynaptic slow inward currents. Neuronal excitation induced by GABA-activated astrocytes partly counteracts the inhibitory effect of GABA. Overall, the model helps to increase knowledge regarding the involvement of astrocytes in neuronal regulation using simulated bath perfusion of GABA, which may be useful for exploring the effects of GABA-type antiepileptic drugs.

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Contradictory effects of GABA-B receptor agonists on cortical epileptic afterdischarges in immature rats

Cited by 18 publications

References 29 publications

An Antagonist of GABA-B Receptors Potentiates Activity of Cortical Epileptic Foci

An Antagonist of GABA-B Receptors Potentiates Activity of Cortical Epileptic Foci

Seizures in Patients with Multiple Sclerosis

A Computational Model to Investigate GABA-Activated Astrocyte Modulation of Neuronal Excitation

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