Eeg changes induced by convulsants interfering with GABAergic inhibition in rats. I. Cortical recordings

Mareš, Pavel; Zouhar, A; Koryntová, H; Rokyta, Richard; Mareš, J

doi:10.1016/s0370-4475(85)80051-4

Revue d&'apos;Electroencéphalographie et de Neurophysiologi

1985

DOI: 10.1016/s0370-4475(85)80051-4

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Eeg changes induced by convulsants interfering with GABAergic inhibition in rats. I. Cortical recordings

Pavel Mareš

A Zouhar

H Koryntová

et al.

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Cited by 3 publications

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“…Bicuculline, a commonly used convulsant drug (Woodbury, 1980; Swinyard and Woodhead, 1982), is a specific antagonist of GABA, receptors (Enna and Karbon, 1986; Krogsgaard-Larsen et al, 1986). Conversely, electrocorticographic (ECoG) changes have been described not only in adult rabbits (Florio and Longo, 1972) and rats (Mares et al, 1985) but in immature rats (de Feo et al, 1985). Conversely, electrocorticographic (ECoG) changes have been described not only in adult rabbits (Florio and Longo, 1972) and rats (Mares et al, 1985) but in immature rats (de Feo et al, 1985).…”

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confidence: 99%

Motor and Electrocorticographic Epileptic Activity Induced by Bicuculline in Developing Rats

et al. 1989

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Motor seizures were induced by intraperitoneally (i.p.) injected bicuculline in 270 rats aged 7, 12, 18, 25, or 90 days. Bicuculline was able to elicit both minimal (clonic) and major (tonic-clonic) seizures in all age groups, but in 7-day-old rats minimal seizures were only noted exceptionally. CD50s (for major seizures) ranged from 2.48 to 2.85 mg/kg in the three younger groups and increased to approximately 7 mg/kg in 25- and 90-day-old rats. An intravenous (i.v.) administration of bicuculline in 67 rats, 18 and 25 days old, caused identical CD50s in these groups, indicating that the difference that occurs with an i.p. administration is due to pharmacokinetic reasons. Electrocorticographic (ECoG) studies in acute experiments as well as in young rats with implanted electrodes demonstrated general principles of the development of EEG: an increase in frequency of individual elements, in generalization of the epileptic activity, in synchronization of activity among various cortical regions, and in the correlation between ECoG and motor phenomena. An exception occurred as an age-related phenomenon: rhythmic activity of the spike-and-wave type. This activity appeared in 18-day-old and older rats and was invariably accompanied by "freezing" of the animals.

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confidence: 99%

Motor and Electrocorticographic Epileptic Activity Induced by Bicuculline in Developing Rats

et al. 1989

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Regional brain activation by bicuculline visualized by functional magnetic resonance imaging. Time-resolved assessment of bicuculline-induced changes in local cerebral blood volume using an intravascular contrast agent

et al. 2000

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Physiology, Pharmacology, and Topography of Cholinergic Neocortical Oscillations In Vitro

Lukatch

MacIver

1997

Journal of Neurophysiology

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Rat neocortical brain slices generated rhythmic extracellular field [microelectroencephalogram (micro-EEG)] oscillations at theta frequencies (3-12 Hz) when exposed to pharmacological conditions that mimicked endogenous ascending cholinergic and GABAergic inputs. Use of the specific receptor agonist and antagonist carbachol and bicuculline revealed that simultaneous muscarinic receptor activation and gamma-aminobutyric acid-A (GABA(A))-mediated disinhibition were necessary to elicit neocortical oscillations. Rhythmic activity was independent of GABA(B) receptor activation, but required intact glutamatergic transmission, evidenced by blockade or disruption of oscillations by 6-cyano-7-nitroquinoxaline-2,3-dione and (+/-)-2-amino-5-phosphonovaleric acid, respectively. Multisite mapping studies showed that oscillations were localized to areas 29d and 18b (Oc2MM) and parts of areas 18a and 17. Peak oscillation amplitudes occurred in layer 2/3, and phase reversals were observed in layers 1 and 5. Current source density analysis revealed large-amplitude current sinks and sources in layers 2/3 and 5, respectively. An initial shift in peak inward current density from layer 1 to layer 2/3 indicated that two processes underlie an initial depolarization followed by oscillatory activity. Laminar transections localized oscillation-generating circuitry to superficial cortical layers and sharp-spike-generating circuitry to deep cortical layers. Whole cell recordings identified three distinct cell types based on response properties during rhythmic micro-EEG activity: oscillation-ON (theta-ON) and -OFF (theta-OFF) neurons, and transiently depolarizing glial cells. Theta-ON neurons displayed membrane potential oscillations that increased in amplitude with hyperpolarization (from -30 to -90 mV). This, taken together with a glutamate antagonist-induced depression of rhythmic micro-EEG activity, indicated that cholinergically driven neocortical oscillations require excitatory synaptic transmission. We conclude that under the appropriate pharmacological conditions, neocortical brain slices were capable of producing localized theta frequency oscillations. Experiments examining oscillation physiology, pharmacology, and topography demonstrated that neocortical brain slice oscillations share many similarities with the in vivo and in vitro theta EEG activity recorded in other brain regions.

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Eeg changes induced by convulsants interfering with GABAergic inhibition in rats. I. Cortical recordings

Cited by 3 publications

References 9 publications

Motor and Electrocorticographic Epileptic Activity Induced by Bicuculline in Developing Rats

Motor and Electrocorticographic Epileptic Activity Induced by Bicuculline in Developing Rats

Regional brain activation by bicuculline visualized by functional magnetic resonance imaging. Time-resolved assessment of bicuculline-induced changes in local cerebral blood volume using an intravascular contrast agent

Physiology, Pharmacology, and Topography of Cholinergic Neocortical Oscillations In Vitro

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