Secondary Epileptogenesis in Frog Forebrain: Effect of Inhibition of Protein Synthesis

Morrell, Frank; Tsuru, Noriko; Hoeppner, Thomas J.; Morgan, David; Harrison, William

doi:10.1017/s0317167100020552

Cited by 44 publications

(16 citation statements)

References 30 publications

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“…Cycloheximide produced no obvious effect on normal EEG recordings as has been reported (Cohen et al, 1966;Morrell et al, 1975). Usually, overt signs of acute intoxication within several hours after the injection were not recognizable in both systemic and intraventricular administrations.…”

Section: General Toxic Effects Of Cycloheximidesupporting

confidence: 55%

“…In this respect, it has been suggested that the kindling may be regarded as a possible analogue for memory engram formation (Goddard et al. 1969;Racine, 1972;Morrell et al, 1975). Morrell et al (1975) studied the effect of cycloheximide, a potent protein synthesis inhibitor, on the epileptogenic focus induced in the hippocampal cortex of the paralyzed bullfrog by means of localized and intermittent electrical stimulation, i.e., kindling procedure.…”

Section: Introductionmentioning

confidence: 99%

“…1969;Racine, 1972;Morrell et al, 1975). Morrell et al (1975) studied the effect of cycloheximide, a potent protein synthesis inhibitor, on the epileptogenic focus induced in the hippocampal cortex of the paralyzed bullfrog by means of localized and intermittent electrical stimulation, i.e., kindling procedure. They reported that cycloheximide blocked the progressive prolongation of afterdischarge duration when subjected to the kindling procedure.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Cycloheximide on Experimental Epilepsy Induced by Daily Amygdaloid Stimulation in Rabbits

Ogata

1977

Epilepsia

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Daily electrical stimulation of the amygdala caused a progressive change in electrographic afterdischarge and behavioral responses that ultimately resulted in generalized convulsions (kindling). Cycloheximide blocked the completion of kindling when administered 4 hours prior to daily electrical stimulations of the amygdala, but exerted no effect when administered shortly before the stimulation. The temporal relation between administration of cycloheximide and stimulation of the amygdala revealed that the blockade of kindling by cycloheximide was due to the suppression of focal afterdischarge rather than to the persistent inhibition of cerebral protein synthesis during the interstimulus periods.

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Section: General Toxic Effects Of Cycloheximidesupporting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of Cycloheximide on Experimental Epilepsy Induced by Daily Amygdaloid Stimulation in Rabbits

Ogata

1977

Epilepsia

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“…This enduring enhancement of synaptic efficacy, its extension only along synaptically linked stations of the stimulated circuit (7), and its strict dependence on protein synthesis (8,9) and axonal transport (7,10) have suggested that kindling should be associated with some morphological alteration of the synapse itself. It seemed reasonable to assume that a possible mechanism of long-lasting facilitation of synaptic transmission during kindling might be an increase in the number of synaptic contacts.…”

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confidence: 99%

Remodeling of synaptic architecture during hippocampal "kindling".

Geinisman

Morrell

deToledo-Morrell

1988

Proc. Natl. Acad. Sci. U.S.A.

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The "kindling" phenomenon is associated with long-lasting facilitation of synaptic transmission. A possible mechanism of such facilitation could involve changes in the number of synaptic contacts. However, previous attempts to demonstrate a synaptic morphological alteration that could account for the long-term effects ofkindling had failed, possibly due to the unavailability, at the time, of unbiased methods for synapse quantitation. Using the unbiased stereological disector technique, we estimated the number of synapses per neuron in the middle molecular layer of the hippocampal dentate gyrus in rats kindled by electrical stimulation of the medial perforant path with implanted electrodes. Unkindled but stimulated (coulodibit control) and unstimulated but implanted rats served as controls. Animals were coded and killed 4 weeks after reaching the kindling criterion of five generalized seizures. The most important results were obtained when axospinous synapses with continuous or discontinuous postsynaptic densities ("nonperforated" or "perforated" synapses) were differentially analyzed. Kindling resulted in a selective loss of nonperforated synaptic contacts in contrast to preservation of perforated ones. Furthermore, the ratio of perforated to nonperforated synapses was increased by 45% or 40% in kindled rats relative to unstimulated or coulombic controls, respectively. These findings suggest that synaptic efficacy may depend on a balance of the two synaptic types; selective elimination of nonperforated synapses may augment the potency ofremaining synaptic contacts, a process reminiscent of synaptic remodeling during development."Kindling" may be viewed as an experimental model of the formation of an engram in the brain (1, 2). It differs from all other models of synaptic plasticity (or neuronal models of memory) by reason of its extraordinary duration. After only a few exposures to a low-level, localized electrical stimulus, the synaptic responsiveness of the stimulated circuit undergoes an augmentation that persists, without further reinforcement, for many months.In the kindling paradigm (3, 4), a subthreshold electrical stimulus is repeatedly delivered to a local brain area once or twice a day for a duration of 1-2 sec. When first applied, the electrical stimulation results in only brief afterdischarge (AD) and no behavioral alteration. Without any change in stimulation parameters, the AD gradually increases in duration and spreads from the stimulated area to increasingly distant, though synaptically connected, brain regions. A progressive alteration of behavior is also seen, beginning with momentary arrest of ongoing locomotor activity and proceeding through localized twitching to a generalized seizure. Once generalized seizures have occurred, cessation of stimulation for weeks, months, or even years does not result in loss of the newly acquired, electrophysiologically and behaviorally defined change (2, 5, 6). Reintroduction of the original stimulus, which was behaviorally ineffective to begin with, ...

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“…Conversely, cooling of a homotopic cortical site disinhibits contralateral unit activity (21). Similarly, disruption of a primary epileptogenic focus causes enhancement of interictal discharge at a mirror focus (22,23). The findings suggest that an epileptogenic focus exerts a tonic inhibitory effect on a distant site.…”

Section: Secondary-site Kindling Inhibitionmentioning

confidence: 91%

Lasting Secondary Antiepileptogenesis Induced by Cingulate Kindling

Wada

Hirayasu

2004

Epilepsia

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Summary:Purpose: To test the validity of a hypothesis that kindling-induced enduring kindling inhibition of the homotopic secondary site is not a primate species-specific effect but occurs also in feline species.Methods: Five mature male cats were kindled at the anterior (AC) and posterior (PC) cingulate cortex followed by secondarysite kindling and primary-site retest.Results: Kindling was characterized by a marked seizure-stage instability and a progressive afterdischarge threshold elevation in all the animals. A protracted nonconvulsive seizure stage was followed by convulsive evolution and rapid generalization. At the secondary site, positive transfer effect was absent, and kindling did not occur. Primary-site retest activated kindled seizure within three stimulations. Recurrent spontaneous seizures, identical to the primary-site kindled seizure, occurred in two AC-kindled animals. Subsequent to this, a markedly elevated afterdischarge threshold also was found at some distant cortical and subcortical sites, to which the afterdischarge propagated. Kindling of the amygdala ipsilateral to the kindled AC or PC was tardy, with no positive transfer effect. However, it was associated with afterdischage threshold reduction.Conclusions: Cingulate kindling-induced enduring kindling inhibition at a homotopic secondary site is not a primate speciesspecific effect and occurs also in feline species. It is not limited to a homotopic site and represents a lasting secondary antiepileptogenesis, presumably due to enhanced intrinsic inhibitory mechanism(s) available to the mammalian brain. A selective afterdischarge threshold elevation concurrently observed is suspected to be a feline species-specific effect.

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Secondary Epileptogenesis in Frog Forebrain: Effect of Inhibition of Protein Synthesis

Cited by 44 publications

References 30 publications

Effects of Cycloheximide on Experimental Epilepsy Induced by Daily Amygdaloid Stimulation in Rabbits

Effects of Cycloheximide on Experimental Epilepsy Induced by Daily Amygdaloid Stimulation in Rabbits

Remodeling of synaptic architecture during hippocampal "kindling".

Lasting Secondary Antiepileptogenesis Induced by Cingulate Kindling

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