Effects of cannabidiol and of diphenylhydantoin on the hippocampus and on learning

Izquierdo, Iván; Nasello, Antonia G.

doi:10.1007/bf00419816

Cited by 33 publications

(6 citation statements)

References 17 publications

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“…Previous studies from this laboratory had shown that moder ate afferent stimulation (15) or localized hippocampal perfusion with moderate ly high K+ concentrations (7) caused an increase of hippocampal RNA levels, whereas more rapid stimulation (15) or too high K+ concentrations in the perfu sion fluid (7) had an opposite effect. This was in agreement with most studies on neuronal RNA, which show increased synthesis and concentration with moder ate stimulation and increased turnover and lowered concentration with exagger ated stimulation (3,5 In the present study, first the effects of metrazol, electroshock and hypo natremia (17) on one hand, and those of cannabidiol (6,10,12), diphenylhydantoin, phénobarbital and trimethadione (6,17) on the other, were exam ined in awake animals. Since, as will be seen, no effect on hippocampal or neocortical RNA was found, we turned to an anesthetized preparation (6,8,(10)(11)(12)(13) where the effect of epileptogenic stimulation of the fornix (8, 11) on hippocampal RNA was studied, and its antagonism by the four mentioned anti convulsant agents.…”

supporting

confidence: 78%

“…Thus, the present data strongly suggest that hippocampal RNA falls caused by seizures are not dependent on K+ release, as was previously thought (7), in contrast to the RNA buildup which occurs upon more moderate afferent stimu lation (15) and is K+-dependent (10,13).…”

Section: Discussionmentioning

confidence: 36%

“…It is interesting that they did so in spite of being unable to actually prevent seizure discharges and of having diverse mechanisms of anti epileptic action (6,10,17). In the hippocampus, for example, where all of them have been shown to raise seizure threshold (6,9,12), diphenylhydantoin and cannabidiol apparently act by blocking K+ release (9,12), whereas phénobarbital and trimethadione do not affect K+ release and presumably act somewhere further on in the chain of events triggered by high K+ (14).…”

Section: Discussionmentioning

confidence: 99%

“…One was left unstimulated during 35 min after surgery and the other one, after 10 min of rest, received a 20-sec stimulation to the fornix for 25 min, adjusted so that seizures occurred after a few seconds and continued then throughout stimulation. Surgical, stimulation and recording procedures v. ere in all respects as described in detail elsewhere (8,(10)(11)(12)(13). At the end of these periods Ae left hippocampus (which was the one with seizures in stimulated rats) was quickly removed, weighed and homogenized as mentioned above, and similarly processed for RNA assay.…”

Section: Methodsmentioning

confidence: 99%

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Effect of Seizures and Anticonvulsant Agents on Hippocampal RNA Concentration

Tannhauser¹,

Izquierdo²

1974

Pharmacology

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Epileptogenic stimulation of the fornix during 25 min caused a fall of total hippocampal RNA concentration in rats. This fall was prevented by the preadministration of phenobarbital, trimethadione, diphenylhydantoin or cannabidiol, which, however, were unable to block seizure discharges in most cases. The administration of any of these anticonvulsant agents to awake animals had no effect on neocortical and hippocampal RNA levels. Generalized convulsions provoked in awake animals by metrazol, electroshock or hyponatremia also had no effect on neocortical or hippocampal RNA.

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supporting

confidence: 78%

Section: Discussionmentioning

confidence: 36%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Effect of Seizures and Anticonvulsant Agents on Hippocampal RNA Concentration

Tannhauser¹,

Izquierdo²

1974

Pharmacology

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“…This led to further investigations on the anticonvulsant action first of extracts and then of isolated compounds of the plant (111, 212,275,276,280) and almost simultaneously to effects of Cannabis and its compounds on fear learning (212,275,288,467) in the laboratory of E. A. Carlini in São Paulo. Concerning the anticonvulsant effects, the nonpsychotropic natural cannabinoid cannabidiol is now beginning to draw generalized attention through a variety of effects aside from the anticonvulsant one: anxiolytic (67) and perhaps neuroprotective (161,600).…”

Section: Cannabinoidsmentioning

confidence: 99%

Fear Memory

Izquierdo

Furini

Myskiw

2016

Physiological Reviews

384

259

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Fear memory is the best-studied form of memory. It was thoroughly investigated in the past 60 years mostly using two classical conditioning procedures (contextual fear conditioning and fear conditioning to a tone) and one instrumental procedure (one-trial inhibitory avoidance). Fear memory is formed in the hippocampus (contextual conditioning and inhibitory avoidance), in the basolateral amygdala (inhibitory avoidance), and in the lateral amygdala (conditioning to a tone). The circuitry involves, in addition, the pre-and infralimbic ventromedial prefrontal cortex, the central amygdala subnuclei, and the dentate gyrus. Fear learning models, notably inhibitory avoidance, have also been very useful for the analysis of the biochemical mechanisms of memory consolidation as a whole. These studies have capitalized on in vitro observations on long-term potentiation and other kinds of plasticity. The effect of a very large number of drugs on fear learning has been intensively studied, often as a prelude to the investigation of effects on anxiety. The extinction of fear learning involves to an extent a reversal of the flow of information in the mentioned structures and is used in the therapy of posttraumatic stress disorder and fear memories in general.

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Levonantradol Potentiates the Anticonvulsant Effects of Diazepam and Valproic Acid in the Kindling Model of Epilepsy

Ehlers

Henriksen

Bloom

1981

The Journal of Clinical Pharma

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The anticonvulsant effects of the cannabinoid derivative levonantradol and its ability to potentiate the anticonvulsant effects of diazepam and valproic acid were studied in rats with previously established amygdala‐kindled seizures. Levonantradol administered in doses of 100 to 400 μg/kg did not block any components of the motor seizure. However, levonantradol did increase the latency of appearance of fully kindled seizures at the 400 μg/kg dose. Administration of diazepam at doses of 1 or 2 mg/kg or valproic acid at doses of 100 or 200 mg/kg produced seizure control as measured by a reduction in motor components of the seizure or a reduction in afterdischarge length or both. The anticonvulsant effects of diazepam and valproic acid were potentiated by administration of 100 μg/kg levonantradol without apparent increases in sedation. Although the mechanism underlying this potentiation of the antiepileptic effects of valproic acid and diazepam remains unknown, levonantradol may have potential as adjunctive therapy in the treatment of complex partial seizures.

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Effects of cannabidiol and of diphenylhydantoin on the hippocampus and on learning

Cited by 33 publications

References 17 publications

Effect of Seizures and Anticonvulsant Agents on Hippocampal RNA Concentration

Effect of Seizures and Anticonvulsant Agents on Hippocampal RNA Concentration

Fear Memory

Levonantradol Potentiates the Anticonvulsant Effects of Diazepam and Valproic Acid in the Kindling Model of Epilepsy

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