Dexamethasone and Hormones Related to the Hypothalamic-Pituitary-Adrenal Axis Modulate Inherited Neocortical Spindling in DBA/2J Mice

Capasso, Anna; Sorrentino, L.; Giannuario, A. Di; Palazzesi, Sergio; Pieretti, Stefano; Loizzo, Alberto

doi:10.1159/000119077

Cited by 10 publications

(9 citation statements)

References 23 publications

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“…Furthermore, these data indicate that the time necessary for the appearance of this effect is very similar to that observed previously on brain excitability after DEX administration in vivo [4,5] and in vitro [4,33]. These data and those obtained with actinomycin D are consistent with the genomic activation induced by DEX via an intracellular receptor mechanism, in agreement with the steroid hormone mechanism of action model proposed by Thompson and Lippman [66].…”

Section: Dopaminergic Pathwaysupporting

confidence: 90%

“…Also, it is well known that glucocorticoids effects may become evident a few minutes [28,29] or 1-2 hr after administration: in this case, glucocorticoids exert their effect through a genomic activation [30][31][32]. Also, some previous studies are in according with the latter findings because DEX needs a certain lag-rime (15-30 min) to reduce brain excitability and cycloheximide was able to block the DEX effects [4,5,33]. Therefore, to verify a possible involvement of a genomic activation in the reducing effect of DEX on morphine, amphetamine and cocaine hypermotility, the steroid was administered at different time intervals before morphine, amphetamine or cocaine injection, and the influence of actinomycin D (dacrinomycin), a protein synthesis inhibitor [34], on the steroid effects was considered.…”

Section: Introductionmentioning

confidence: 98%

“…The author has studied some steroid effects on brain excitability by using different experimental procedures showing that ACTH or corticosteroids prevent the appearance of EEG ictal episodes induced by intracerebrally injected CRF in rabbits [3], that DEX is able to block the epileptiform activity induced by opioids in vivo and in vitro experiments [4] and that DEX and HPA axis hormones are able to reduce the spike and wave neocortical spindling occurrence of DBA/2J mice [5]. However, how mechanisms which really underlie attenuation of the brain excitability by corticosteroids are still unclear.…”

Section: Introductionmentioning

confidence: 99%

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Glucocorticoids Involvement in the Control of CNS Excitability

Capasso

2007

RPCN

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The effect of dexamethasone (DEX) and its interaction with psychostimulants agents (morphine, cocaine and amphetamine) has been studied on locomotor activity and straub reaction in mice: a) Morphine administration, (30-75-150 mg/kg,ip) induced a dose-related increase of the locomotor activity of mice, whereas DEX per se (0.1-1.0-10 mg/kg,ip) did not modify the activity of control mice. Pretreatment of mice with DEX 0.1 mg did not alter the hyperactivity produced by the three doses of morphine. In contrast, DEX administered at 1.0 mg reduced the morphine effects on locomotor activity, whereas DEX at 10 mg potentiated the morphine hypermotility. b) Cocaine (10 mg/kg/i.p.) and amphetamine (5 mg/kg/i.p.) increased markedly locomotor activity of mice whereas DEX per se (0.1-1.0-10 mg/kg/i.p.) did not modify the activity of control mice. DEX pretreatment decreased the stimulating effects induced by cocaine and amphetamine. DEX pretreatment 0, 15, 30, 60 and 120 min before amphetamine or cocaine strongly decreased both amphetamine and cocaine effects, but no dose-related effect was observed. The time-course study performed with DEX revealed differences in its reducing effect on cocaine and amphetamine hypermotility when the groups of animals treated with the steroid immediately before the cocaine (or amphetamine) injection when compared to those treated with the steroid later (15, 30, 60 and 120 min). Furthermore, actinomycin D was able to block the reducing effect of DEX on both amphetamine and cocaine hypermotility. c) When morphine was administered in doses of 7.5, 15 and 30 mg/kg/i.p, a dose-dependent straub reaction was produced. DEX per se (0.1-1.0-10 mg /kg,i.p.) did not modify the tail of control mice. Pre-treatment with DEX 120 min before morphine injection caused a dose-dependent reduction of straub reaction. Cycloheximide (15 mg/kg,i.p.) administered 2h before morphine did not change morphine-induced straub reaction, but was able to prevent the effects of DEX on morphine-induced straub reaction. The glucocorticoid receptor antagonist RU-38486 (15 mg/kg,i.p.) did not affect morphine-induced straub reaction, whereas it was able to block the effects of dexamethasone on morphine-induced straub reaction. Our results suggest that DEX may play an important regulatory role on the central effects of morphine, cocaine and amphetamine through a differential modulation of brain excitability systems indicating that DEX may play an important role on the stimulating effects of morphine, cocaine and amphetamine and that it may be of some utility in the clinical management of psychastimuants abuse. The ability of actinomicyn D and/or cycloheximide as well as of RU-38486 to block dexamethasone's effects indicates that the steroid's interference with psychostimulants-mediated effects involve a protein-synthesis-dependent mechanism via glucocorticoid receptors. The patents related to psychostimulant agent and glucocorticoids are also discussed in this article.

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Section: Dopaminergic Pathwaysupporting

confidence: 90%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Glucocorticoids Involvement in the Control of CNS Excitability

Capasso

2007

RPCN

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“…Moreover, the WAG/ Rij rats, an absence epilepsy model, show a rapid, albeit transient increase in the number of absence seizures in response to the administration of CORT (Schridde and van Luijtelaar, 2004). In contrast, administration of CORT to absence seizure-prone DBA/2J mice decreased the number of spontaneous spike and wave discharges observed (Capasso et al, 1994).…”

Section: Effects Of Corticosterone On Seizuresmentioning

confidence: 96%

Stress and Epilepsy: Multiple Models, Multiple Outcomes

Sawyer

Escayg

2010

Journal of Clinical Neurophysiology

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Human studies show a link between stress and epilepsy, with stress causing an increase in seizure frequency and severity in patients with epilepsy. Many different animal model systems have been used to better understand this connection and the possible mechanisms involved. This review highlights the results of such studies relating stress and seizure susceptibility, with a focus on the hypothalamic-pituitary-adrenal axis and its relationship to seizure generation. The effects of hypothalamic-pituitary-adrenal axis mediators, acute stress, chronic stress, and early life stress on the seizure phenotype are summarized. Results suggest that stress has both anticonvulsive and proconvulsive properties, depending on the animal strain and the stress/seizure induction paradigm used. Attempts to interpret the stress-epilepsy literature must take these variables into account. The growing availability of genetically modified mice that carry either human epilepsy mutations or mutations in stress pathway genes now provide the opportunity to examine the relationship between stress and epilepsy more directly.

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“…Experimental data showed that cortisone and hydrocortisone facilitate kindling development [16,17], lower the seizure threshold [18,19] Di Giannuario/Pieretti/Sagratella/Loizzo spikes in the hippocampus, hypothalamus, amygdala and septum [20]. On the other hand, it has been reported that dexamethasone reduces spontaneous spike and spindling episodes (S&W) in DBA/2J mice [21] and blocks the epileptiform activity induced by morphine in the rabbit hippocampus in vivo [10] and by the Ì-opioid agonist [DAla 2 -N,Me-Phe 4 -Gly 5 -ol]enkephalin (DAMGO), or by picrotoxin in rat hippocampal slices [10] and in organotypic cell culture in vitro [22]. Clinical data also confirm that glucocorticoids may have anti-epileptic properties as observed in the early treatment of some infantile spasms with ACTH or corticosteroids which produce a remission of seizure activity and epileptiform EEG patterns [23][24][25].…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone Blocking Effects on Mu- and Delta-Opioid-Induced Seizures Involves Kappa-Opioid Activity in the Rabbit

Giannuario

Pieretti²,

Sagratella³

et al. 2001

Neuropsychobiology

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Previous data indicate that intracerebroventricular administration of agonists for µ- and δ-opioid receptors induces limbic seizures in rats, but no data are reported in rabbits. We found that the µ- and δ-opioid peptides [D-Ala²-N,Me-Phe⁴-Gly⁵-ol]enkephalin (DAMGO), β-endorphin and deltorphin II, induced EEG non-convulsive hippocampal seizures, and changes in hippocampal background EEG, physical parameters and overt behaviour after central administration. Dexamethasone pre-treatment prevented DAMGO-, deltorphin II- and β-endorphin-induced seizures as well as changes in background EEG, physical parameters and overt behaviour induced by µ-opioid agonists. Dexamethasone antagonism on opioid action was blocked by pre-treatment with a protein synthesis inhibitor, cycloheximide or by the ĸ-opioid antagonist nor-binaltorphimine. Our data suggest that dexamethasone influences opioid actions at µ- and δ-receptors via a protein synthesis mechanism involving ĸ-opioid receptors.

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Dexamethasone and Hormones Related to the Hypothalamic-Pituitary-Adrenal Axis Modulate Inherited Neocortical Spindling in DBA/2J Mice

Cited by 10 publications

References 23 publications

Glucocorticoids Involvement in the Control of CNS Excitability

Glucocorticoids Involvement in the Control of CNS Excitability

Stress and Epilepsy: Multiple Models, Multiple Outcomes

Dexamethasone Blocking Effects on Mu- and Delta-Opioid-Induced Seizures Involves Kappa-Opioid Activity in the Rabbit

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