Seizure susceptibility to various convulsant stimuli in dystrophin-deficient mdx mice

Sarro, Giovambattista De; Ibbadu, Guido Ferreri; Marra, Rosario; Rotiroti, Domenicantonio; Loiacono, Antonella; Paola, Eugenio Donato Di; Russo, Emilio

doi:10.1016/j.neures.2004.05.007

Cited by 34 publications

(33 citation statements)

References 39 publications

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“…Results indicate that the development of kindled convulsions was directly proportional and cumulative with repeated exposure to PTZ. About 4-5 weeks of treatment was needed to achieve a stage 4 seizure intensity and, therefore, kindling was achieved with about 16 injections of PTZ, similarly to our previous results [34,50]. None of the animals convulsed on the first administration, and only 12/108 did not reach the kindling status after 8 weeks.…”

Section: Development Of Pentylenetetrazol Kindlingsupporting

confidence: 84%

“…For the study of the persistence of kindling status, an independent challenge experiment was performed using PTZ (25 mg/kg, s.c.) 45 days after withdrawal from the last PTZ (30 mg/kg, s.c.) treatment, as previously described [50]. The mice were observed for 120 min after injection in order to determine the incidence of convulsions.…”

Section: Challenge With Pentylenetetrazolmentioning

confidence: 99%

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Lamotrigine positively affects the development of psychiatric comorbidity in epileptic animals, while psychiatric comorbidity aggravates seizures

Russo

Chimirri

Aiello

et al. 2013

Epilepsy & Behavior

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Section: Development Of Pentylenetetrazol Kindlingsupporting

confidence: 84%

Section: Challenge With Pentylenetetrazolmentioning

confidence: 99%

Lamotrigine positively affects the development of psychiatric comorbidity in epileptic animals, while psychiatric comorbidity aggravates seizures

Russo

Chimirri

Aiello

et al. 2013

Epilepsy & Behavior

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“…Dystrophin mutations in Mdx mice or in patients with Duchenne muscular dystrophy are often accompanied by cognitive deficits, as well as a higher risk for epilepsy and autism spectrum disorder (ASD) (4,41). Dystroglycanopathies display similar phenotypes including severe intellectual disability and epilepsy (4).…”

Section: Discussionmentioning

confidence: 99%

Dystroglycan mediates homeostatic synaptic plasticity at GABAergic synapses

Pribiag

Peng

Shah

et al. 2014

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

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Dystroglycan (DG), a cell adhesion molecule well known to be essential for skeletal muscle integrity and formation of neuromuscular synapses, is also present at inhibitory synapses in the central nervous system. Mutations that affect DG function not only result in muscular dystrophies, but also in severe cognitive deficits and epilepsy. Here we demonstrate a role of DG during activitydependent homeostatic regulation of hippocampal inhibitory synapses. Prolonged elevation of neuronal activity up-regulates DG expression and glycosylation, and its localization to inhibitory synapses. Inhibition of protein synthesis prevents the activity-dependent increase in synaptic DG and GABA A receptors (GABA A Rs), as well as the homeostatic scaling up of GABAergic synaptic transmission. RNAi-mediated knockdown of DG blocks homeostatic scaling up of inhibitory synaptic strength, as does knockdown of like-acetylglucosaminyltransferase (LARGE)-a glycosyltransferase critical for DG function. In contrast, DG is not required for the bicuculline-induced scaling down of excitatory synaptic strength or the tetrodotoxin-induced scaling down of inhibitory synaptic strength. The DG ligand agrin increases GABAergic synaptic strength in a DG-dependent manner that mimics homeostatic scaling up induced by increased activity, indicating that activation of this pathway alone is sufficient to regulate GABA A R trafficking. These data demonstrate that DG is regulated in a physiologically relevant manner in neurons and that DG and its glycosylation are essential for homeostatic plasticity at inhibitory synapses. muscular dystrophy | excitation-inhibition balance | dystrophin |

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“…Dilute brown agouti coat color/2 mice are particularly susceptible not only to convulsant agents such as pentylenetetrazole, picrotoxin, bicuculline, DMCM, and β-CCM acting predominantly by impairing GABA neurotransmission [29,62,68], but also to excitatory neurotransmitter agonists such as AMPA, kainic acid, and NMDA acting through ionotropic glutamate receptors and 4-AP blocking K + channels [56,68,69]. Furthermore, DBA/2 mice are more susceptible to convulsant doses of imipenem, a broad spectrum antibiotic of the carbapenem class, than Swiss and NMRl mice [52,70].…”

Section: Susceptibility Of Dba/2 Mice To Convulsant Compoundsmentioning

confidence: 99%

Genetically epilepsy-prone rats (GEPRs) and DBA/2 mice: Two animal models of audiogenic reflex epilepsy for the evaluation of new generation AEDs

Sarro¹,

Russo²,

Citraro³

et al. 2017

Epilepsy & Behavior

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Seizure susceptibility to various convulsant stimuli in dystrophin-deficient mdx mice

Cited by 34 publications

References 39 publications

Lamotrigine positively affects the development of psychiatric comorbidity in epileptic animals, while psychiatric comorbidity aggravates seizures

Lamotrigine positively affects the development of psychiatric comorbidity in epileptic animals, while psychiatric comorbidity aggravates seizures

Dystroglycan mediates homeostatic synaptic plasticity at GABAergic synapses

Genetically epilepsy-prone rats (GEPRs) and DBA/2 mice: Two animal models of audiogenic reflex epilepsy for the evaluation of new generation AEDs

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