Epilepsy in patients with insulin-dependent diabetes and relation to glutamic acid decarboxylase 65

Mahmoud, Adel A.; Abdelmagid, Tayseer; AlGhofely, Mohammed A.; Hamed, A.M.; Sharif, Roaa Al

doi:10.17712/nsj.2020.3.20190057

Cited by 3 publications

(2 citation statements)

References 14 publications

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“…The residual glutamate in the extracellular space is, potentially, neurotoxic. One of the major functions of astrocytes is to uptake most of the synaptically-released glutamate, which optimizes synaptic transmission prevents glutamate excitotoxicity(Fellin and Carmignoto 2004;Mahmoud et al 2020). Absence epilepsy have been proposed to be associated with an imbalance in the level of -aminobutyrate (GABA) and glutamate neurotransmitters(Panayiotopoulos 2001;Cope et al 2009).…”

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confidence: 99%

RETRACTED ARTICLE: Comparing astrocytic gap junction of genetic absence epileptic rats with control rats: an experimental study

et al. 2021

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The synchronization of astrocytes via gap junctions (GJ) is a crucial mechanism in epileptic conditions, contributing to the synchronization of the neuronal networks. Little is known about the endogenous response of GJ in genetic absence epileptic animal models. We evaluated and quanti ed astrocyte GJ protein connexin 30 (Cx30) and 43 (Cx43) in the somatosensory cortex (SSCx), ventrobasal (VB), centromedian (CM), lateral geniculate (LGN) and thalamic reticular (TRN) nuclei of thalamus of genetic absence epilepsy rats from Strasbourg (GAERS), Wistar albino glaxo rats from Rijswijk (WAG/Rij) and control Wistar animals using immunohistochemistry and Western Blot.The Cx30 and Cx43 immunopositive astrocytes in per unite area were quanti ed for each region of the three animal strains. Further, Cx30 and Cx43 Western Blot was applied to the tissue samples from the same regions of the three strain.The number of Cx30 immunopositive astrocytes showed signi cant increase in both GAERS and WAG/Rij compared to control Wistar in all brain regions studied except LGN of WAG/Rij animals. Furthermore, Cx43 in both GAERS and WAG/Rij showed signi cant increase in SSCx, VB and TRN. The percentage of dual expression of Cx30 and Cx43 in the same astrocyte ranged between 17-100% for the 5 brain regions of the 3 animal strains studied. The protein expression of both Cx30 and Cx43 in the two epileptic strain showed an increase compared to Wistar control animals.The signi cant increase in the astrocytic GJ proteins Cx30 and Cx43 and the differences in the dual expression of Cx30 and Cx43 in the genetically absence epileptic strains compared to control animals may suggest that astrocytic Cx's may be involved in the mechanism of absence epilepsy. Increased number of astrocytic Cx's in GAERS and WAG/Rij may represent a compensatory response of the thalamocortical circuitry to the absence seizures or may be related to the production of absence seizures.

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confidence: 99%

RETRACTED ARTICLE: Comparing astrocytic gap junction of genetic absence epileptic rats with control rats: an experimental study

et al. 2021

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“…ICH rat model Iron induced rat or cat model Epilepsy patients N/C EEG discharges and behavioral convulsions N/C Focal aware motor seizures Iron [221] Iron [222] Iron [223] Ischemic and hemorrhagic stroke patients Rat hippocampal slice model of glutamate injury Spontaneous, recurrent epileptiform discharges Neuroinflammation [224] Glutamate [225] Baicalein [226] COVID-19 SARS-CoV-2/Human interactome (master regulator analysis) TLE rat model N/A Limbic seizure, tonic clonic seizures ACE2 [227] ACE2 [228] N/C Higher Seizure Susceptibility and SE-related mortality Hyperglycemic were less seizure sensitive, and diabetic hyperglycemic mice were seizure sensitive GAD antibodies [229] GAD antibodies [230] GAD antibodies [231] GAD antibodies/GABA [232] Hyperglycemia [233] Hypoglycemia/hyperglycemia [234] KD [235] Cardiovasc ular disease…”

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confidence: 99%