An aqueous extract of Canarium schweinfurthii attenuates seizures and potentiates sleep in mice: Evidence for involvement of GABA Pathway

An aqueous extract of Khaya senegalensis (Desv.) A. Juss. (Meliaceae) prevents seizures and reduces anxiety in kainate-treated rats: modulation of GABA neurotransmission, oxidative stress, and neuronal loss in the hippocampus

“…Despite the exact molecular mechanisms underlying neuronal loss in these regions being unclear, the activation of astrocytes and microglia, oxidative stress, and proinflammatory cytokines may be involved in SE-induced neuronal loss ( Azcoitia et al., 1998 ; Buckmaster and Jongen-Rêlo, 1999 ). Histological analysis of dentate gyrus of rats treated with the extract (100 and 200 mg/kg) revealed a reduction in perivascular edema, granulovascular degeneration, and neuronal loss and suggested a neuroprotective effect of the extract ( Azcoitia et al., 1998 ; Buckmaster and Jongen-Rêlo, 1999 ; Kandeda et al., 2021a , Kandeda et al., 2021b ). These changes were confirmed by the higher number of surviving neurons compared to the KA + DW group.…”

“…As a result, epilepsy represents the second most common reason for consultation in neurology (16%) in Cameroon, clearly making it a major public health concern ( Mapoure et al., 2015 ; Angwafor et al., 2021 ; Morin et al., 2021 ). Of all types of epilepsy, temporal lobe epilepsy (TLE) accounts for 70–80% of adult epilepsies and is highly drug-resistant ( Lévesque et Avoli, 2013 ; D'Alessio et al., 2020 ; Kandeda et al., 2021b ; Kandeda et al., 2022 ).…”

GABA content and an antioxidant profile positively correlated with the anticonvulsive activity of Microcos paniculata in acute seizure mice

“…This is because reactive oxygen species (ROS) from oxidative stress can cause neuronal injury and alter GABAergic neurotransmission [ 37 , 38 ], which is critical for the control of neuronal excitability and the prevention of seizures [ [39] , [40] , [41] ]. Studies have shown that oxidative stress can alter GABA synthesis and lead to the depletion of GABA content and other neurotransmitters, which may contribute to the development and progression of epilepsy [ [42] , [43] , [44] ]. Many studies have revealed that antioxidant compounds have properties that attenuate seizure events by restoring normal GABAergic signaling [ [45] , [46] , [47] , [48] ].…”

Ameliorative Potential of (-) Pseudosemiglabrin in Mice with Pilocarpine-Induced Epilepsy: Antioxidant, Anti-Inflammatory, Anti-Apoptotic, and Neurotransmission Modulation

“…Acute animal models, such as the pilocarpine-induced epilepsy model, are believed to be useful for initial anti-epileptic pharmacological screening [ 29 ]. The pilocarpine epilepsy model resulted in persistent epileptic-like disorders that accurately mimic the symptoms and pharmacology of the most common type of human epilepsy, refractory temporal lobe epilepsy, and helped the studying of the pathophysiology, behavioral, and electroencephalographic aspects of epilepsy [ 1 , 30 , 31 , 32 ]. Pilocarpine is a nonselective muscarinic agonist with a relatively high affinity for muscarinic receptors in the central nervous system.…”

“…Pilocarpine is a nonselective muscarinic agonist with a relatively high affinity for muscarinic receptors in the central nervous system. When administered intraperitoneally, it induces tonic-clonic seizures since it activates excitatory neurons in specific brain regions, including the amygdala, hippocampus, and entorhinal cortex, with glutamate release [ 31 , 32 , 33 , 34 ].…”