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(continue) ? We thank the reviewer for having paid a good deal of attention to that kainate (KA) has been used as a powerful tool to evaluate pharmacological and mechanistic properties of glutamate receptors. Indeed, KA, as an agonist for the AMPA/KA class of glutamate receptor, is widely used to induce status epilepticus and kindling. Using these models of epilepsy, neurobiologists have well defined patterns of neuronal degeneration in the hippocampus and other brain regions. Neuronal alterations in KA-induced seizures have widely been investigated by testing hippocampal hyperexcitability, cIEGs (cellular immediate-early genes) response in vivo, oxidative DNA damage, neuronal death, hormone release, and substrate metabolism. These indicate that KA administration is commonly considered to be an experimental model for the neurological damage and has been used extensively in neurobiological research as it preferentially damages neurones in the limbic system, particularly the hippocampus, although it is not a natural ligand of AMPA/KA receptors. The generation of ROS by KA and its correlation with excitotoxicity have been reviewed. Furthermore, many substances such as melatonin, ascorbate, nimesulide, propofol and ganglioside that play roles in neuroprotection against oxidative lesions have been investigated, using KA-induced seizure models. Accordingly, it is understandable that we used the model of KA- but not glutamate-induced excitotoxicity and seizures to investigate TMP neuroprotection against oxidative lesions. Anyhow, the reviewer’s suggestion will be beneficial for our better understanding of KA excitotoxicity. We thank the reviewer. After resubmission days you may receive: Accepted or rejected information Weeks after you will receive: PDF file of Proof Offprints order form Copyright transfer agreement … COPYRIGHT TRANSFER AGREEMENT Date: Contributor name: __________________________________