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Experimental Models of Status Epilepticus
Published in Steven L. Peterson, Timothy E. Albertson, Neuropharmacology Methods in Epilepsy Research, 2019
Flurothyl, hexaflurodiethyl ether (Flura Corp., Newport, TN), is a convulsant gas that when inhaled induces seizure activity.15,16,88 It has been hypothesized that flurothyl induces seizure activity by opening sodium channels.15 Flurothyl has been used to induce SE but not as often as the previously discussed models. The advantages of flurothyl are that it induces SE that is accompanied by a predictable pattern of irreversible neuronal damage; physiologic parameters during SE can be controlled and monitored; and the duration of the seizures can be determined by the investigator.16 In order to use flurothyl, the laboratory must be equipped with a closed gas inhalation delivery system for rodents so the investigator is not exposed to the flurothyl, otherwise all experiments must be done in a laboratory fume hood. These animals also require significant instrumentation in order to monitor and control the physiologic changes that occur during SE.
Stimulatory and inhibitory effects of morphine on pentylenetetrazol-induced epileptic activity in rat
Published in International Journal of Neuroscience, 2021
Samrand Rashan, Yousef Panahi, Emad Khalilzadeh
Morphine is an opioid that delays the onset of pentylenetetrazol (PTZ)-and flurothyl-induced seizures and suppresses audiogenic seizures (AGSs) [2]. It has biphasic effects. It exerts anticonvulsant effects at lower doses and proconvulsant effects at higher doses [3]. The proconvulsant or anticonvulsant activity of an opioid has a close affinity with a specific opioid receptor, dose, route of administration, and animal model [1]. The systemic administration of pentazocine, fentanyl, meperidine, and morphine protects against seizures [4]. In-vivo studies indicate that the proconvulsant action of morphine is mediated by morphine-3-glucuronide [5] or nitric oxide [6]. Other studies demonstrate that opioid, adrenergic, and glutamate receptors trigger opioid-induced seizures [7]. Moreover, opioids antagonize gamma-aminobutyric acid (GABA)-ergic neurotransmission [8].
Aberrant plasticity in the hippocampus after neonatal seizures
Published in International Journal of Neuroscience, 2018
Xiaoqian Zhang, Huiling Qu, Ying Wang, Shanshan Zhao, Ting Xiao, Chuansheng Zhao, Weiyu Teng
With respect to flurothyl-induced seizures, there were different effects on the proliferation of newly formed neurons depending on the time point when the toxin was administered. Holmes et al. demonstrated that neonatal rats subjected to a series of 25 brief flurothyl-induced seizures had more newly formed DGCs than controls when assessed 45 d later [17]. McCabe et al. detected a reduction in the proliferation of newly formed DGCs from neonatal rats experiencing 25 flurothyl-induced seizures at postnatal day 0 (P0)-P4, and this reduction persisted for 6 d following the last seizure [41]. Furthermore, McCabe et al. also demonstrated that a very large percentage of the newly formed cells were neurons and immature rats subjected to a single seizure did not differ from controls in terms of the newly formed DGCs.