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Brain Slice Model of Epilepsy: Neuronal Networks and Actions of Antiepileptic Drugs
Published in Carl L. Faingold, Gerhard H. Fromm, Drugs for Control of Epilepsy:, 2019
Suzanne Clark, Wilkie A. Wilson
In addition to traditional anticonvulsants, many of the following studies have explored the antiepileptic properties of excitatory amino acid antagonists. These antagonists fall into several different classes based upon the type of antagonism they exert at the different types of glutamate receptors. For example, the NMDA receptor channel complex is competitively blocked by 2-amino-phosphonovalerate (APV)19,37,38 and DL-2-amino-7-phosphonoheptanoic acid (AP7);38 the channel is blocked by agents exemplified by dizocilpine maleate (MK-801).39,40 Compounds such as these are of interest in the study of epilepsy for several reasons: (1) many of the areas of the brain implicated in epilepsy have high levels of NMDA receptors,41 (2) the NMDA antagonists have exhibited anticonvulsant properties in certain in vivo models,42 and (3) certain NMDA antagonists have exhibited antiepileptogenic properties in the kindling model of epilepsy.42 Therefore, although the NMDA antagonists are not currently used as anticonvulsants in clinical settings, we will discuss their effects on brain slices in light of their potential usefulness.
Developing the theory of the extended amygdala with the use of the cupric-silver technique
Published in Journal of the History of the Neurosciences, 2023
Soledad de Olmos, Alfredo Lorenzo
It took a decade of trials and modifications aimed at revealing different types of neuronal injuries with great sensitivity until the final version of the new amino-cupric-silver technique (A-Cu-Ag) was optimized (Beltramino et al. 1993; de Olmos, Beltramino, and de Olmos de Lorenzo 1994). The A-Cu-Ag not only stained the normal granular argyrophilic “control” cells of the lateral hypothalamus (the cells described by Knoche; see Figure 4a), it was also used to reveal the degeneration patterns in the CNS induced by metamphetamine (Jensen et al. 1993) and other neurotoxic drugs such as doxorubicine, dizocilpine maleate, quinolinic acid, and trimethyltin (Figure 4b–f). The sensitivity of the A-Cu-Ag technique made it ideal for analyzing the effects of both neurotoxic and neuroprotective drugs (Beltramino et al. 1993; de Olmos, Beltramino, and de Olmos de Lorenzo 1994; Switzer 1993).
Short-term propofol anaesthesia down-regulates clock genes expression in the master clock
Published in Chronobiology International, 2018
Nawfel Ben-Hamouda, Vincent-Joseph Poirel, Garance Dispersyn, Paul Pévet, Etienne Challet, Laure Pain
Some data suggest that circadian effects of anaesthetics result from the inhibition of the biding of the complex CLOCK:BMAL1 (Circadian Locomotor Output Cycles Kaput: Brain and Muscle Arnt-like 1 protein) via glycogen synthase kinase 3β (GSK3β) (Poulsen et al. 2018). In physiological conditions, CLOCK:BMAL1 complex promotes Per genes transcription (Ko and Takahashi 2006). Ketamine, propofol anaesthesia or long-term sevoflurane exposure leads to (GSK3β) inactivation (Poulsen et al. 2018). This effect has also been observed in the presence of dizocilpine maleate (an NMDA receptor antagonist) (Hetman et al. 2000) suggesting an anti-NMDA mechanism of ketamine and sevoflurane, but another not yet elucidated mechanism for propofol.