“Although most anti-epileptic drugs are considered to have a primary molecular target, it is clear that their actions are unlikely to be limited to effects on a single aspect of inhibitory synaptic transmission, excitatory transmission or voltage-gated
ion channels. Systemically administered drugs can obviously selleck simultaneously access all possible targets, so we have attempted to determine the overall effect of diverse agents on the balance between GABAergic inhibition, glutamatergic excitation and cellular excitability in neurones of the rat entorhinal cortex in vitro. We used an approach developed for estimating global background synaptic excitation and inhibition from fluctuations in membrane potential obtained by intracellular recordings. We have previously validated www.selleckchem.com/products/lazertinib-yh25448-gns-1480.html this approach in entorhinal cortical neurones [Greenhill and Jones (2007a) Neuroscience 147:884-892]. Using this approach, we found that, despite their differing pharmacology, the drugs tested (phenytoin, lamotrigine, valproate, gabapentin, felbamate, tiagabine) were unified in their ability to increase the ratio of background GABAergic inhibition to glutamatergic excitation. This could occur as a result of decreased excitation concurrent with increased inhibition (phenytoin, lamotrigine, valproate), a decrease in excitation alone
(gabapentin, felbamate), or even with a differential increase in both (tiagabine). Additionally, we found that the effects on global synaptic conductances agreed well with whole cell patch recordings of spontaneous
glutamate and GABA release (our previous studies and further data presented here). The consistency with which the synaptic inhibition:excitation ratio was increased by the antiepileptic drugs tested was matched by an ability of all drugs to concurrently reduce intrinsic neuronal excitability. Thus, it seems possible that specific molecular targets among antiepileptic drugs are less important than the ability to increase the inhibition:excitation ratio and reduce overall neuronal and network excitability. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Accurate Diflunisal endoleak classification is essential following fenestrated endovascular aneurysm repair (f-EVAR). Both endoleak type and exact source of endoleak have implications upon the urgency and complexity of future management strategies. Herein we report on a patient with a documented endoleak post-f-EVAR, in which the source of blood flow into the aneurysm sac could not be determined using conventional computed tomographic angiography. Consequently, dynamic volumetric computed tomographic angiography (DV-CTA) was employed, which clearly illustrated the site of origin of the endoleak.