TY - JOUR
T1 - N-ethyl lidocaine (QX-314) protects striatal neurons against ischemia
T2 - An in vitro electrophysiological study
AU - Armogida, Marta
AU - Giustizieri, Michela
AU - Zona, Cristina
AU - Piccirilli, Silvia
AU - Nisticò, Robert
AU - Mercuri, Nicola B.
PY - 2010/2
Y1 - 2010/2
N2 - In this study, we have investigated the neuroprotective actions of the membrane impermeable, lidocaine analog, N-ethyl lidocaine (QX-314) in the striatum. The effects of this drug were compared with those caused by the strictly-related-compound and sodium channel blocker lidocaine. To address this issue, electrophysiological recordings were performed in striatal slices, in control condition (normoxia) and during combined oxygen and glucose deprivation (in vitro ischemia). Either QX-314 or lidocaine induced, to some extent, a protection of the permanent electrophysiological alteration (field potential loss) caused by a period (12 min) of ischemia. Thus, both compounds permitted a partial recovery of the ischemic depression of the corticostriatal transmission and reduced the amplitude of the ischemic depolarization in medium spiny neurons. However, while QX-314, at the effective concentration of 100 μM, slightly reduced the amplitude of the excitatory field potential and did not affect the current-evoked spikes discharge of medium spiny striatal neurons, equimolar lidocaine depressed the field potential and eliminated repetitive spikes on a depolarizing step. On the basis of these observations, our results suggest the use of QX-314 as a neuroprotective agent in ischemic brain disorders.
AB - In this study, we have investigated the neuroprotective actions of the membrane impermeable, lidocaine analog, N-ethyl lidocaine (QX-314) in the striatum. The effects of this drug were compared with those caused by the strictly-related-compound and sodium channel blocker lidocaine. To address this issue, electrophysiological recordings were performed in striatal slices, in control condition (normoxia) and during combined oxygen and glucose deprivation (in vitro ischemia). Either QX-314 or lidocaine induced, to some extent, a protection of the permanent electrophysiological alteration (field potential loss) caused by a period (12 min) of ischemia. Thus, both compounds permitted a partial recovery of the ischemic depression of the corticostriatal transmission and reduced the amplitude of the ischemic depolarization in medium spiny neurons. However, while QX-314, at the effective concentration of 100 μM, slightly reduced the amplitude of the excitatory field potential and did not affect the current-evoked spikes discharge of medium spiny striatal neurons, equimolar lidocaine depressed the field potential and eliminated repetitive spikes on a depolarizing step. On the basis of these observations, our results suggest the use of QX-314 as a neuroprotective agent in ischemic brain disorders.
KW - Field potentials
KW - Ischemia
KW - Ischemic depolarization
KW - Medium spiny neurons
KW - Neuroprotection
KW - Patch-clamp
KW - Sodium channel blockers
KW - Synaptic transmission
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U2 - 10.1002/syn.20735
DO - 10.1002/syn.20735
M3 - Article
C2 - 19852070
AN - SCOPUS:72449179416
VL - 64
SP - 161
EP - 168
JO - Synapse
JF - Synapse
SN - 0887-4476
IS - 2
ER -