We used field potential recording techniques to examine whether felbamate (FBM), lamotrigine (LTG), and lidocaine (LID) protect against the irreversible functional damage induced by transient ischemia. Five minutes of ischemia caused a depression of the field potential in rat cortical slices, which did not recover even after more than 1 h of washout. The N-methyl-D-aspartate (NMDA) antagonist ketamine (50 μM) protected against depres- sion of the field caused by ischemia. On the other hand, the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2.3-dione (CNQX) (10 μM) had protective effects only if co-applied with ketamine. We found that either FBM (30–300 μM), which did not modify the amplitude of the field EPSP, or LTG (10–300 μM), which reversibly depressed the excitatory synaptic transmission, had a marked protective effect when superfused before and during the ischemic insult. After FBM (100 μM) and LTG (100 μM), the field EPSP recovered by 84 1% and 73 2.7% of control, respectively. Furthermore, LID (30–300 μM) was less effective than FBM and LTG in inducing a functional recovery from the damage caused by ischemia (58 1.8%). The rank order of potency, based on the maximal protection caused by the three drugs, was FBM LTG LID. Our results suggest that a noticeable neuroprotection can be obtained during glucose and O2 deprivation by preventive therapeutic regimens which use the two recently marketed anticonvulsant drugs, FBM and LTG.

An electrophysiological analysis of the protective effects of felbamate, lamotrigine, and lidocaine on the functional recovery from in vitro ischemia in rat neocortical slices.

GUATTEO, EZIA;
1998

Abstract

We used field potential recording techniques to examine whether felbamate (FBM), lamotrigine (LTG), and lidocaine (LID) protect against the irreversible functional damage induced by transient ischemia. Five minutes of ischemia caused a depression of the field potential in rat cortical slices, which did not recover even after more than 1 h of washout. The N-methyl-D-aspartate (NMDA) antagonist ketamine (50 μM) protected against depres- sion of the field caused by ischemia. On the other hand, the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2.3-dione (CNQX) (10 μM) had protective effects only if co-applied with ketamine. We found that either FBM (30–300 μM), which did not modify the amplitude of the field EPSP, or LTG (10–300 μM), which reversibly depressed the excitatory synaptic transmission, had a marked protective effect when superfused before and during the ischemic insult. After FBM (100 μM) and LTG (100 μM), the field EPSP recovered by 84 1% and 73 2.7% of control, respectively. Furthermore, LID (30–300 μM) was less effective than FBM and LTG in inducing a functional recovery from the damage caused by ischemia (58 1.8%). The rank order of potency, based on the maximal protection caused by the three drugs, was FBM LTG LID. Our results suggest that a noticeable neuroprotection can be obtained during glucose and O2 deprivation by preventive therapeutic regimens which use the two recently marketed anticonvulsant drugs, FBM and LTG.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11367/53684
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