Figure 4: Spreading neuroprotection against a direct excitotoxic challenge requires GABAB receptor function.
From: Neuronal networks provide rapid neuroprotection against spreading toxicity
(a) GABAA (muscimol or diazepam) or GABAB (baclofen) receptor activity attenuates glutamate excitotoxicity, although prior exposure (60 minutes) is required for GABAB neuroprotection to develop (n = 3). (b) Spreading toxicity to downstream chambers (−2, −1, 1, 2) is blocked by enhancing GABAergic inhibition (100 μM muscimol, 5 μM diazepam, or 100 μM baclofen, n = 3). (c) Downstream Ca2+ spiking spread by an excitotoxic challenge is abolished by muscimol or baclofen (n = 3). Traces are representative of individual neuronal responses (light color) and the mean for all recorded cells (dark color). (d) Spreading neuroprotection from a direct excitotoxic challenge (100 GG, 1 hour) is blocked by CGP (n = 3), but not bicuculline (n = 6). Basal cell death is indicated by the dotted line (UT). Data are expressed as mean ± S.E.M (one-way ANOVA with post hoc Tukey’s test. ‘ns’ denotes p > 0.05, *denotes p < 0.05, **denotes p < 0.01, ***denotes p < 0.001, relative to control). Experiments were performed using independent neuronal preparations.
