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Fig. 1 | BMC Neuroscience

Fig. 1

From: Re-engineering a neuroprotective, clinical drug as a procognitive agent with high in vivo potency and with GABAA potentiating activity for use in dementia

Fig. 1

Retention of GABAA potentiating, and attenuated sedative activity in NMZ relative to CMZ. a Oocytes expressing the α1β2γ2 GABAA receptor (n = 6) showed a dose response to increasing concentrations of NMZ in the presence of GABA (6 µM). Addition of picrotoxin (200 µM) caused 96 ± 2 % inhibition of the potentiated GABA response (n = 4) (O). Data show mean ± SD normalized to the saturated 200 µM GABA response. b Male C57Bl/6 mice (n = 5–16) were injected i.p. with CMZ (45 mg/kg) or an equimolar dose of NMZ before testing for their latency to fall on a rotating rod (RR). NMZ showed less sedation than CMZ at various time points. Data show mean ± SEM. Statistical significance relative to vehicle is indicated by *p < 0.05, **p < 0.01, ***p < 0.001, using one-way ANOVA with Dunnett’s post hoc test. c Male C57BL/6 mice (n = 4–5) were injected with escalating doses of CMZ and NMZ and loss of righting reflex (LORR) was measured over 2 h. NMZ showed less sedation than CMZ, and no LORR was observed for NMZ until 125 mg/kg. Data show mean ± SEM. Non-zero statistical significance by one-sample t test is indicated by *p < 0.05, ***p < 0.001

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