Skip to main content
. Author manuscript; available in PMC: 2014 Aug 5.
Published in final edited form as: J Neurosci Res. 2012 Dec 26;91(3):416–425. doi: 10.1002/jnr.23155

Fig. 3.

Fig. 3

Fig. 3

Fig 3A: At 0.1 μM BMI decreases pair-pulse inhibition without secondary PSs. A cumulative dose response curve of BMI was done to determine the lowest concentration necessary to decrease paired-pulse inhibition. Schaffer collaterals were stimulated once per min with paired-pulses of 20 ms interpulse interval and the synaptically evoked PSs were recorded from stratum pyramidale. The concentration of BMI was incremented every 20 min. The recordings shown are the average of the last 5 responses for each concentration. The black arrow shows the primary PSs elicited by the second stimulus at 0.1 μM BMI. The white arrows show secondary PSs elicited by the first and the second stimuli.

Fig 3B: Preexposure to specific concentrations of BMI protected against NMDA excitotoxicity. Slices were pre-exposed for 1 hour to either ACSF or to the various BMI concentrations. BMI was removed by superfusion with ACSF for another hour after which the standard NMDA toxic stimulus was applied. After NMDA the slices were superfused for 1 hour with ACSF and the final PSs were recorded. The recovery of PSs in slices preincubated with 0.1 and 0.5 μM BMI was significantly larger than in NMDA controls exposed only to NMDA (white bar) or to 0.05 or 1 μM BMI (* p<0.05). The number of slices per condition was 42, 21, 90, 21, 14, and 21, respectively. The black line on top indicates the experimental groups exposed to 0.5 mM NMDA for 10 min. The gray bar below indicates the groups exposed to BMI. The hatched bar shows the lack of effect of superfusion for 1 hour with 0.1 μM BMI on the PSs. See Fig 1 for details of design.