Figure 3

The effect of anise oil on hypoxic events and synaptic plasticity. Anise oil extended the latency of the induction of anoxic terminal negativity (ATN) by hypoxia (deprivation of O2) and inhibited induction of long-term potentiation (LTP) in rat hippocampal slices. (A) Recordings of ATN of the DC-potential and of evoked potentials in control (A1), with pre-treatment of anise oil (A2; 20 μg/l), with pretreatment with APV (A3; 10 μmol/l), and pre-treatment with APV and anise oil (A4) in CA1 areas of the hippocampus. (B) Statistical evaluation of the latency of the appearance of ATN in control as well as pre-treatment with anise oil at 10 and 20 μg/l (B1; * indicate p = 0.03, ANOVA test), pre-treatment with NMDA as well as NMDA and anise oil (B2; ** indicate P = 0.007, Mann-Whitney rank sum test), pre-treatment with APV (B3; 10 μmol/l), and pre-treatment with APV and anise oil (B4; ** indicate p = 0.04, Mann-Whitney rank sum test). Anis oil significantly extended the latency of the induction of ATN, possibly by inhibition of glutamate NMDA sub-receptors. (C) Tetanic stimulation produces a rapid and stable potentiation in the amplitude of the evoked field potentials, calculated as a percentage of baseline mean response amplitude. (C1) Open triangle and solid circles show the evoked fEPSP after application of anise oil and control, respectively. Arrow shows the time of tetanic stimulation, 60 min after application of anise oil (20 μg/l) or ACSF (control). The time points given refer to substance application. Application of anise oil significantly inhibited LTP of the evoked field potentials (Mann-Whitney rank sum test, p = 0.006), calculated as a percentage of baseline mean response amplitude. (C2) Representative examples of the evoked field potentials before and after titanic stimulation in control and anise oil -treated slices.