LTP (Wigström and Gustafsson, 1986), we used a relatively weak concentration of PTX (50 μM) to partially block GABA(A) receptors and to mimic CB1-mediated suppression of neurotransmission. Application of PTX prevented the WIN block of LTP in stress slices (159.57 ± 1.54%, Fig. 5a) but was not as effective in non-stress slices (107.19 ± 1.69%, Fig 5b). For comparison, Figure 6 summarizes all the LTP experiments. A one-way ANOVA comparing LTP levels among all the experimental conditions was significant (F (5, 89) = 734.04, p = 0.000), allowing for further analysis between groups. Post-hoc tests revealed that in stress (S) animals, WIN application significantly impaired LTP compared to control LTP (S; p = 0.000) and compared to S_WIN_PTX LTP levels (p = 0.000). However, S_WIN_PTX was also significantly lower than control LTP (p = 0.000). In non-stress (NS) animals, WIN also inhibited LTP compared to control levels (p = 0.000). LTP in the NS_WIN_PTX also was significantly different from control LTP (p = 0.000), indicating that PTX did not effectively prevent the WIN impairment. Although, the NS_WIN_PTX group was also significantly different from the NS_WIN (p = 0.000), showing that a weak level of plasticity is still possible in these
