for additional plasticity. Indeed, blocking GABA(A) receptors with picrotoxin rescued LTP in slices from CMS animals. Interestingly, picrotoxin did not rescue LTP in non-stress slices even though blocking GABA did produce slightly-larger LTP in non-stress slices compared to normal non-stress controls. These results indicate that as previously determined, CB1-mediated block of LTP depends on CB1-activation on glutamatergic terminals in non-stress animals, however in CMS-animals, the LTP inhibition shifts to being dependent on CB1-activation on GABAergic terminals (see Fig 8). This, of course, does not rule out that glutamatergic-CB1 activation does not contribute to blocking LTP in stress slices. Collectively, these findings demonstrate how chronic mild stress re-shapes CB1-mediated synaptic physiology and plasticity.
