Figure 3. Inhibition of cerebellar plasticity in ipsi-lesional flocculus prevents the increase in intrinsic excitability of MVN neurons during compensation.

Mean in vitro discharge rates (±s.e.m.) of rostral ipsi-lesional MVN neurons in slices prepared from animals that were unilaterally labyrinthectomised under urethane anaesthesia, and which remained anaesthetised for 4 h post-UL. The number of cells recorded in each experimental condition is shown at the base of the columns. A, in animals treated with dexamethasone i.p. at the time of UL (UL_4h+ Dex), the mean in vitro discharge rate of the MVN neurons was significantly elevated compared to that in control MVN slices, while in slices from animals that did not receive dexamethasone i.p. (UL_4h - Dex) the mean in vitro discharge rate is not different from control. B, effects of intrafloccular micro-injection of the metabotropic glutamate receptor antagonist AIDA, the PKC inhibitor BIS-I and the serene-threonine kinase inhibitor H-7 at the time of UL, on the mean in vitro discharge rates of MVN neurons in slices prepared 4 h post-UL. In each of these groups dexamethasone was given i.p. at the time of UL. Intrafloccular micro-injection of AIDA and BIS-I abolished the expected increase in intrinsic excitability of the MVN neurons (AIDA_F, BIS-I_F groups). H-7 had no effect when micro-injected at the time of UL (H-7_F group), but did abolish the increase in intrinsic excitability when micro-injected 2 h post-UL (H-7_F2h group). C, ffects of intra-floccular microinjection of dexamethasone (Dex_F group) and the GR antagonist RU38486 (RU_F group). The Dex_F group did not receive dexamethasone i.p.; instead dexamethasone was micro-injected into the ipsi-lesional floccular lobe at the time of UL. The RU_F group received dexamethasone i.p. at the time of UL, but RU38486 was micro-injected into the ipsi-lesional flocculus to block GR.