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Received May 10, 2002
Accepted after revision September 26, 2002
1 Department of Biomedical Sciences (Physiology), Edinburgh University Medical School, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK
2 Molecular Medicine Centre, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK
3 Department Of Biomedical Sciences (Physiology), Edinburgh University Medical School, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK
* To whom correspondence should be addressed. E-mail: m.b.dutia{at}ed.ac.uk.
We investigated the role of the cerebellar flocculus in mediating the adaptive changes that occur in the intrinsic properties of brainstem medial vestibular nucleus (MVN) neurons during vestibular compensation. Ipsi-lesional, but not contra-lesional, flocculectomy prevented the compensatory increase in intrinsic excitability (CIE) that normally occurs in the de-afferented MVN neurons within 4 h after unilateral labyrinthectomy (UL). Flocculectomy did not, however, prevent the down-regulation of efficacy of GABA receptors that also occurs in these neurons after UL, indicating that these responses of the MVN neurons to deafferentation are discrete, parallel processes. CIE was also abolished by intra-floccular microinjection of the metabotropic glutamate receptor (mGluR) antagonist AIDA, and the protein kinase C inhibitor bisindolymaleimide I (BIS-I). The serene-threonine kinase inhibitor H-7 had no effect when microinjected at the time of de-afferentation, but abolished CIE if microinjected 2 h later. These cellular effects are in line with the retardatory effects of BIS-I and H-7 on behavioural recovery after UL reported by Balaban et al. (Brain Research 845, 97-101, 1999). They demonstrate that the development of CIE in MVN neurons during vestibular compensation requires mGluR activation and protein phosphorylation in cerebellar cortex. Furthermore, microinjection of the glucocorticoid receptor (GR) antagonist RU38486 into the ipsi-lesional flocculus also abolished CIE in MVN neurons. Thus an important site for glucocorticoids in facilitating vestibular compensation is within the cerebellar cortex. These observations ascribe functional significance to the high levels of GR and 11-ß-HSD Type 1 expression in cerebellum.
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