C. Dewaele et al., DISTRIBUTION OF GLUTAMATERGIC RECEPTORS AND GAD MESSENGER-RNA-CONTAINING NEURONS IN THE VESTIBULAR NUCLEI OF NORMAL AND HEMILABYRINTHECTOMIZED RATS, European journal of neuroscience, 6(4), 1994, pp. 565-576
Vestibular compensation is an attractive model for investigations of c
ellular mechanisms underlying post-lesional plasticity in the adult ce
ntral nervous system. Immediately after hemilabyrinthectomy, the spont
aneous activity in the deafferented second-order vestibular neurons fa
lls to zero, resulting in a strong asymmetry between the resting disch
arge of the vestibular complexes on the lesioned and intact sides. Thi
s asymmetry most probably causes the static and dynamic vestibular def
icits observed in the acute stage. After similar to 50 h, the deaffere
nted vestibular neurons recover a quasi-normal resting activity which
is thought to be the key of the compensation of the static vestibular
syndromes. However, the molecular mechanisms underlying this recovery
are unknown. In this study, we investigate possible changes in the dis
tribution of glutamatergic N-methyl-D-aspartate (NMDA) and glutamate m
etabotropic receptors and of glutamate decarboxylase 67k (GAD 67k) mRN
As in the deafferented vestibular neurons induced by the labyrinthine
lesion. Specific radio-active oligonucleotides were used to probe sect
ions of rat vestibular nuclei according to in situ hybridization metho
ds. Animals were killed at different times (5 h, 3 days and 3 weeks) f
ollowing the lesion. Signal was detected by means of film or emulsion
autoradiography. In the normal animals, several brainstem regions incl
uding the medial, lateral, inferior and superior vestibular nuclei wer
e densely labelled by the antisense oligonucleotide NMDAR1 probe. Howe
ver, the vestibular nuclei were not labelled by the glutamate metabotr
opic oligonucleotide antisense probe (mGluR 1). The GAD 67k antisense
oligonucleotide probe labelled numerous small- to medium-sized central
vestibular neurons but not the larger cell bodies in the lateral vest
ibular nucleus. This agrees with previous studies. In the hemilabyrint
hectomized rats, no asymmetry could be detected, at either the autorad
iographic or cellular levels, between the two medial vestibular nuclei
whatever the probe used and whatever the delay following the lesion.
However, for the NMDAR1 probe, the mean density of silver grains in bo
th the deafferented and intact medial vestibular neurons was 20% lower
5 h after the lesion. Three days and 3 weeks later, the intensity of
labelling over all cells was the same as in the control group. Further
studies are necessary to confirm the relatively weak modification of
the NMDAR1 mRNAs expression and to exclude a change of GAD 65 and of o
ther NMDA subunit mRNAs during the vestibular compensation process.