S. Consolo et al., Increased striatal expression of glutamate decarboxylase 67 after priming of 6-hydroxydopamine-lesioned rats, NEUROSCIENC, 89(4), 1999, pp. 1183-1187
Previous single exposure (priming) to a dopamine receptor agonist greatly e
nhances the contralateral turning behaviour elicited by dopamine D-1 recept
or agonists in unilaterally 6-hydroxydopamine lesioned rats. In the present
study we have investigated the levels of glutamate decarboxylase 67 and gl
utamate decarboxylase 65 messenger RNA in the striatum of 6-hydroxydopamine
-lesioned rats primed with L-3,4-dihydroxyphenylalanine (L-DOPA) and challe
nged with the D-1 receptor agonist SKF 38393, three days thereafter. As pre
viously reported, levels of glutamate decarboxylase 67 messenger RNA increa
sed in the striatum denervated by the 6-hydroxydopamine lesion as compared
with the intact one. Striatal glutamate decarboxylase 67 messenger RNA leve
ls, measured three days after priming with L-DOPA (50 mg/kg), further incre
ased in the lesioned striatum while were not modified in the intact one. Ad
ministration of SKF 38393 (3 mg/kg) elicited a more intense contralateral t
urning behaviour in primed than in drug-naive 6-hydroxydopamine-lesioned ra
ts but did not induce any change in striatal glutamate decarboxylase 67 mes
senger RNA. In contrast, striatal levels of glutamate decarboxylase 65 mess
enger RNA were not modified by either 6-hydroxydopamine lesions or priming
with L-DOPA.
The results show that priming with L-DOPA induces long-lasting changes in G
ABAergic neurons of the 6-hydroxydopamine-lesioned striatum. These changes
might play a role in the increased behavioural response of striatal D-1 rec
eptors induced by priming. (C) 1999 IBRO. Published by Elsevier Science Ltd
.