The effect of a single injection of 3-acetylpyridine (3-AP), which led to a degeneration of the excitatory cerebellar climbing fibers, was studied on the binding of [3H]MK-801, a non-competitive NMDA antagonist, in the rat cerebellar cortex. The same treatment increased also the binding of [3H]CGP 39653, a new NMDA competitive antagonist. Saturation isotherms showed a significant increase of the maximal number of binding sites (Bmax) for [3H]CGP 39653 and [3H]MK-801 (+48 and 36% respectively) with no change in the affinity 4-9 days after the administration of 3-AP. Our data demonstrate that in the cerebellar cortex both NMDA recognition site labelled by [3H]CGP 39653 and its modulatory site labelled by [3H]MK-801 may undergo plastic changes when the glutamatergic receptors and transmission are denervated.
The degeneration of the excitatory climbing fibers enhances [3H]MK-801 and [3H]CGP 39653 binding sites in the rat cerebellar cortex.
SERRA, MARIANGELA;
1992-01-01
Abstract
The effect of a single injection of 3-acetylpyridine (3-AP), which led to a degeneration of the excitatory cerebellar climbing fibers, was studied on the binding of [3H]MK-801, a non-competitive NMDA antagonist, in the rat cerebellar cortex. The same treatment increased also the binding of [3H]CGP 39653, a new NMDA competitive antagonist. Saturation isotherms showed a significant increase of the maximal number of binding sites (Bmax) for [3H]CGP 39653 and [3H]MK-801 (+48 and 36% respectively) with no change in the affinity 4-9 days after the administration of 3-AP. Our data demonstrate that in the cerebellar cortex both NMDA recognition site labelled by [3H]CGP 39653 and its modulatory site labelled by [3H]MK-801 may undergo plastic changes when the glutamatergic receptors and transmission are denervated.
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