TRANSSYNAPTIC CELL-DEATH OF NEURONS FOLLOWING STRIATOPALLIDAL LESIONSDOES NOT OCCUR IN SUBSTANTIA-NIGRA PARS RETICULATA IN DEVELOPING RATS

In adult rats, combined lesions of the striatum and globus pailidus (G P) cause transsynaptic cell death of neurons in the substantia nigra p ars reticulata (SNr) which becomes apparent 1-2 weeks after the lesion s. This delayed cell death of SNr neurons has been explained to be cau sed by over-excitation of SNr neurons which results from an imbalance between excitatory and inhibitory inputs due to two simultaneous event s: acceleration of the excitatory input from the disinhibited subthala mic nucleus (STN) and deprivation of the inhibitory input from the str iatum. To examine whether the transsynaptic neuronal death in SNr is c aused by the same lesions in developing rats, we destroyed the striatu m and GP in rats on postnatal days 10 (P10), P15, P20, P25, P30, P35 a nd P60 by injecting ibotenic acid. We found that cell death did not oc cur in SNr neurons in rats younger than P20 and that Fos expression in duced in STN neurons after these striatopallidal lesions in P10 and P2 0 rats was lower than that in P30 or P60 rats. These findings suggest that excitation of STN neurons is not enough to cause cell death of SN r neurons in rats younger than P20. Immature functional connection bet ween the cerebral cortex and STN in the early developing animals may c ontribute to the resistivity of SNr neurons to transsynaptic delayed c ell death. (C) 1998 Elsevier Science B.V.