Sachdev R N, Gilman S, Aldridge J W
Department of Neurology, University of Michigan, Ann Arbor 48104.
Brain Res. 1989 Nov 6;501(2):295-306. doi: 10.1016/0006-8993(89)90646-x.
Striatal projections to the globus pallidus and entopeduncular nucleus are thought to be GABAergic and inhibitory. Thus, striatal lesions might be expected to increase the spontaneous discharge rate of neurons in these nuclei. To test this prediction, we recorded spontaneous single unit activity from awake cats sitting quietly before and 7-160 days after striatal lesions. Striatal lesions were produced by injecting ibotenic acid into the caudate nucleus and putamen. Median, standard deviation, mean, and coefficient of variation of the interspike intervals were calculated for each unit. In globus pallidus the striatal lesion resulted in a significant decrease in median interval length, i.e. an increase in the discharge rate. The prelesion median of 36 ms (S.E.M. = 2.3) decreased 11% to a postlesion value of 32 ms (S.E.M. = 2.1). The lesion also resulted in a significant decrease in the variability of interspike intervals. The coefficient of variation, 1.31 (S.E.M. = 0.08) before the lesion, decreased 25% to 0.97 (S.E.M. = 0.06) after the lesion. In entopeduncular nucleus, the lesion had no statistically significant effect on the rate of activity, but a significant decrease in the variability of activity occurred. The median interval was 33 ms (S.E.M. = 3.3) before the lesion and decreased 2% to 32 ms (S.E.M. = 2.4). The coefficient of variation decreased 48% from 1.44 (S.E.M. = 0.1) to 0.73 (S.E.M. = 0.03). These observations support the hypothesis that loss of GABAergic inputs to the globus pallidus results in disinhibition. The discharge rate in entopeduncular nucleus was not affected by the striatal lesion, suggesting that striatal substance P or subthalamic excitatory inputs may have a role in regulating discharge rate in the entopeduncular nucleus.
