LOSS OF CHOLINERGIC NEURONS IN THE NUCLEUS BASALIS INDUCES NEOCORTICAL ELECTROENCEPHALOGRAPHIC AND PASSIVE-AVOIDANCE DEFICITS

被引：51

作者：

RIEKKINEN, P ^{[1
]}

RIEKKINEN, M ^{[1
]}

SIRVIO, J ^{[1
]}

MIETTINEN, R ^{[1
]}

RIEKKINEN, P ^{[1
]}

机构：

[1] UNIV KUOPIO, DEPT PATHOL, SF-70211 KUOPIO, FINLAND

来源：

NEUROSCIENCE | 1992年 / 47卷 / 04期

关键词：

D O I：

10.1016/0306-4522(92)90032-W

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The present experiments were designed to examine the hypothesis that the degeneration of cholinergic nucleus basalis is related to the cognitive and neurophysiological deficits found in old age. Aged (26 months) rats were impaired both in the acquisition of spatial (water-maze) task and retention of passive avoidance task. During aging, neocortical electroencephalographic fast activity was decreased and high-voltage spindles increased. Loss of choline acetyltransferase-positive neurons correlated with the high-voltage spindle incidence and passive avoidance retention deficit. Unilateral ibotenate nucleus basalis lesioning decreased choline acetyltransferase activity in the cortex and produced a large nonspecific subcortical cell loss in young rats. Ibotenate-lesioned rats were impaired in spatial learning and passive avoidance retention in young rats. Quisqualic acid produced a greater decrease in cortical choline acetyltransferase activity and smaller nonspecific subcortical cell loss than ibotenate lesioning. Spatial learning was not impaired, but passive avoidance performance was disrupted. Slow waves and high-voltage spindles were increased and beta activity decreased on the side of either quisqualate or ibotenate nucleus basalis lesioning. These results demonstrate that age-related neurophysiological and cognitive deficits result partially from the loss of cholinergic neurons in the nucleus basalis and that quisqualic acid nucleus basalis-lesioning in young rats may be used as a pharmacological model of the age-related cholinergic neuron loss.

引用

页码：823 / 831

页数：9

共 38 条

[21] LEARNING AND MEMORY DEFICITS AFTER LESIONS OF THE NUCLEUS BASALIS MAGNOCELLULARIS - REVERSAL BY PHYSOSTIGMINE [J].