Effect of XXXX and @entity2475 on central cholinergic mechanisms and active-avoidance acquisition.

@entity2475 @entity1617 @entity1877 @entity35 @entity11348 @entity4159 @entity934
@entity4159 at 100 and 300 mg/kg i.p. dose levels increased @entity934 ( @entity1617 ) utilization in the @entity35 cerebral cortex and hippocampus. @entity1617 utilization was assessed by measuring, with a gas chromatographic method, the decrease in @entity1617 level after inhibiting its synthesis by 15 micrograms intracerebroventricularly (i.c.v.) injection of @entity11348 (HC-3). @entity1617 steady state levels were not affected. @entity2475 (300 mg/kg i.p.) also increased @entity1617 utilization in the hippocampus. Repeated daily administration of @entity4159 100 mg/kg i.p. caused a 31% increase in high-affinity @entity1877 uptake (HACU) in the hippocampus. A single administration of 300 mg/kg i.p. of @entity4159 and @entity2475 also increased HACU rate in the hippocampus. However, the effect of @entity2475 was over within 3 h, while 3 h after its administration @entity4159 still caused a 40% increase in HACU rate. @entity4159 (100 mg/kg i.p.) significantly antagonized the impairment in the acquisition of an active-avoidance conditioned response (pole climbing) associated with the inhibition of @entity1617 synthesis by HC-3. These results indicate that @entity4159 enhances the activity of the septohippocampal cholinergic pathways, and to a lesser extent, of the cortical cholinergic network.
