Pretraining or previous non-spatial experience improves spatial learning in the Morris water maze of nucleus basalis lesioned rats.
Previous experiments have shown that infusions of ibotenic acid in the nucleus basalis magnocellularis (NBM) induce a strong impairment in spatial navigation for a hidden platform in the Morris water maze. This effect was initially attributed to a cholinergic deficit, but later studies showed that performance level did not correlate with the degree of cholinergic denervation. Therefore, this impairment is due to a combined cholinergic and non-cholinergic deficit. However, it is not clear in which particular processes the NBM is involved. In this study we have evaluated the origin of behavioural impairment in spatial navigation in the water maze after an ibotenic acid-induced lesion of NBM. In the first experiment, Wistar rats were trained preoperatively in an allocentric navigation task. Postoperatively, they were tested in the same task. All lesioned animals showed a performance level similar to controls. Lesions did not impede the acquisition of new positions in the water maze, nor did affect the ability of animals to remember new platform positions after an intertrial interval of 20s, even if animals had received only allocentric experience with the platform position, or allocentric and path integration information concurrently. Lesions also failed to affect the ability to locate a hidden platform in a new environment. However, hippocampal infusions of scopolamine (5 microg) produced a severe impairment in NBM-damaged animals, without impairing performance of controls. In the second experiment Wistar rats with the same lesion were first trained in a visual-guided task in the water maze, and subsequently evaluated in the spatial task. In both tasks lesioned animals were not different from controls. These results suggest that the NBM played an important role during acquisition phases but not in the execution of spatial navigation. Moreover, the excessive emotional response displayed by lesioned animals is postulated as a relevant cause for the impairment observed in spatial navigation after NBM damage.
Nieto-Escámez
Francisco A
FA
Departamento de Neurociencia y Ciencias de la Salud, Universidad de Almería, Ctra Sacramento s/n 04120, Almería, Spain.
Sánchez-Santed
Fernando
F
de Bruin
Jan P C
JP
D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects / Q000502:physiology; D020532:Basal Nucleus of Meynert / Q000187:drug effects / Q000473:pathology*; D003463:Cues; D004193:Discrimination Learning / Q000187:drug effects / Q000502:physiology; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology; D007051:Ibotenic Acid / Q000633:toxicity; D008297:Male; D018782:Maze Learning / Q000502:physiology*; D018727:Muscarinic Antagonists / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D012193:Reversal Learning / Q000187:drug effects / Q000502:physiology; D012601:Scopolamine / Q000494:pharmacology; D013037:Spatial Behavior / Q000502:physiology*
D018690:Excitatory Amino Acid Agonists; D018727:Muscarinic Antagonists; D007051:Ibotenic Acid; D012601:Scopolamine