• D K Hannesson and R W Skelton.
• Department of Psychology, University of Victoria, BC, Canada.
• Behav. Brain Res. 1998 Jan 1; 90 (1): 35-56.

AbstractThe present study investigated whether spatial performance in the Morris water maze (MWM) recovers after bilateral transection of the fimbria/fornix (FF) in rats, whether such recovery results from restored or residual spatial cognitive capacity, and what contribution, if any, pre-operative training makes to such recovery. Following surgery, rats were administered extensive training to a constant submerged platform location with frequent probe tests to assess performance strategies. Following the attainment of asymptotic performance levels, rats were tested for acquisition of a second platform location. FF lesions were found to produce a severe impairment both in pre-operatively trained rats (a retention or retrieval deficit) and in naive rats (an acquisition deficit) as shown by the use of indirect routes to the platform on submerged platform trials and an absence of localized searching in the platform's area on probe trials. However, with further training, performance recovered in both groups, such that they eventually used direct escape routes to the submerged platform and showed highly localized searching in its area on probe trials. When tested for acquisition of a second platform location, a substantial deficit reappeared, but was again overcome with additional training. Pre-operative training was found to attenuate the initial post-operative deficit and speed recovery of performance but did not affect asymptotic performance levels nor acquisition of the second platform location. These data show that, though spatial cognition as assessed in the MWM is impaired by FF lesions, spatial performance eventually recovers. Moreover, pre-operative training, though of some initial post-operative benefit, is not essential for this recovery. The deficit shown in acquisition of the second platform location argues against recovery of spatial cognition and suggests that the basis of recovered performance is residual spatial cognitive capacity. Several limitations of this residual capacity are apparent: (i) rate of acquisition of spatial information is reduced; (ii) utilization of spatial information stored pre-operatively is restricted; and (iii) translation of spatial information into navigational behaviour is less efficient. The neural bases of this residual system are speculated to include spared intra-hippocampal storage mechanisms and/or mechanisms involved in extra-hippocampal long-term memory consolidation while the neural bases of the FF's contribution to spatial information storage in the intact brain are speculated to involve theta synchronization of hippocampal activity and the induction and expression of hippocampal long-term potentiation.

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