Detailed behavioral analysis of water maze acquisition under APV or CNQX: Contribution of sensorimotor disturbances to drug-induced acquisition deficits.

Abstract

A detailed behavioral analysis of water-maze acquisition showed that the N-methyl-D-aspartate (NMDA) antagonist NPC17742 and the muscarinic antagonist scopolamine caused sensorimotor disturbances in behaviors required for maze performances and that these correlated with acquisition impairments in both hidden and visible platform versions of the maze in male rats. Behavioral disturbances included thigmotaxic swimming, swimming over and deflecting off the platform, abnormal swim behavior, and hyperactivity. Rats familiar with the behavioral strategies involved in the task performed normally under NPC17742 or scopolamine. The results indicated that drug-induced sensorimotor disturbances contributed to poor acquisition scores in naive rats. NMDA or muscarinic activity may contribute to but do not appear to be essential for spatial learning in the water maze.

A Behavioral Analysis of the Spatial Learning Deficit Induced by the NMDA Receptor Antagonist MK-801 (Dizocilpine) in the Rat

“…The results show that the effects of systemically administered MK-801 on spatial learning in the water maze task cannot be dissociated from motor and/or sensory disturbances. This supports the view that NMDA receptors probably contribute to, but seem not to be crucial for, spatial learning (Cain 1998;Cain et al 1996;Saucier et al 1996).…”

The effect of nonspatial water maze pretraining in rats subjected to serotonin depletion and muscarinic receptor antagonism: a detailed behavioural assessment of spatial performance

“…Thus, this behaviour would have severely lirnited the opportunity of the 'laive SC0 rats to spontaneously encounter the platform. which likely interfered with subsequent rnaze acquisition [6,25]. The Naive S C 0 group also had a greater number of platform contacts that were deflections and swimovers.…”

“…and combined muscarinic and serotonergic antagonism. The combination of a detailed behavioural analysis and NSP was chosen because it has proven useful in clarifying the role of some neurorransrnitter receptor populations in the field of learning and memory [1,4,6,28,29].…”

Hippocampal synaptic plasticity, spatial memory and anxiety

“…However, given the i.c.v. route of drug administration, there followed considerable debate, (i) as to the brain locus of these effects (hippocampal (CA and DG subfields) vs. extrahippocampal), and (ii) whether the watermaze deficit in these animals reflected a learning impairment or a non-specific disruption of sensorimotor or motivational aspects of task performance 27,30,31 . Furthermore, subsequent pharmacological experiments showed that AP5-treated rats could in fact solve the SRM watermaze task, if they had received watermaze pretraining in a different spatial environment prior to testing with the drug (the spatial upstairs/downstairs task) 32,38 .…”

“…In particular, the idea that LTP (or an LTP-like mechanism) in the hippocampus supports associative spatial memory formation (i.e. associating particular spatial locations within a cognitive map with particular events or outcomes or stimuli) has been widely accepted 26 , and has only rarely been questioned [27][28][29][30][31][32] . However, recent evidence from a novel genetically modified mouse line challenges the relationship between hippocampal LTP and long-term, associative spatial memory formation 33 .…”