Source Paper
Synaptic plasticity and learning: selective impairment of learning rats and blockade of long-term potentiation in vivo by the N-methyl-D- aspartate receptor antagonist AP5
Journal of Neuroscience • 1989
View Abstract
This paper reports a series of 5 experiments concerned with a possible role for N-methyl-D-aspartate (NMDA) receptors in certain types of learning. The results show that chronic intraventricular infusion of the NMDA receptor antagonist D,L-2-amino-5-phosphonopentanoic acid (D,L- AP5) caused an impairment of spatial but not of visual discrimination learning in rats. Such selectivity of the learning impairment occurred despite widespread distribution of the drug throughout the CNS. AP5 sometimes caused a disturbance of sensorimotor function during learning, but one experiment addressing whether this disturbance could be responsible for the spatial learning impairment established that it was statistically independent. Another experiment showed that AP5 did not affect the retention of previously acquired spatial information. These behavioral effects were all obtained with a concentration of AP5 that, in a final study, was found to be sufficient to block hippocampal long-term potentiation (LTP) in vivo without affecting normal synaptic transmission. Taken together, these observations (1) implicate NMDA receptors in certain types of learning, and (2) extend recent work showing that saturation of LTP causes an anterograde spatial amnesia (McNaughton et al., 1986). A preliminary report of parts of this work has been published (Morris et al., 1986a).
Sensorimotor Function Assessment
Objective: Evaluation of sensorimotor disturbances caused by AP5 to determine independence from spatial learning impairment
This is a Sensorimotor Function Assessment protocol using rat as the model organism. The procedure involves 3 procedural steps, 1 materials. Extracted from a 1989 paper published in Journal of Neuroscience.
Model and subjects
rat
Study window
Estimated timing pending
Core workflow
Chronic intraventricular infusion of AP5 • Assess sensorimotor function during learning • Determine statistical independence of sensorimotor disturbance from spatial learning impairment
Primary readouts
- Presence and severity of sensorimotor disturbances
- Statistical independence of sensorimotor effects from spatial learning impairment
Key equipment and reagents
Verified items
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Direct vendor links
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Protocol Steps
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Chronic intraventricular infusion of AP5
Administer D,L-AP5 chronically via intraventricular infusion to rats
Note: Drug concentration was sufficient to block hippocampal long-term potentiation in vivo without affecting normal synaptic transmission
View evidence from paper
“chronic intraventricular infusion of the NMDA receptor antagonist D,L-2-amino-5-phosphonopentanoic acid (D,L-AP5)”
Assess sensorimotor function during learning
Evaluate sensorimotor disturbances in rats receiving AP5 during learning tasks
Note: AP5 sometimes caused a disturbance of sensorimotor function during learning
View evidence from paper
“AP5 sometimes caused a disturbance of sensorimotor function during learning”
Determine statistical independence of sensorimotor disturbance from spatial learning impairment
Conduct experiment to establish whether sensorimotor disturbance could be responsible for the spatial learning impairment
Note: One experiment addressing whether this disturbance could be responsible for the spatial learning impairment established that it was statistically independent
View evidence from paper
“one experiment addressing whether this disturbance could be responsible for the spatial learning impairment established that it was statistically independent”