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The hippocampus has been implicated in temporal learning. Plasticity within the hippocampus requires NMDA receptor‐dependent glutamatergic neurotransmission. We tested the prediction that hippocampal NMDA receptors are required for learning about time by testing mice that lack postembryonal NMDARs in the CA1 and dentate gyrus (DG) hippocampal subfields on three different appetitive temporal learning procedures. The conditional knockout mice (Grin1ΔDCA1) showed normal sensitivity to cue duration, responding at a higher level to a short duration cue than compared to a long duration cue. Knockout mice also showed normal precision and accuracy of response timing in the peak procedure in which reinforcement occurred after 10 s delay within a 30 s cue presentation. Mice were tested on the matching of response rates to reinforcement rates on instrumental conditioning with two levers reinforced on a concurrent variable interval schedule. Pressing on one lever was reinforced at a higher rate than the other lever. Grin1ΔDGCA1 mice showed normal sensitivity to the relative reinforcement rates of the levers. In contrast to the lack of effect of hippocampal NMDAR deletion on measures of temporal sensitivity, Grin1ΔDGCA1 mice showed increased baseline measures of magazine activity and lever pressing. Furthermore, reversal learning was enhanced when the reward contingencies were switched in the lever pressing task, but this was true only for mice trained with a large difference between relative reinforcement rates between the levers. The results failed to demonstrate a role for NMDARs in excitatory CA1 and DG neurons in learning about temporal information. [ABSTRACT FROM AUTHOR]

Spatial properties of stimuli are sometimes encoded even when incidental to the demands of a particular learning task. Incidental encoding of spatial information may interfere with learning by (i) causing a failure to generalize learning between trials in which a cue is presented in different spatial locations and (ii) adding common spatial features to stimuli that predict different outcomes. Hippocampal lesions have been found to facilitate acquisition of certain tasks. This facilitation may occur because hippocampal lesions impair incidental encoding of spatial information that interferes with learning. To test this prediction mice with lesions of the hippocampus were trained on appetitive simple simultaneous discrimination tasks using inserts in the goal arms of a T-maze. It was found that hippocampal lesioned mice were facilitated at learning the discriminations, but they were sensitive to changes in spatial information in a manner that was similar to control mice. In a second experiment it was found that both control and hippocampal lesioned mice showed equivalent incidental encoding of egocentric spatial properties of the inserts, but both groups did not encode the allocentric information. These results demonstrate that mice show incidental encoding of egocentric spatial information that decreases the ability to solve simultaneous discrimination tasks. The normal egocentric spatial encoding in hippocampal lesioned mice contradicts theories of hippocampal function that suggest that the hippocampus is necessary for incidental learning per se, or is required for modulating stimulus representations based on the relevancy of information. The facilitated learning suggests that the hippocampal lesions can enhance learning of the same qualitative information as acquired by control mice. © 2011 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Spatial alternation, win-shift behavior has been claimed to be a test of working memory in rodents that requires active maintenance of relevant, trial-specific information. In this review, we describe work with GluA1 AMPA receptor subunit knockout mice that show impaired spatial alternation, but normal spatial reference memory. Due to their selective impairment on spatial alternation, GluA1 knockout mice provide a means by which the psychological processes underlying alternation can be examined. We now argue that the spatial alternation deficit in GluA1 knockout mice is due to an inability to show stimulus-specific, short-term habituation to recently experienced stimuli. Short-term habituation involves a temporary reduction in attention paid to recently presented stimuli, and is thus a distinct process from those that are involved in working memory in humans. We have recently demonstrated that GluA1 knockout mice show impaired short-term habituation, but, surprisingly, show enhanced long-term spatial habituation. Thus, GluA1 deletion reveals that there is competition between short-term and long-term processes in memory. © 2010 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]