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The glycine transporter (GlyT1) regulates levels of the neurotransmitter glycine, a coagonist of the
N
-methyl-
d
-aspartate receptor (NMDAR), and as such may represent a novel site for developing cognition-enhancing drugs. Genetically modified mice with reduced levels of GlyT1 have been generated to test this hypothesis.
P. Singer, D. Boison, H. Möhler, J. Feldon, and B. K. Yee (2007)
now show, through a spontaneous exploration task, that mice in which GlyT1 has been deleted, specifically in neurons in the forebrain, demonstrate enhanced object recognition memory. Whereas both control and mutant mice show a preference for a novel object over a familiar object 2 min after the initial presentation of 1 of the objects, only the mutant mice show a preference for the novel object when tested after a 2-hr delay. The longer-lasting habituation displayed by the GlyT1 mice is consistent with a role for glycine/NMDAR-dependent synaptic plasticity in supporting a nonassociative, short-term memory trace of a recently experienced stimulus. This short-term habituation process may be independent of associative learning mechanisms and may be best described by
A. R. Wagner's (1981)
sometimes opponent process model.