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. 2014 Aug 13;34(33):11007–11015. doi: 10.1523/JNEUROSCI.0956-14.2014

Figure 1.

Figure 1.

Incidental taste learning, attenuation of taste neophobia, and long-term safe taste memory formation do not require hippocampal plasticity. A, Subregion-specific NMDA receptor subunit NR1 deletion (indicated by arrow) revealed by in situ hybridization. DAPI (left) and NR1 (right) probe labeling of hippocampi of control, CA1-, CA3-, and DG-NR1 KO mice. B, CA1-, CA3-, and DG-NR1 KOs showed clear deletion of NR1 gene restricted to the appropriate layer of the hippocampus. C, Outline of the behavioral procedure. Following habituation to drink from pipettes for 20 min per day for 2 d, the mice were tested for taste recognition and neophobia (Test 1), attenuation of taste neophobia (Tests 1, 2, and 3) and long-term memory for the familiarized taste. D, CA1-, CA3-, and DG-NR1 KOs demonstrated normal unpalatable bitter (quinine) taste recognition. E, Separate cohorts of CA1-, CA3-, and DG-NR1 KO mice also showed a normal neophobia to palatable novel sweet (saccharin) taste. F, G, CA1-, CA3-, and DG-NR1KOs also exhibited normal attenuation of taste neophobia (saccharin; F) and long-term taste memory storage (saccharin; G).