The different effects of over-expressing murine NMDA receptor 2B subunit in the forebrain on conditioned taste aversion.
The glutamate transmission system and the N-methyl-D-aspartate receptor (NMDA-R), in particular its 2B subunit (NR2B), have been reported to be possibly related to taste memory as a result of treatment with NMDA antagonists and agonists. In order to further study the role of the NR2B subunit in gustation memory, we applied four different taste aversive tasks to observe the behavior of a transgenic mice model in which the NR2B subunit was specifically over-expressed in the forebrain. We found that in both short- and long-term conditioned taste aversion (CTA) experiments, mice with forebrain expression of the NR2B transgene (Tg) showed significantly enhanced CTA 2 days after training. However, both the Tg and the wild-type (Wt) mice shared the same level of aversive memory on the 30th day after training. In both fast and slow extinction experiments, Tg mice maintained a higher CTA memory than that of control mice in most extinction trials. The third experiment, which involved testing the memory for familiar taste, demonstrated that NR2B augmentation had no benefit on the latent inhibition (LI) of CTA. In addition, the last experiment (two-taste LI) showed a suppression of enhanced CTA in Tg mice when the mice were exposed to both novel and familiar tastes. These data suggested that forebrain NR2B over-expression had different effects on gustatory learning and memory. The transgenic animals were only sensitive to novel but not familiar tastes, and up-regulation of NR2B resulted in enhanced CTA function for only a short period of time.
Li
Shijia
S
Shanghai Children's Medical Center, Shanghai Key Laboratory of Children's Environmental Health, Shanghai Jiaotong University, School of Medicine, Shanghai 200127, China; Shanghai Institute of Brain Functional Genomics, and Key Laboratory of Brain Functional Genomics, MOE & STCSM, East China Normal University, Shanghai 200062, China.
Gu
Yiran
Y
Shanghai Institute of Brain Functional Genomics, and Key Laboratory of Brain Functional Genomics, MOE & STCSM, East China Normal University, Shanghai 200062, China.
Meng
Bo
B
Shanghai Institute of Brain Functional Genomics, and Key Laboratory of Brain Functional Genomics, MOE & STCSM, East China Normal University, Shanghai 200062, China.
Mei
Bing
B
Shanghai Institute of Brain Functional Genomics, and Key Laboratory of Brain Functional Genomics, MOE & STCSM, East China Normal University, Shanghai 200062, China. Electronic address: bmei@brain.ecnu.edu.cn.
Li
Fei
F
Shanghai Children's Medical Center, Shanghai Key Laboratory of Children's Environmental Health, Shanghai Jiaotong University, School of Medicine, Shanghai 200127, China. Electronic address: lifei5861_cn@yahoo.com.cn.
D000818:Animals; D001362:Avoidance Learning / Q000502:physiology*; D003214:Conditioning, Classical / Q000502:physiology*; D005108:Extinction, Psychological / Q000502:physiology; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D008822:Mice, Transgenic; D016548:Prosencephalon / Q000378:metabolism*; D021122:Protein Subunits / Q000096:biosynthesis* / Q000235:genetics; D016194:Receptors, N-Methyl-D-Aspartate / Q000096:biosynthesis* / Q000235:genetics; D013649:Taste / Q000235:genetics*
C121001:NR2B NMDA receptor; D021122:Protein Subunits; D016194:Receptors, N-Methyl-D-Aspartate