N-methyl-D-aspartate receptor 2B subunit (GRIN2B) gene variation is associated with alerting, but not with orienting and conflicting in the Attention Network Test

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Abstract

Appropriate attention levels are pivotal for cognitive processes, and individual differences in attentional functioning are related to variations in the interplay of neurotransmitters. The attention network theory reflects attention as a non-homogenous set of separate neural networks: alerting, orienting and conflicting. In the present study, the role of variations in GRIN2B, which encodes the NR2B subunit of N-methyl-d-aspartate (NMDA) receptors, was explored with regard to the regulation of arousal and attention by comparing the efficiency of the three attentional networks as measured with the Attention Network Test (ANT). Two synonymous SNPs in GRIN2B, rs1806201 (T888T) and rs1806191 (H1178H) were genotyped in 324 young Caucasian adults. Results revealed a highly specific modulatory influence of SNP rs1806201 on alerting processes with subjects homozygous for the frequent C allele displaying higher alerting network scores as compared to the other two genotype groups (CT and TT). This effect is due to the fact that in the no cue condition faster reaction times were evident in participants carrying at least one of the rare T alleles, possibly as a result of more effective glutamatergic neurotransmission. The results might be further explained by a dissociation between tonic and phasic alertness modulated by the GRIN2B genotype and by a ceiling effect, meaning that subjects cannot be phasicly alert in excess to a certain level. Altogether, the results show that variations in GRIN2B have to be taken into consideration when examining attentional processes. © 2012 Elsevier Ltd. All rights reserved.

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Schulz, S., Arning, L., Pinnow, M., Epplen, J. T., & Beste, C. (2012). N-methyl-D-aspartate receptor 2B subunit (GRIN2B) gene variation is associated with alerting, but not with orienting and conflicting in the Attention Network Test. Neuropharmacology, 63(2), 259–265. https://doi.org/10.1016/j.neuropharm.2012.02.024

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