. The brain cytoplasmic RNA BC1 regulates dopamine D2 receptor-mediated transmission in the striatum. J Neurosci. 2007 Aug 15;27(33):8885-92. PubMed.

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  1. The thrust of this paper is that the noncoding RNA BC1 is responsible for regulating D2-mediated synaptic transmission. Perhaps the greatest strength of the study is the robust neurophysiology and pharmacology with tight controls. That data set shows, using corticostriatal slice preparations, that the dopaminergic perturbation (hypersensitivity) is specific for the D2 receptor in BC1-knockout mice. This is especially important in light of the “anxiety” phenotype these mice express, and the probable role(s) of striatal dopamine in human psychiatric diseases. The authors then show that BC1 is apparently present in axons and in striatal GABAergic cells.

    A challenge for this work is that the actual mechanism by which BC1 works is as yet poorly understood. That BC1 may be present in axons has been shown previously; however, the significance of axonal BC1 remains obscure. The authors show that D2DR mRNA and protein levels are not dramatically decreased (protein appears increased) in the BC1 KO mice, and thus conclude that “D2DR-mediated transmission in this brain area is under the control of BC1 RNA, through a process likely to be mediated by a negative influence on D2DR insertion, turnover, and/or stability.”

    The subject matter is complex. It relates to the diverse fields of noncoding RNA, synaptic regulation, dopamine pharmacology and physiology, transgenic mice, cell biology, and translational regulation in neurons. Few investigators are expert in all of these fields, and I tip my cap to these authors for undertaking the challenge. In a general sense, they have added another piece to the amazing puzzle of noncoding RNA biology. More specifically, they demonstrate expertise and a possibly ideal model to tease out the complex mechanism of the brain-enriched noncoding RNA termed BC1.

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