In:
The Journal of Neuroscience, Society for Neuroscience, Vol. 27, No. 33 ( 2007-08-15), p. 8885-8892
Abstract:
Dopamine D 2 receptor (D 2 DR)-mediated transmission in the striatum is remarkably flexible, and changes in its efficacy have been heavily implicated in a variety of physiological and pathological conditions. Although receptor-associated proteins are clearly involved in specific forms of synaptic plasticity, the molecular mechanisms regulating the sensitivity of D 2 receptors in this brain area are essentially obscure. We have studied the physiological responses of the D 2 DR stimulations in mice lacking the brain cytoplasmic RNA BC1, a small noncoding dendritically localized RNA that is supposed to play a role in mRNA translation. We show that the efficiency of D 2 -mediated transmission regulating striatal GABA synapses is under the control of BC1 RNA, through a negative influence on D 2 receptor protein level affecting the functional pool of receptors. Ablation of the BC1 gene did not result in widespread dysregulation of synaptic transmission, because the sensitivity of cannabinoid CB 1 receptors was intact in the striatum of BC1 knock-out (KO) mice despite D 2 and CB 1 receptors mediated similar electrophysiological actions. Interestingly, the fragile X mental retardation protein FMRP, one of the multiple BC1 partners, is not involved in the BC1 effects on the D 2 -mediated transmission. Because D 2 DR mRNA is apparently equally translated in the BC1-KO and wild-type mice, whereas the protein level is higher in BC1-KO mice, we suggest that BC1 RNA controls D 2 DR indirectly, probably regulating translation of molecules involved in D 2 DR turnover and/or stability.
Type of Medium:
Online Resource
ISSN:
0270-6474
,
1529-2401
DOI:
10.1523/JNEUROSCI.0548-07.2007
Language:
English
Publisher:
Society for Neuroscience
Publication Date:
2007
detail.hit.zdb_id:
1475274-8
SSG:
12
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