Abstract
The brain cytoplasmic (BC1) RNA is a non-coding RNA (ncRNA) involved in neuronal translational control. Absence of BC1 is associated with altered glutamatergic transmission and maladaptive behavior. Here, we show that pyramidal neurons in the barrel cortex of BC1 knock out (KO) mice display larger excitatory postsynaptic currents and increased spontaneous activity in vivo. Furthermore, BC1 KO mice have enlarged spine heads and postsynaptic densities and increased synaptic levels of glutamate receptors and PSD-95. Of note, BC1 KO mice show aberrant structural plasticity in response to whisker deprivation, impaired texture novel object recognition and altered social behavior. Thus, our study highlights a role for BC1 RNA in experience-dependent plasticity and learning in the mammalian adult neocortex, and provides insight into the function of brain ncRNAs regulating synaptic transmission, plasticity and behavior, with potential relevance in the context of intellectual disabilities and psychiatric disorders.
Highlights
The brain cytoplasmic (BC1) RNA is a non-coding RNA involved in neuronal translational control
Given the presence of BC1 RNA in several messenger ribonucleoprotein particles (RNPs) involved in synaptic development and function, the lack of BC1 could have a detrimental impact on dendrite elaboration and spine formation
Because αCaMKII has been implicated in glutamate receptors (GluRs) synaptic delivery and it is an FMRP target regulated by BC1 RNA in intact synapses[11, 17], we examined αCaMKII levels in postsynaptic membrane preparations from wild type (WT) and BC1 knock out (KO) mice
Summary
The brain cytoplasmic (BC1) RNA is a non-coding RNA (ncRNA) involved in neuronal translational control. Our study highlights a role for BC1 RNA in experience-dependent plasticity and learning in the mammalian adult neocortex, and provides insight into the function of brain ncRNAs regulating synaptic transmission, plasticity and behavior, with potential relevance in the context of intellectual disabilities and psychiatric disorders. O complex represses translation of a defined subset of FMRP target mRNAs11, 17 and helps recruit additional factors such as cytoplasmic FMRP interacting protein 1 (CYFIP1), which are responsible for translation inhibition[16] This function is of particular relevance at synapses[11], where a fine-tuned regulation of local protein synthesis is crucial for spine structure and function[18]. The understanding of how these ncRNAs regulate brain function and behavior is still very limited
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