The fragile X mental retardation protein (FMRP) is a selective RNA-binding protein whose function is implicated in regulating protein synthesis of its mRNA targets. The lack of FMRP leads to abnormal synapse development in the brain and impaired learning/memory. Although FMRP is predominantly expressed in neurons of the adult brain, whether FMRP also functions in glia during early development remains elusive, since expression of FMRP in glia has not been rigorously examined. This is an important question because recent studies revealed important roles of glia in synaptic development. Here we report that in addition to the observed neuronal expression, FMRP expression is detected in oligodendroglia progenitor cells (OPCs), immature oligodendrocytes and oligodendroglia cell lines, where it interacts with a subgroup of oligodendrocyte-specific mRNAs, including the myelin basic protein (MBP) mRNA. FMRP expression gradually declines as oligodendrocytes differentiate in vitro and in the developing brain. The decline of FMRP expression during oligodendrocyte differentiation is associated with a vigorous up-regulation of the MBP protein. In addition, we show that the MBP 3'untranslated region (3'UTR) is necessary and sufficient for binding FMRP, and mediates translation inhibition of a reporter gene by FMRP specifically in oligodendrocytes. These results support the hypothesis that FMRP may participate in regulating translation of its bound mRNAs in oligodendroglia during early brain development.

There is underreporting of postoperative lumbar plexus nerve injury and a lack of standardization of clinical findings of neural complications related to the minimally invasive lateral retroperitoneal transpsoas approach. The authors provide a diagnostic paradigm that allows for an efficient and accurate classification of postoperative lumbar plexopathies and nerve injuries.

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The object of this study was to evaluate a novel surgical technique in the treatment of adult degenerative scoliosis and present our early experience with the minimally invasive lateral approach for anterior longitudinal ligament release to provide lumbar lordosis and examine its impact on sagittal balance. Methods. All patients with adult spinal deformity (ASD) treated with the minimally invasive lateral retroperitoneal transpsoas interbody fusion (MIS LIF) for release of the anterior longitudinal ligament were examined. Patient demographics, clinical data, spinopelvic parameters, and outcome measures were recorded. Results. Seven patients underwent release of the anterior longitudinal ligament (ALR) to improve sagittal imbalance. All cases were split into anterior and posterior stages, with mean estimated blood loss of 125 cc and 530 cc, respectively. Average hospital stay was 8.3 days, and mean follow-up time was 9.1 months. Comparing pre- and postoperative 36′′ standing X-rays, the authors discovered a mean increase in global lumbar lordosis of 24 degrees, increase in segmental lumbar lordosis of 17 degrees per level of ALL released, decrease in pelvic tilt of 7 degrees, and decrease in sagittal vertical axis of 4.9 cm. At the last followup, there was a mean improvement in VAS and ODI scores of 26.2% and 18.3%. Conclusions. In the authors' early experience, release of the anterior longitudinal ligament using the minimally invasive lateral retroperitoneal transpsoas approach may be a feasible alternative in correcting sagittal deformity.

The genetic lesion in the quakingviable (qk(v)) mutant mice is a deletion 5' to the qkI gene, resulting in severe hypomyelination. qkI produces several QKI protein isoforms via alternative splicing of the C-terminal coding exons. In the qk(v)/qk(v) brain, immunostaining of QKI proteins is diminished in an isoform-differential manner with undefined mechanisms. We examined the expression of QKI protein isoforms and qkI mRNA isoforms in the qk(v)/qk(v) mutants and the non-phenotypic wt/qk(v) littermates. Our results indicated significant reduction of all qkI mRNA isoforms in the central and peripheral nervous system during active myelination without detectable post-transcriptional abnormalities. In the early stage of myelin development, qkI mRNAs are differentially reduced, which appeared to be responsible for the reduction of the corresponding QKI protein isoforms. The reduced qkI expression was a specific consequence of the qk(v) lesion, not observed in other hypomyelination mutants. Further more, no abnormal qkI expression was found in testis, heart and astroglia of the qk(v)/qk(v) mice, suggesting that the reduction of qkI mRNAs occurred specifically in myelin-producing cells of the nervous system. These observations suggest that diminished qkI expression results from deletion of an enhancer that promotes qkI transcription specifically in myelinating glia during active myelinogenesis.