Browsing by Subject "spine"
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(2019)Classical and rapid-acting antidepressant drugs have been shown to reinstate juvenile-like plasticity in the adult brain, allowing mature neuronal networks to rewire in an environmentally-driven/activity-dependent process. Indeed, antidepressant drugs gradually increase expression of brain-derived neurotrophic factor (BDNF) and can rapidly activate signaling of its high-affinity receptor TRKB. However, the exact mechanism of action underlying drug-induced restoration of juvenile-like plasticity remains poorly understood. In this study we first characterized acute effects of classical and rapid-acting antidepressant drugs on the interaction between TRKB and postsynaptic density (PSD) proteins PSD-93 and PSD-95 in vitro. PSD proteins constitute the core of synaptic complexes by anchoring receptors, ion channels, adhesion proteins and various signaling molecules, and are also involved in protein transport and cell surface localization. PSD proteins have in common their role as key regulators of synaptic structure and function, although PSD-93 and PSD-95 are associated with different functions during development and have opposing effects on the state of plasticity in individual synapses and neurons. Secondly, we investigated changes in mobility of TRKB in dendritic structures in response to treatment with antidepressant drugs in vitro. We found that antidepressant drugs decrease anchoring of TRKB with PSD-93 and PSD-95, and can rapidly increase TRKB turnover in dendritic spines. Our results contribute to the mechanistic model explaining drug-induced restoration of juvenile-like neuronal plasticity, and may provide a common basis for the effects of antidepressant drugs.
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(2020)Study Design: A prospective follow-up study. Objective: To investigate if early lumbar disc degeneration (DD) in young low back pain (LBP) patients predicts progression of degenerative changes, pain, or disability in a 30-year follow-up. Summary of Background Data: MRI is an accurate method for studying degenerative changes in intervertebral discs. Decreased signal intensity (SI) can be used as indication of decreased water content. Long-term prognosis of early DD remains unclear. Methods: In an earlier study, 75 conscripts aged 20 years with LBP, had their lumbar spine examined by MRI. At a follow-up of 30 years, the subjects were contacted; 35/69 filled a pain and disability questionnaire, and 26/35 were also re-examined clinically and by MRI. The images were evaluated for decreased SI and other degenerative changes. Association between decreased SI of a disc at baseline and the presence of more severe degenerative changes in the same disc space at follow-up was analyzed using Fisher’s exact test. Association between decreased baseline SI and pain/disability scores from the questionnaire was analyzed with Kruskal-Wallis H test. Results: The total number of lumbar discs with decreased SI increased from 23/130 (18%) to 92/130 (71%) – from 0.9 to 3.5 per subject during the follow-up. Distribution of DD changed from being mostly in L4 – L5 and L5 – S1 discs to being almost even between the four lowermost discs. Discs that had even slightly decreased SI at baseline were more likely to have severely decreased SI at follow-up, compared to healthy discs (57% vs 11%, p<0.001). Other degenerative changes were also more common in these discs. Severity of DD at baseline did not have a significant association with current pain or disability. Conclusions: In young LBP patients, early degeneration in lumbar discs predicts progressive degenerative changes in the respective discs, but not pain, disability, or clinical symptoms.
Now showing items 1-2 of 2