The first olfactory processing center in the larval Drosophila brain uses information about feeding state to shape behavior.

Purpose Osteoporosis affects more than 200 million individuals worldwide and predisposes to vertebral compression fractures (VCFs). Given undertreatment of fragility fractures, including VCFs, we investigate current anti-osteoporotic medication prescribing trends. Methods Patients 50 and older with a diagnosis of primary closed thoracolumbar VCF between 2004 and 2019 were identified from the Clinformatics® Data Mart database. Multivariate analysis was performed for demographic and clinical treatment and outcome variables. Results Of 143 081 patients with primary VCFs, 16 780 (11.7%) were started on anti-osteoporotic medication within a year; 126 301 (88.3%) patients were not started on medication. The medication cohort was older (75.4 ± 9.3 vs 74.0 ± 12.3 years, P < .001), had higher Elixhauser Comorbidity Index scores (4.7 ± 6.2 vs 4.3 ± 6.7, P < .001), was more likely to be female (81.1% vs 64.4%, P < .001), and was more likely to have a formal osteoporosis diagnosis (47.8% vs 32.9%) than the group that did not receive medication. Alendronate (63.4%) and calcitonin (27.8%) were the most commonly initiated medications. The proportion of individuals receiving anti-osteoporotic medication within the year following VCF peaked in 2008 (15.2%), then declined until 2012 with a modest increase afterward. Conclusions Osteoporosis remains undertreated after low-energy VCFs. New anti-osteoporotic medication classes have been approved in recent years. Bisphosphonates remain the most prescribed class. Increasing recognition and treatment of osteoporosis is paramount to decreasing the risk of subsequent fractures.

All drugs of abuse induce long-lasting changes in synaptic transmission and neural circuit function that underlie substance use disorders. Here, we demonstrate that dopaminergic neuronal activity-regulated myelin plasticity is a key modulator of dopaminergic circuit function and opioid reward. Oligodendroglial lineage cells respond to dopaminergic neuronal activity evoked by either optogenetic stimulation or by morphine administration specifically within the reward center ventral tegmental area (VTA), but not along the axonal projections in the medial forebrain bundle nor within the target nucleus accumbens (NAc). Genetic blockade of oligodendrogenesis dampens NAc dopamine release dynamics, which is critical for reward learning, and impairs behavioral conditioning to morphine. Our findings identify dopaminergic neuronal activity-regulated myelin plasticity as an important circuit modification that is required for opioid reward. One-Sentence Summary: Activity-dependent myelin plasticity in the ventral tegmental area modulates dopaminergic circuit function and opioid reward