Synaptogenesis is essential in forming new neurocircuits during development, and this is mediated in part by astrocyte-released thrombospondins (TSPs) and activation of their neuronal receptor, α2δ-1. Here, we show that this developmental synaptogenic mechanism is utilized during cocaine experience to induce spinogenesis and the generation of AMPA receptor-silent glutamatergic synapses in the adult nucleus accumbens shell (NAcSh).
 
  Using multidisciplinary approaches including astrocyte Ca
  imaging, genetic mouse lines, viral-mediated gene transfer, and operant behavioral procedures, we monitor the response of NAcSh astrocytes to cocaine administration and examine the role of astrocytic TSP-α2δ-1 signaling in cocaine-induced silent synapse generation as well as the behavioral impact of astrocyte-mediated synaptogenesis and silent synapse generation.
 
  Cocaine administration acutely increases Ca
  events in NAcSh astrocytes, while decreasing astrocytic Ca
  blocks cocaine-induced generation of silent synapses. Furthermore, knockout of TSP2, or pharmacological inhibition or viral-mediated knockdown of α2δ-1, prevents cocaine-induced generation of silent synapses. Moreover, disrupting TSP2-α2δ-1-mediated spinogenesis and synapse generation in NAcSh decreases cue-induced cocaine seeking after withdrawal from cocaine self-administration and cue-induced reinstatement of cocaine seeking after drug extinction.
 
  These results establish that silent synapses are generated by an astrocyte-mediated synaptogenic mechanism in response to cocaine experience and embed critical cue-associated memory traces that promote cocaine relapse.
 These results establish that silent synapses are generated by an astrocyte-mediated synaptogenic mechanism in response to cocaine experience and embed critical cue-associated memory traces that promote cocaine relapse.
  The use of general anesthesia in infants involves both short-term and long-term risks. The aim of this study is to evaluate the efficacy of brain MRI without anesthesia in infants younger than 3-month-old immobilized with a pillow.
 
  This prospective case-control study was done in 2019. Cases were stable patients less than 3 months old who did not require ventilatory support for whom brain MRI was indicated. Patients were fed so they would fall asleep and placed in the scanner with an immobilizing pillow. Controls were clinically unstable patients matched for age and sex referred for brain MRI under general anesthesia. Three pediatric radiologists evaluated the success of the MRI study (whether it answered the clinical question), recorded whether it was necessary to repeat the study, and rated the presence of motion artifacts on a scale ranging from 1 to 4.
 
  A total of 47 cases were included (28 boys and 19 girls; mean age, 31 days). Of these, 42 (89%) MRI studies were considered successful. The proportion of successful MRI studies was lower in outpatients than in inpatients (p=0.02). The quality of MRI in cases was considered optimal in 60% and suboptimal (motion artifacts in one or two sequences) in 30%. No safety issues related with the technique were detected. The mean duration of the studies was 16.6minutes (range, 6-30minutes).  https://www.selleckchem.com/products/gsk2193874.html  All of the MRI studies in controls were considered successful; quality was considered optimal in 89% and suboptimal in 11%. In the first year in which we used this technique, we avoided the use of general anesthesia in 47 MRI studies in 42 newborns.
 
  Brain MRI using the feed and sleep technique in infants younger than 3-month-old immobilized with a pillow can be done safely and efficaciously without general anesthesia.
 Brain MRI using the feed and sleep technique in infants younger than 3-month-old immobilized with a pillow can be done safely and efficaciously without general anesthesia.Diseases of the spinal cord often have devastating consequences and imaging studies are indispensable for their diagnosis. The fundamental imaging technique to evaluate these diseases is magnetic resonance imaging of the spine. The diagnostic approach must be based on the clinical context, the time elapsed since the onset of symptoms and signs, and the imaging findings; for this reason, it sometimes necessary to broaden the study to include the brain. The first step in the diagnostic algorithm is to rule out spinal cord compression before evaluating other causes of myelopathy, which sometimes has multiple causes. This paper includes a broad review of the different diseases that can cause myelopathy, their imaging manifestations, their differential diagnoses, and diagnostic algorithms. Using an appropriate radiological approach will result in better management and prognosis of these patients.Making an intraoral digital scan for fixed mandibular implant-supported complete-arch prostheses is a clinical challenge. The absence of references in the mandibular arch for precise scan alignment may complicate the correct digital design of the prosthesis framework. This article presents a straightforward method that allows a completely digital approach to digital scanning for fixed mandibular implant-supported prostheses.Skeletal muscle is the largest tissue in the body, and plays a remarkable role in energy and metabolic homeostasis. Disorder in lipid metabolism and glucose utilization could impair the quality and function of skeletal muscle. Glutaredoxin-1 (Grx1) acts as a vital metabolic regulator of redox homeostasis. Recent studies have shown that Grx1 regulates hepatic lipid metabolism. The skeletal muscle also contains abundant Grx1, but the role of Grx1 in skeletal muscle remains unknown. Therefore, we investigated the effect of Grx1 on skeletal muscle. In this study, we found that Grx1-deficient mice (Grx1-/-) spontaneously developed muscle atrophy by 3 months of age. And the p-AMPK activity and Sirt1 activity were inhibited in Grx1-/- mice, which led to intramuscular lipid deposition and glucose utilization disorder in skeletal muscle. However, intraperitoneal injection of metformin for 15 consecutive days ameliorated skeletal muscle atrophy caused by Grx1 deficiency to a certain extent. Taken together, these findings indicate that Grx1 deficiency might induce skeletal muscle atrophy by regulating the intramuscular lipid deposition and glucose utilization, which could be attenuated by metformin.