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The AlSi10Mg alloy produced by casting (AC) and additive manufacturing (AM) technology of laser powder bed fusion (L -PBF) has been investigated through mechanical spectroscopy (MS). In addition to the grain boundary peak P GB the Q −1 curves of both materials exhibit two other relaxation peaks, P1 (H = 0.8 ± 0.05 eV; τ 0 = 10−11±1 s) and P2 (H = 1.0 ± 0.05 eV; τ 0 = 10−13±1 s), depending on the interaction of dislocations with solute elements (Si and Mg). Relaxation strengths of P1, P2 and P GB of AM alloy are greater than those of the AC one owing to the finer structure of Al cells and the higher amount of Si and Mg in supersaturated solid solution induced by the rapid solidification typical of the L -PBF process. After successive MS test runs relaxation strengths of P1 and P2 peaks in both the examined materials decrease due to the precipitation of Si atoms and dislocation density recovery. Such decrease is more pronounced in AM alloy where change of cell shape and increase of cell size is observed. Dynamic modulus of AM alloy exhibits an anomalous trend in the first test run that is no more present in successive runs. The irreversible process giving rise to such anomalous behavior is the closure of pores of nanometric size. • AlSi10Mg produced by casting (AC) and additive manufacturing (AM) has been investigated through mechanical spectroscopy (MS). • Q-1 curves of both materials exhibit the grain boundary peak P GB and two other relaxation peaks (P1 and P2). • The MS results have been correlated to microstructural information from light microscopy, XRD, TEM and SEM. • The P1 and P2 peaks depend on the interaction of dislocations with solute elements (Si and Mg). • Dynamic modulus of AM alloy exhibits an anomalous trend in the first test run that is no more present in successive runs. [ABSTRACT FROM AUTHOR]

Abstract: SR58611A is a selective β3-adrenoceptor (Adrb3) agonist which has demonstrated antidepressant and anxiolytic properties in rodents. The present study confirmed the detection of Adrb3 mRNA transcript in rodent brain sub-regions and evaluated the effect of SR58611A on serotonergic and noradrenergic transmission in rats and mice in an attempt to elucidate the mechanism(s) underlying these properties. SR58611A (3 and 10 mg/kg, p.o.) increased the synthesis of 5-HT and tryptophan (Trp) levels in several rodent brain areas (cortex, hippocampus, hypothalamus, striatum). Moreover, SR58611A (10 mg/kg, p.o.) increased the release of 5-HT assessed by in vivo microdialysis in rat prefrontal cortex. Systemic (3 mg/kg, i.v.) or chronic administration of SR58611A (10 mg/kg, p.o.), in contrast to fluoxetine (15 mg/kg, p.o.), did not modify the activity of serotonergic neurons in the rat dorsal raphe nucleus. The increase in 5-HT synthesis induced by SR58611A was not observed in Adrb3s knockout mice, suggesting a selective involvement of Adrb3s in this effect. SR58611A (3 and 10 mg/kg, p.o.) did not modify norepinephrine synthesis and metabolism but increased its release in rat brain. Repeated administration of SR58611A (10 mg/kg, p.o.) did not modify basal norepinephrine release in rat prefrontal cortex whereas it prevented its tail-pinch stress-induced enhancement similarly to reboxetine (15 mg/kg, p.o.). Finally SR58611A increased the firing rate of noradrenergic neurons in the rat locus coeruleus following systemic (3 mg/kg, i.v.) or local (0.01 and 1 μM) but not chronic (10 mg/kg, p.o.) administration. These results suggest that the anxiolytic- and antidepressant-like activities of SR58611A involve an increase of brain serotonergic and noradrenergic neurotransmissions, triggered by activation of Adrb3s. [Copyright &y& Elsevier]