Electronic measurement and control of spin transport in Silicon

The electron spin lifetime and diffusion length are transport parameters that define the scale of coherence in spintronic devices and circuits. Since these parameters are many orders of magnitude larger in semiconductors than in metals, semiconductors could be the most suitable for spintronics. Thus far, spin transport has only been measured in direct-bandgap semiconductors or in combination with magnetic semiconductors, excluding a wide range of non-magnetic semiconductors with indirect bandgaps. Most notable in this group is silicon (Si), which (in addition to its market entrenchment in electronics) has long been predicted a superior semiconductor for spintronics with enhanced lifetime and diffusion length due to low spin-orbit scattering and lattice inversion symmetry. Despite its exciting promise, a demonstration of coherent spin transport in Si has remained elusive, because most experiments focused on magnetoresistive devices; these methods fail because of universal impedance mismatch obstacles, and are obscured by Lorentz magnetoresistance and Hall effects. Here we demonstrate conduction band spin transport across 10 microns undoped Si, by using spin-dependent ballistic hot-electron filtering through ferromagnetic thin films for both spin-injection and detection. Not based on magnetoresistance, the hot electron spin-injection and detection avoids impedance mismatch issues and prevents interference from parasitic effects. The clean collector current thus shows independent magnetic and electrical control of spin precession and confirms spin coherent drift in the conduction band of silicon.Comment: Single PDF file with 4 Figure

Direct electronic measurement of the spin Hall effect

The generation, manipulation and detection of spin-polarized electrons in nanostructures define the main challenges of spin-based electronics[1]. Amongst the different approaches for spin generation and manipulation, spin-orbit coupling, which couples the spin of an electron to its momentum, is attracting considerable interest. In a spin-orbit-coupled system, a nonzero spin-current is predicted in a direction perpendicular to the applied electric field, giving rise to a "spin Hall effect"[2-4]. Consistent with this effect, electrically-induced spin polarization was recently detected by optical techniques at the edges of a semiconductor channel[5] and in two-dimensional electron gases in semiconductor heterostructures[6,7]. Here we report electrical measurements of the spin-Hall effect in a diffusive metallic conductor, using a ferromagnetic electrode in combination with a tunnel barrier to inject a spin-polarized current. In our devices, we observe an induced voltage that results exclusively from the conversion of the injected spin current into charge imbalance through the spin Hall effect. Such a voltage is proportional to the component of the injected spins that is perpendicular to the plane defined by the spin current direction and the voltage probes. These experiments reveal opportunities for efficient spin detection without the need for magnetic materials, which could lead to useful spintronics devices that integrate information processing and data storage.Comment: 5 pages, 4 figures. Accepted for publication in Nature (pending format approval

Activation of the dopamine 1 and dopamine 5 receptors increase skeletal muscle mass and force production under non-atrophying and atrophying conditions

<p>Abstract</p> <p>Background</p> <p>Control of skeletal muscle mass and force production is a complex physiological process involving numerous regulatory systems. Agents that increase skeletal muscle cAMP levels have been shown to modulate skeletal muscle mass and force production. The dopamine 1 receptor and its closely related homolog, the dopamine 5 receptor, are G-protein coupled receptors that are expressed in skeletal muscle and increase cAMP levels when activated. Thus we hypothesize that activation of the dopamine 1 and/or 5 receptor will increase skeletal muscle cAMP levels thereby modulating skeletal muscle mass and force production.</p> <p>Methods</p> <p>We treated isolated mouse tibialis anterior (TA) and medial gastrocnemius (MG) muscles in tissue bath with the selective dopamine 1 receptor and dopamine 5 receptor agonist SKF 81297 to determine if activation of skeletal muscle dopamine 1 and dopamine 5 receptors will increase cAMP. We dosed wild-type mice, dopamine 1 receptor knockout mice and dopamine 5 receptor knockout mice undergoing casting-induced disuse atrophy with SKF 81297 to determine if activation of the dopamine 1 and dopamine 5 receptors results in hypertrophy of non-atrophying skeletal muscle and preservation of atrophying skeletal muscle mass and force production.</p> <p>Results</p> <p>In tissue bath, isolated mouse TA and MG muscles responded to SKF 81297 treatment with increased cAMP levels. Treating wild-type mice with SKF 81297 reduced casting-induced TA and MG muscle mass loss in addition to increasing the mass of non-atrophying TA and MG muscles. In dopamine 1 receptor knockout mice, extensor digitorum longus (EDL) and soleus muscle mass and force was not preserved during casting with SKF 81297 treatment, in contrast to significant preservation of casted wild-type mouse EDL and soleus mass and EDL force with SKF 81297 treatment. Dosing dopamine 5 receptor knockout mice with SKF 81297 did not significantly preserve EDL and soleus muscle mass and force although wild-type mouse EDL mass and force was significantly preserved SKF 81297 treatment.</p> <p>Conclusions</p> <p>These data demonstrate for the first time that treatment with a dopamine 1/5 receptor agonist results in (1) significant preservation of EDL, TA, MG and soleus muscle mass and EDL muscle force production during periods of atrophy and (2) hypertrophy of TA and MG muscle. These effects appear to be mainly mediated by both the dopamine 1 and dopamine 5 receptors.</p

Structure of the D2 dopamine receptor bound to the atypical antipsychotic drug risperidone

Dopamine is a neurotransmitter that has been implicated in processes as diverse as reward, addiction, control of coordinated movement, metabolism and hormonal secretion. Correspondingly, dysregulation of the dopaminergic system has been implicated in diseases such as schizophrenia, Parkinson's disease, depression, attention deficit hyperactivity disorder, and nausea and vomiting. The actions of dopamine are mediated by a family of five G-protein-coupled receptors. The D2 dopamine receptor (DRD2) is the primary target for both typical and atypical antipsychotic drugs, and for drugs used to treat Parkinson's disease. Unfortunately, many drugs that target DRD2 cause serious and potentially life-threatening side effects due to promiscuous activities against related receptors. Accordingly, a molecular understanding of the structure and function of DRD2 could provide a template for the design of safer and more effective medications. Here we report the crystal structure of DRD2 in complex with the widely prescribed atypical antipsychotic drug risperidone. The DRD2-risperidone structure reveals an unexpected mode of antipsychotic drug binding to dopamine receptors, and highlights structural determinants that are essential for the actions of risperidone and related drugs at DRD2. © 2018 Macmillan Publishers Limited, part of Springer Nature. All rights reserved