Investigation of the impact of neutron irradiation on SiC power MOSFETs lifetime by reliability tests

High temperature reverse-bias (HTRB), High temperature gate-bias (HTGB) tests and electrical DC characterization were performed on planar-SiC power MOSFETs which survived to accelerated neutron irradiation tests carried out at ChipIr-ISIS (Didcot, UK) facility, with terrestrial neutrons. The neutron test campaigns on the SiC power MOSFETs (manufactered by ST) were con-ducted on the same wafer lot devices by STMicroelectronics and Airbus, with different neutron tester systems. HTGB and HTRB tests, which characterise gate-oxide integrity and junction robustness, show no difference between the non irradiated devices and those which survived to the neutron irradiation tests, with neutron fluence up to 2 × 1011 (n/cm2). Electrical characterization performed pre and post-irradiation on different part number of power devices (Si, SiC MOSFETs and IGBTs) which survived to neutron irradiation tests does not show alteration of the data-sheet electrical parameters due to neutron interaction with the device

A low-voltage activated, transient calcium current is responsible for the time-dependent depolarizing inward rectification of rat neocortical neurons in vitro

Intracellular recordings were obtained from rat neocortical neurons in vitro. The current-voltage-relationship of the neuronal membrane was investigated using current- and single-electrode-voltage-clamp techniques. Within the potential range up to 25 mV positive to the resting membrane potential (RMP: –75 to –80 mV) the steady state slope resistance increased with depolarization (i.e. steady state inward rectification in depolarizing direction). Replacement of extracellular NaCl with an equimolar amount of choline chloride resulted in the conversion of the steady state inward rectification to an outward rectification, suggesting the presence of a voltage-dependent, persistent sodium current which generated the steady state inward rectification of these neurons. Intracellularly injected outward current pulses with just subthreshold intensities elicited a transient depolarizing potential which invariably triggered the first action potential upon an increase in current strength. Single-electrode-voltage-clamp measurements reveled that this depolarizing potential was produced by a transient calcium current activated at membrane potentials 15–20 mV positive to the RMP and that this current was responsible for the time-dependent increase in the magnitude of the inward rectification in depolarizing direction in rat neocortical neurons. It may be that, together with the persistent sodium current, this calcium current regulates the excitability of these neurons via the adjustment of the action potential threshold

DISC1 genetics, biology and psychiatric illness

Psychiatric disorders are highly heritable, and in many individuals likely arise from the combined effects of genes and the environment. A substantial body of evidence points towards DISC1 being one of the genes that influence risk of schizophrenia, bipolar disorder and depression, and functional studies of DISC1 consequently have the potential to reveal much about the pathways that lead to major mental illness. Here, we review the evidence that DISC1 influences disease risk through effects upon multiple critical pathways in the developing and adult brain

Control of Ca2+ influx by cannabinoid and metabotropic glutamate receptors in rat cerebellar cortex requires K+ channels

In the rodent cerebellum, both presynaptic CB1 cannabinoid receptors and presynaptic mGluR4 metabotropic glutamate receptors acutely depress excitatory synaptic transmission at parallel fibre-Purkinje cell synapses. Using rat cerebellar slices, we have analysed the effects of selective CB1 and mGluR4 agonists on the presynaptic Ca2+ influx which controls glutamate release at this synapse.Changes in presynaptic Ca2+ influx were determined with the Ca2+-sensitive dyes fluo-4FF AM or fluo-3 AM. Five stimulations delivered at 100 Hz or single stimulations of parallel fibres evoked rapid and reproducible transient increases in presynaptic fluo-4FF or fluo-3 fluorescence, respectively, which decayed to prestimulus levels within a few hundred milliseconds. Bath application of the selective CB1 agonist WIN55,212-2 (1 μm) markedly reduced the peak amplitude of these fluorescence transients. This effect was fully reversed by the selective CB1 antagonist SR141716-A (1 μm).Bath application of the selective mGluR4 agonist l-AP4 (100 μm) also caused a transient decrease in the peak amplitude of the fluorescence transients evoked by parallel fibre stimulation.Bath application of the potassium channel blocker 4-AP (1 mm) totally prevented both the WIN55,212-2- and the l-AP4-induced inhibition of peak fluorescence transients evoked by parallel fibre stimulation.The present study demonstrates that activation of CB1 and mGluR4 receptors inhibits presynaptic Ca2+ influx evoked by parallel fibre stimulation via the activation of presynaptic K+ channels, suggesting that the molecular mechanisms underlying this inhibition involve an indirect inhibition of presynaptic voltage-gated Ca2+ channels rather than their direct inhibition