Radiation damage in silicon first semiannual report, oct. 15, 1963 - apr. 15, 1964

Observed paramagnetic center, effects of impurities on radiation damage of silicon, and low energy proton bombardment of silicon and gallium arsenide solar cell

Quasiperiodic oscillations in bright galactic-bulge X-ray sources

Quasiperiodic oscillations with frequencies in the range 5-50 Hz have recently been discovered in X-rays from two bright galactic-bulge sources and Sco X-1. These sources are weakly magnetic neutron stars accreting from disks which the plasma is clumped. The interaction of the magnetosphere with clumps in the inner disk causes oscillations in the X-ray flux with many of the properties observed

Medial prefrontal cortex neuronal activation and synaptic alterations after stress-induced reinstatement of palatable food seeking: a study using c-fos-GFP transgenic female rats

Relapse to maladaptive eating habits during dieting is often provoked by stress and there is evidence for a role of ovarian hormones in stress responses and feeding. We studied the role of these hormones in stress-induced reinstatement of food seeking and medial prefrontal cortex (mPFC) neuronal activation in c-fos-GFP transgenic female rats, which express GFP in strongly activated neurons. Food-restricted ovariectomized or sham-operated c-fos-GFP rats were trained to lever-press for palatable food pellets. Subsequently, lever-pressing was extinguished and reinstatement of food seeking and mPFC neuronal activation was assessed after injections of the pharmacological stressor yohimbine (0.5-2 mg/kg) or pellet priming (1-4 noncontingent pellets). Estrous cycle effects on reinstatement were also assessed in wild-type rats. Yohimbine- and pellet-priming-induced reinstatement was associated with Fos and GFP induction in mPFC; both reinstatement and neuronal activation were minimally affected by ovarian hormones in both c-fos-GFP and wild-type rats. c-fos-GFP transgenic rats were then used to assess glutamatergic synaptic alterations within activated GFP-positive and nonactivated GFP-negative mPFC neurons following yohimbine-induced reinstatement of food seeking. This reinstatement was associated with reduced AMPA receptor/NMDA receptor current ratios and increased paired-pulse facilitation in activated GFP-positive but not GFP-negative neurons. While ovarian hormones do not appear to play a role in stress-induced relapse of food seeking in our rat model, this reinstatement was associated with unique synaptic alterations in strongly activated mPFC neurons. Our paper introduces the c-fos-GFP transgenic rat as a new tool to study unique synaptic changes in activated neurons during behavio

Role of dopamine in dorsal medial prefrontal cortex in yohimbine-induced reinstatement of food seeking in rats

In humans, relapse to maladaptive eating habits during dieting is often provoked by stress.Weadapted a drug relapse-reinstatement model to study the role of stress in relapse to food seeking (Nair et al., Prog. Neurobiol., 2009). In our model, the anxiogenic drug yohimbine, an alpha-2 adrenoceptor antagonist, that causes stress-like responses in humans and laboratory animals, reliably reinstates food seeking.Werecently found that yohimbine-induced reinstatement of food seeking is attenuated by systemic injections of SCH23390 (a D1-family receptor antagonist) but not clonidine (an alpha-2 adrenoceptor agonist). Here, we studied the role of the medial prefrontal cortex (mPFC) in yohimbine-induced reinstatement. We trained food-restricted rats to lever-press for 35% high-fat pellets every other day (9–15 3 h sessions). We then extinguished the food-reinforced operant responding for 10–14 days by removing the pellets. Subsequently, we tested the effect of systemic injections of yohimbine (0, 2 mg/kg) on reinstatement of food seeking. In Exp. 1we found that yohimbine-induced reinstatement was associated with strong induction of Fos (a marker of neuronal activity) in the dorsal mPFC and weaker Fos induction in the ventral mPFC. In Exp. 2 we found that dorsal but not ventral mPFC injections of the D1-family receptor antagonist SCH23390 (0.5, 1.0g/side) decreased yohimbine-induced reinstatement of food seeking. Our data indicate a critical role of dorsal mPFC dopamine in reinstatement food seeking induced by the pharmacological stressor yohimbine

Indirect Detection of Kaluza-Klein Dark Matter from Latticized Universal Dimensions

We consider Kaluza-Klein dark matter from latticized universal dimensions. We motivate and investigate two different lattice models, where the models differ in the choice of boundary conditions. The models reproduce relevant features of the continuum model for Kaluza-Klein dark matter. For the model with simple boundary conditions, this is the case even for a model with only a few lattice sites. We study the effects of the latticization on the differential flux of positrons from Kaluza-Klein dark matter annihilation in the galactic halo. We find that for different choices of the compactification radius, the differential positron flux rapidly converges to the continuum model results as a function of the number of lattice sites. In addition, we consider the prospects for upcoming space-based experiments such as PAMELA and AMS-02 to probe the latticization effect.Comment: 25 pages, 9 figures, LaTeX. Final version published in JCA

Long-Term Stability of an Area-Reversible Atom-Interferometer Sagnac Gyroscope

We report on a study of the long-term stability and absolute accuracy of an atom interferometer gyroscope. This study included the implementation of an electro-optical technique to reverse the vector area of the interferometer for reduced systematics and a careful study of systematic phase shifts. Our data strongly suggests that drifts less than 96 $\mu$deg/hr are possible after empirically removing shifts due to measured changes in temperature, laser intensity, and several other experimental parameters.Comment: 4 pages, 4 figures, submitted to PR

An accretion disk model for periodic timing variations of pulsars

The long-term, highly periodic and correlated variations in both the pulse shape and the rate of slow-down of two isolated pulsars (PSRs) PSR B1828-11 and PSR B1642-03 were discovered recently. This phenomenon may provide evidence for "free precession" as suggested in the literature. Some authors presented various kinds of models to explain this phenomenon within the framework of free precession. Here we present an accretion disk model for this precession phenomenon instead. Under reasonable parameters, the observed phenomenon can be explained by an isolated pulsar with a fossil disk. This may link radio pulsars and anomalous X-ray pulsars (AXPs) and present an indirect evidence for the existence of the fossil disk in nature.Comment: 4 pages, 2 figures, to appear in A&A Lette

Involvement of Noradrenergic Neurotransmission in the Stress- but not Cocaine-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Role for β-2 Adrenergic Receptors

The responsiveness of central noradrenergic systems to stressors and cocaine poses norepinephrine as a potential common mechanism through which drug re-exposure and stressful stimuli promote relapse. This study investigated the role of noradrenergic systems in the reinstatement of extinguished cocaine-induced conditioned place preference by cocaine and stress in male C57BL/6 mice. Cocaine- (15 mg/kg, i.p.) induced conditioned place preference was extinguished by repeated exposure to the apparatus in the absence of drug and reestablished by a cocaine challenge (15 mg/kg), exposure to a stressor (6-min forced swim (FS); 20–25°C water), or administration of the α-2 adrenergic receptor (AR) antagonists yohimbine (2 mg/kg, i.p.) or BRL44408 (5, 10 mg/kg, i.p.). To investigate the role of ARs, mice were administered the nonselective β-AR antagonist, propranolol (5, 10 mg/kg, i.p.), the α-1 AR antagonist, prazosin (1, 2 mg/kg, i.p.), or the α-2 AR agonist, clonidine (0.03, 0.3 mg/kg, i.p.) before reinstatement testing. Clonidine, prazosin, and propranolol failed to block cocaine-induced reinstatement. The low (0.03 mg/kg) but not high (0.3 mg/kg) clonidine dose fully blocked FS-induced reinstatement but not reinstatement by yohimbine. Propranolol, but not prazosin, blocked reinstatement by both yohimbine and FS, suggesting the involvement of β-ARs. The β-2 AR antagonist ICI-118551 (1 mg/kg, i.p.), but not the β-1 AR antagonist betaxolol (10 mg/kg, i.p.), also blocked FS-induced reinstatement. These findings suggest that stress-induced reinstatement requires noradrenergic signaling through β-2 ARs and that cocaine-induced reinstatement does not require AR activation, even though stimulation of central noradrenergic neurotransmission is sufficient to reinstate

Fos-expressing neuronal ensemble in rat ventromedial prefrontal cortex encodes cocaine seeking but not food seeking in rats

Neuronal ensembles in ventromedial prefrontal cortex (vmPFC) play a role in both cocaine and palatable food seeking. However, it is unknown whether similar or different vmPFC neuronal ensembles mediate food and cocaine seeking. Here, we used the Daun02 inactivation procedure to assess whether the neuronal ensembles mediating food and cocaine seeking can be functionally distinguished. We trained male and female Fos-LacZ rats to self-administer palatable food pellets and cocaine on alternating days for 18 days. We then exposed the rats to a brief nonreinforced food- or cocaine-seeking test to induce Fos and β-gal in neuronal ensembles associated with food or cocaine seeking, respectively and infused Daun02 into vmPFC to ablate the β-gal-expressing ensembles. Two days later, we tested the rats for food or cocaine seeking under extinction conditions. Although inactivation of the food-seeking ensemble did not influence food or cocaine seeking, inactivation of the cocaine-seeking ensemble reduced cocaine seeking but not food seeking. Results indicate that the neuronal ensemble activated by cocaine seeking in vmPFC is functionally separate from the ensemble activated by food seeking