Gate control of low-temperature spin dynamics in two-dimensional hole systems

We have investigated spin and carrier dynamics of resident holes in high-mobility two-dimensional hole systems in GaAs/Al$_{0.3}$Ga$_{0.7}$As single quantum wells at temperatures down to 400 mK. Time-resolved Faraday and Kerr rotation, as well as time-resolved photoluminescence spectroscopy are utilized in our study. We observe long-lived hole spin dynamics that are strongly temperature dependent, indicating that in-plane localization is crucial for hole spin coherence. By applying a gate voltage, we are able to tune the observed hole g factor by more than 50 percent. Calculations of the hole g tensor as a function of the applied bias show excellent agreement with our experimental findings.Comment: 8 pages, 7 figure

Motion and pattern cortical potentials in adults with high-functioning autism spectrum disorder

Purpose: Autism spectrum disorder (ASD) is a condition in which visual perception to both static and moving stimuli is altered. The aim of this study was to investigate the early cortical responses of subjects with ASD to simple patterns and moving radial rings using visual evoked potentials (VEPs). Methods: Male ASD participants (n = 9) and typically developing (TD) individuals (n = 7) were matched for full, performance and verbal IQ (p > 0.263). VEPs were recorded to the pattern reversing checks of 50′ side length presented with Michelson contrasts of 98 and 10 % and to the onset of motion—either expansion or contraction of low-contrast concentric rings (33.3 % duty cycle at 10 % contrast). Results: There were no significant differences between groups in the VEPs elicited by pattern reversal checkerboards of high (98 %) or low (10 %) contrast. The ASD group had a significantly larger N160 peak (1.85 x) amplitude to motion onset VEPs elicited by the expansion of radial rings (p = 0.001). No differences were evident in contraction VEP peak amplitudes nor in the latencies of the motion onset N160 peaks. There was no evidence of a response that could be associated with adaptation to the motion stimulus in the interstimulus interval following an expansion or contraction phase of the rings. Conclusion: These data support a difference in processing of motion onset stimuli in this adult high-functioning ASD group compared to the TD group

Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil–DNA glycosylase impair learning in a mouse model of vascular cognitive impairment

Dietary deficiencies in folic acid result in elevated levels of plasma homocysteine, which has been associated with the development of dementia and other neurodegenerative disorders. Previously, we have shown that elevated levels of plasma homocysteine in mice deficient for a DNA repair enzyme, uracil–DNA glycosylase (UNG), result in neurodegeneration. The goal of this study was to evaluate how deficiencies in folic acid and UNG along with elevated levels of homocysteine affect vascular cognitive impairment, via chronic hypoperfusion in an animal model. Ung+/+ and Ung−/− mice were placed on either control (CD) or folic acid deficient (FADD) diets. Six weeks later, the mice either underwent implantation of microcoils around both common carotid arteries. Post-operatively, behavioral tests began at 3-weeks, angiography was measured after 5-weeks using MRI to assess vasculature and at completion of study plasma and brain tissue was collected for analysis. Learning impairments in the Morris water maze (MWM) were observed only in hypoperfused Ung−/− FADD mice and these mice had significantly higher plasma homocysteine concentrations. Interestingly, Ung+/+ FADD produced significant remodeling of the basilar artery and arterial vasculature. Increased expression of GFAP was observed in the dentate gyrus of Ung−/− hypoperfused and FADD sham mice. Chronic hypoperfusion resulted in increased cortical MMP-9 protein levels of FADD hypoperfused mice regardless of genotypes. These results suggest that elevated levels of homocysteine only, as a result of dietary folic acid deficiency, don’t lead to memory impairments and neurobiochemical changes. Rather a combination of either chronic hypoperfusion or UNG deficiency is required

Hippocampal-Dependent Spatial Memory in the Water Maze is Preserved in an Experimental Model of Temporal Lobe Epilepsy in Rats

Cognitive impairment is a major concern in temporal lobe epilepsy (TLE). While different experimental models have been used to characterize TLE-related cognitive deficits, little is known on whether a particular deficit is more associated with the underlying brain injuries than with the epileptic condition per se. Here, we look at the relationship between the pattern of brain damage and spatial memory deficits in two chronic models of TLE (lithium-pilocarpine, LIP and kainic acid, KA) from two different rat strains (Wistar and Sprague-Dawley) using the Morris water maze and the elevated plus maze in combination with MRI imaging and post-morten neuronal immunostaining. We found fundamental differences between LIP- and KA-treated epileptic rats regarding spatial memory deficits and anxiety. LIP-treated animals from both strains showed significant impairment in the acquisition and retention of spatial memory, and were unable to learn a cued version of the task. In contrast, KA-treated rats were differently affected. Sprague-Dawley KA-treated rats learned less efficiently than Wistar KA-treated animals, which performed similar to control rats in the acquisition and in a probe trial testing for spatial memory. Different anxiety levels and the extension of brain lesions affecting the hippocampus and the amydgala concur with spatial memory deficits observed in epileptic rats. Hence, our results suggest that hippocampal-dependent spatial memory is not necessarily affected in TLE and that comorbidity between spatial deficits and anxiety is more related with the underlying brain lesions than with the epileptic condition per se

Guidelines for diagnosis and management of the cobalamin-related remethylation disorders cblC, cblD, cblE, cblF, cblG, cblJ and MTHFR deficiency

BACKGROUND: Remethylation defects are rare inherited disorders in which impaired remethylation of homocysteine to methionine leads to accumulation of homocysteine and perturbation of numerous methylation reactions. OBJECTIVE: To summarise clinical and biochemical characteristics of these severe disorders and to provide guidelines on diagnosis and management. DATA SOURCES: Review, evaluation and discussion of the medical literature (Medline, Cochrane databases) by a panel of experts on these rare diseases following the GRADE approach. KEY RECOMMENDATIONS: We strongly recommend measuring plasma total homocysteine in any patient presenting with the combination of neurological and/or visual and/or haematological symptoms, subacute spinal cord degeneration, atypical haemolytic uraemic syndrome or unexplained vascular thrombosis. We strongly recommend to initiate treatment with parenteral hydroxocobalamin without delay in any suspected remethylation disorder; it significantly improves survival and incidence of severe complications. We strongly recommend betaine treatment in individuals with MTHFR deficiency; it improves the outcome and prevents disease when given early

Visual mismatch negativity elicited by magnocellular system activation

AbstractThe processing of visual motion was tested by means of event related potentials recording (ERP) using a paradigm designed to produce a visual mismatch negativity effect. The stimuli were unattended and presented in the peripheral visual field (outside the central 15°). The standard stimulus consisted of an up/down motion sequence, whilst the deviant stimulus of a down/up motion sequence. Significant ERP differences between the standard and deviant conditions were found in 8 out of 10 adult subjects already in 80ms and prevailingly in interval 145–260ms from the initial stimulus presentation. The results demonstrate that the magnocellular information undergoes processing capable of detecting differences in the sequence of unattended peripheral motion stimuli