Electrical Characteristics of the Junction between PEDOT:PSS and Thiophene-Functionalized Silicon Microwires.

Thiophene moieties have been attached to Si microwires (Si MWs) by a two-step chlorination/alkylation reaction method. X-ray photoelectron spectroscopy indicated that saturation of the surface occurred after 30 min of reaction time. Electrical measurements using a standard probe station indicated that the junction between individual thiophene-functionalized Si MWs and the conducting polymer poly(3,4-ethylenedioxythiophene)/poly(styrenesulfonate) ( PEDOT: PSS) became more ohmic as more thiophene was added to the MW surface. Under a light-limited current of 20 nA, representative of operation of Si MWs under 1 Sun illumination conditions, the iR loss of thiophene-n-Si MW/PEDOT-PSS contacts was 20 mV, representing an order of magnitude reduction compared with PEDOT-PSS junctions formed with methyl terminated n-Si MWs. Such iR losses are much less than typical catalytic overpotentials for fuel formation, and hence the thiophene-functionalized Si MW contacts will not limit the performance of a Si MW array-based solar fuels device under 1 Sun illumination.

Strain specific differences in memory and neuropathology in a mouse model of Alzheimer's disease.

AIMS: Studies using transgenic mouse strains that incorporate Alzheimer's disease (AD) mutations are valuable for the identification of signaling pathways, potential drug targets, and possible mechanisms of disease that will aid in our understanding of AD. However, reports on the effects of specific AD mutations (Swedish, KM670/671NL; Indiana, V717F) on behavior (Morris water maze) and neuropathological progression have been inconsistent when comparing different genetic backgrounds in these models. Given this, investigators are compelled to more closely evaluate different background strains. The aim of the present study was to compare two commonly used TgCRND8 backgrounds, the 129SvEvTac/C57F1 strain and the C3H/C57F1 strain. MAIN METHODS: Memory function was assessed by the Morris water maze, a test for assaying hippocampal-dependent memory. We also stained with ThioflavinS in order to visualize and quantify amyloid beta (Abeta) plaques. Real time polymerase chain reaction (PCR) was used to measure insulin-degrading enzyme (IDE), an enzyme that also degrades amyloid beta. KEY FINDINGS: We found deficits in the 129SvEvTac/C57F1 strain in several parameters of the Morris water maze. In addition, amyloid plaque load expression was significantly greater in the 129SvEvTac/C57F1 as compared to the C3H/C57F1 strain as demonstrated by histochemical staining. We also observed a significant decrease in IDE, in the 129SvEvTac/C57F1 strain. SIGNIFICANCE: This study supports the notion that strain specific differences are apparent in tests of spatial memory and neuropathologic progression in AD.

Controlled pulse delivery of electrical stimulation differentially reduces epileptiform activity in Mg2+-free-treated hippocampal slices.

Electrical stimulation for applications in epilepsy has been attempted in multiple brain regions [corrected] using high- or low-frequency stimulation protocols. Data suggest that specific frequencies may have more benefit at controlling seizure activity. To this end, investigators have tested low-frequency stimulation (LFS) protocols (0.1 to 25 Hz) in both animal models and in human epileptic patients and reported reduced epileptiform synchronization, afterdischarge thresholds, and seizure activity in general. Collectively, these studies imply that LFS may have benefit in reducing epileptiform activity, however, the effectiveness of various electrical parameters still needs to be determined in specific targets. This study aimed to systematically control the total number of stimulation pulses when using primarily LFS protocols (0.5, 0.75, 1, 2, 5, 10, and 25 Hz) delivered for the suppression of seizure-like activity in the hippocampal brain slice using a Mg2+-free model of epilepsy. Fifty Hz was also tested as a reference higher frequency protocol. Regulating the total number of pulses also controlled the amount of electrical work delivered. Of the LFS protocols tested, 0.5 Hz, and 1 Hz were optimal and significantly (p<0.05) reduced several measures of epileptiform activity. However, the higher frequency protocol, 50 Hz was similarly effective at significantly (p < 0.05) suppressing several aspects of epileptiform activity (but not for reduction of population-spike amplitude). The data show that these protocols, which had a controlled number of pulses differentially reduced epileptiform activity in our model where increasing the frequency of stimulation did not result in increased attenuation.

Electrical stimulation protocols for hippocampal synaptic plasticity and neuronal hyper-excitability: are they effective or relevant?

Long-term potentiation (LTP) of synaptic transmission is a widely accepted model that attempts to link synaptic plasticity with memory. LTP models are also now used in order to test how a variety of neurological disorders might affect synaptic plasticity. Interestingly, electrical stimulation protocols that induce LTP appear to display different efficiencies and importantly, some may not be as physiologically relevant as others. In spite of advancements in our understanding of these differences, many types of LTP inducing protocols are still widely used. In addition, in some cases electrical stimulation leads to normal biological phenomena, such as putative memory encoding and in other cases electrical stimulation triggers pathological phenomena, such as epileptic seizures. Kindling, a model of epileptogenesis involving repeated electrical stimulation, leads to seizure activity and has also been thought of, and studied as, a form of long-term neural plasticity and memory. Furthermore, some investigators now use electrical stimulation in order to reduce aspects of seizure activity. In this review, we compare in vitro and in vivo electrical stimulation protocols employed in the hippocampal formation that are utilized in models of synaptic plasticity or neuronal hyperexcitability. Here the effectiveness and physiological relevance of these electrical stimulation protocols are examined in situations involving memory encoding (e.g., LTP/LTD) and epileptiform activity.