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1. Athermal lithium niobate microresonator

   https://doi.org/10.1364/OE.398363  

   Ling, Jingwei ; He, Yang ; Luo, Rui ; Li, Mingxiao ; Liang, Hanxiao ; Lin, Qiang ( July 2020 , Optics Express)

   Lithium niobate (LN), possessing wide transparent window, strong electro-optic effect, and large optical nonlinearity, is an ideal material platform for integrated photonics application. Microring resonators are particularly suitable as integrated photonic components, given their flexibility of device engineering and their potential for large-scale integration. However, the susceptibility to temperature fluctuation has become a major challenge for their implementation in a practical environment. Here, we demonstrate an athermal LN microring resonator. By cladding an x-cut LN microring resonator with a thin layer of titanium oxide, we are able to completely eliminate the first-order thermo-optic coefficient (TOC) of cavity resonance right at room temperature (20^°C), leaving only a small residual quadratic temperature dependence with a second-order TOC of only 0.37 pm/K². It corresponds to a temperature-induced resonance wavelength shift within 0.33 nm over a large operating temperature range of (−10 – 50)^°C that is one order of magnitude smaller than a bare LN microring resonator. Moreover, the TiO₂-cladded LN microring resonator is able to preserve high optical quality, with an intrinsic optical Q of 5.8 × 10⁵that is only about 11% smaller than that of a bare LN resonator. The flexibility of thermo-optic engineering, high optical quality, and device fabrication compatibility show great promisemore »of athermal LN/TiO₂hybrid devices for practical applications, elevating the potential importance of LN photonic integrated circuits for future communication, sensing, nonlinear and quantum photonics.

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2. A High-Resolution Opto-Electrophysiology System with a Miniature Integrated Headstage

   Mendrela, A. E ; Kim, K ; English, D ; McKenzie, S ; Seymour, J.P ; Buzsáki, G ; Yoon, E. ( October 2018 , IEEE transactions on biomedical circuits and systems)

   This work presents a fully integrated neural interface system in a small form factor (1.9 g), consisting of a μLED silicon optoelectrode (12 μLEDs and 32 recording sites in a 4-shank configuration), an Intan 32-channel recording chip, and a custom optical stimulation chip for controlling 12 μLEDs. High-resolution optical stimulation with approximately 68.5 nW radiant flux resolution is achieved by a custom LED driver ASIC, which enables individual control of up to 48 channels with a current precision of 1 μA, a maximum current of 1.024 mA, and an update rate of > 10 kHz. Recording is performed by an off-the-shelf 32- channel digitizing front-end ASIC from Intan®. Two compact custom interface PCBs were designed to link the headstage with a PC. The prototype system demonstrates precise current generation, sufficient optical radiant flux generation (𝚽𝒆 > 𝟎. 𝟏𝟔 𝛍𝐖), and fast turn-on of μLEDs (𝒕𝒓𝒊𝒔𝒆 < 𝟏𝟎 𝛍𝐬). Single animal in vivo experiments validated the headstage’s capability to precisely modulate single neuronal activity and independently modulate activities of separate neuronal populations near neighboring optoelectrode shanks.
3. Artifact propagation in electrocorticography stimulation

   Lim, J. ; Wang, P.T. ; Shaw, S.J. ; Armacost, M. ; Gong, H. ; Liu, C.Y. ; Heydari, P. ; Do, A.H. ; Nenadic, Z. ( May 2018 , Seventh International BCI Meeting, Abstract Book)

   Introduction:Current brain-computer interfaces (BCIs) primarily rely on visual feedback. However, visual feedback may not be sufficient for applications such as movement restoration, where somatosensory feedback plays a crucial role. For electrocorticography (ECoG)-based BCIs, somatosensory feedback can be elicited by cortical surface electro-stimulation [1]. However, simultaneous cortical stimulation and recording is challenging due to stimulation artifacts. Depending on the orientation of stimulating electrodes, their distance to the recording site, and the stimulation intensity, these artifacts may overwhelm the neural signals of interest and saturate the recording bioamplifiers, making it impossible to recover the underlying information [2]. To understand how these factors affect artifact propagation, we performed a preliminary characterization of ECoG signals during cortical stimulation.Materials/Methods/ResultsECoG electrodes were implanted in a 39-year old epilepsy patient as shown in Fig. 1. Pairs of adjacent electrodes were stimulated as a part of language cortical mapping. For each stimulating pair, a charge-balanced biphasic square pulse train of current at 50 Hz was delivered for five seconds at 2, 4, 6, 8 and 10 mA. ECoG signals were recorded at 512 Hz. The signals were then high-pass filtered (≥1.5 Hz, zero phase), and the 5-second stimulation epochs were segmented. Within each epoch, artifact-induced peaks were detectedmore »for each electrode, except the stimulating pair, where signals were clipped due to amplifier saturation. These peaks were phase-locked across electrodes and were 20 ms apart, thus matching the pulse train frequency. The response was characterized by calculating the median peak within the 5-second epochs. Fig. 1 shows a representative response of the right temporal grid (RTG), with the stimulation channel at RTG electrodes 14 and 15. It also shows a hypothetical amplifier saturation contour of an implantable, bi-directional, ECoG-based BCI prototype [2], assuming the supply voltage of 2.2 V and a gain of 66 dB. Finally, we quantify the worstcase scenario by calculating the largest distance between the saturation contour and the midpoint of each stimulating channel.Discussion:Our results indicate that artifact propagation follows a dipole potential distribution with the extent of the saturation region (the interior of the white contour) proportional to the stimulation amplitude. In general, the artifacts propagated farthest when a 10 mA current was applied with the saturation regions extending from 17 to 32 mm away from the midpoint of the dipole. Consistent with the electric dipole model, this maximum spread happened along the direction of the dipole moment. An exception occurred at stimulation channel RTG11-16, for which an additional saturation contour emerged away from the dipole contour (not shown), extending the saturation region to 41 mm. Also, the worst-case scenario was observed at 6 mA stimulation amplitude. This departure could be a sign of a nonlinear, switch-like behavior, wherein additional conduction pathways could become engaged in response to sufficiently high stimulation.Significance:While ECoG stimulation is routinely performed in the clinical setting, quantitative studies of the resulting signals are lacking. Our preliminary study demonstrates that stimulation artifacts largely obey dipole distributions, suggesting that the dipole model could be used to predict artifact propagation. Further studies are necessary to ascertain whether these results hold across other subjects and combinations of stimulation/recording grids. Once completed, these studies will reveal practical design constraints for future implantable bi-directional ECoG-based BCIs. These include parameters such as the distances between and relative orientations of the stimulating and recording electrodes, the choice of the stimulating electrodes, the optimal placement of the reference electrode, and the maximum stimulation amplitude. These findings would also have important implications for the design of custom, low-power bioamplifiers for implantable bi-directional ECoG-based BCIs.References:[1] Hiremath, S. V., et al. "Human perception of electrical stimulation on the surface of somatosensory cortex." PloS one 12.5 (2017): e0176020.[2] Rouse, A. G., et al. "A chronic generalized bi-directional brain-machine interface." Journal of Neural Engineering 8.3 (2011): 036018« less
4. Optogenetic feedback control of neural activity

   https://doi.org/10.7554/eLife.07192  

   Newman, Jonathan P ; Fong, Ming-fai ; Millard, Daniel C ; Whitmire, Clarissa J ; Stanley, Garrett B ; Potter, Steve M ( July 2015 , eLife)

   Optogenetic techniques enable precise excitation and inhibition of firing in specified neuronal populations and artifact-free recording of firing activity. Several studies have suggested that optical stimulation provides the precision and dynamic range requisite for closed-loop neuronal control, but no approach yet permits feedback control of neuronal firing. Here we present the ‘optoclamp’, a feedback control technology that provides continuous, real-time adjustments of bidirectional optical stimulation in order to lock spiking activity at specified targets over timescales ranging from seconds to days. We demonstrate how this system can be used to decouple neuronal firing levels from ongoing changes in network excitability due to multi-hour periods of glutamatergic or GABAergic neurotransmission blockade in vitro as well as impinging vibrissal sensory drive in vivo. This technology enables continuous, precise optical control of firing in neuronal populations in order to disentangle causally related variables of circuit activation in a physiologically and ethologically relevant manner.
5. Cellular and molecular responses to acute cocaine treatment in neuronal-like N2a cells: potential mechanism for its resistance in cell death

   https://doi.org/10.1038/s41420-018-0078-x  

   Badisa, Ramesh B. ; Wi, Sungsool ; Jones, Zachary ; Mazzio, Elizabeth ; Zhou, Yi ; Rosenberg, Jens T. ; Latinwo, Lekan M. ; Grant, Samuel C. ; Goodman, Carl B. ( July 2018 , Cell Death Discovery)

   Cocaine is a highly abused drug that causes psychiatric and neurological problems. Its entry into neurons could alter cell-biochemistry and contribute in the manifestation of early pathological symptoms. We have previously shown the acute cocaine effects in rat C6 astroglia-like cells and found that these cells were highly sensitive to cocaine in terms of manifesting certain pathologies known to underlie psychological disorders. The present study was aimed to discern acute cocaine effects on the early onset of various changes in Neuro-2a (N2a) cells. Whole-cell patch-clamp recording of differentiated cells displayed the functional voltage-gated Na⁺and K⁺channels, which demonstrated the neuronal characteristics of the cells. Treatment of these cells with acute cocaine (1 h) at in vivo (nM to μM) and in vitro (mM) concentrations revealed that the cells remained almost 100% viable. Cocaine administration at 6.25 μM or 4 mM doses significantly reduced the inward currents but had no significant effect on outward currents, indicating the Na⁺channel-blocking activity of cocaine. While no morphological change was observed at in vivo doses, treatment at in vitro doses altered the morphology, damaged the neurites, and induced cytoplasmic vacuoles; furthermore, general mitochondrial activity and membrane potential were significantly decreased. Mitochondrial dysfunction enabled the cells switch to anaerobicmore »glycolysis, evidenced by dose-dependent increases in lactate and H₂S, resulting unaltered ATP level in the cells. Further investigation on the mechanism of action unfolded that the cell’s resistance to cocaine was through the activation of nuclear factor E2-related factor-2 (Nrf-2) gene and subsequent increase of antioxidants (glutathione [GSH], catalase and GSH peroxidase [GPx]). The data clearly indicate that the cells employed a detoxifying strategy against cocaine. On a broader perspective, we envision that extrapolating the knowledge of neuronal resistance to central nervous system (CNS) diseases could delay their onset or progression.

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