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Blue led

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The Blue LED is a light-emitting diode that emits light in the blue region of the visible spectrum. It has a peak wavelength of approximately 450-475 nanometers. The Blue LED is a basic semiconductor device that converts electrical energy into blue light through the process of electroluminescence.

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Lab products found in correlation

Bx51wi, by Olympus (2 mentions) Axopatch 200b amplifier, by Molecular Devices (2 mentions) Optic fiber, by Thorlabs (1 mentions) Pm100d optical power meter, by Thorlabs (1 mentions) S120vc photodiode power sensor, by Thorlabs (1 mentions) Clampfit 10, by Molecular Devices (1 mentions) Pm100d, by Thorlabs (1 mentions) 0.3 na objective, by Olympus (1 mentions) Blue led, by Doric (1 mentions)

10 protocols using blue led

1

Wide-field and Two-photon Imaging of Mouse Whisker Cortex

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Wide-field epifluorescence imaging was used to identify the area of activation in response to whisker stimulation. The mouse was head-fixed. An objective lens (either 4× magnification, 0.10 NA, 18.5 mm WD, Olympus, or 16×, 0.80 NA, 3.0 mm WD, Nikon) was placed over the cranial window and the cortical surface was illuminated with a blue LED (470 nm, Thorlabs). Fluorescence signal was collected with a CCD camera (QIMAGING) at 168 ms per frame and 310 pixels/mm (4×) or 1120 pixels/mm (16×). The field of view was ∼2.24 × 1.67 mm for 4× and 621 × 464 μm for 16×.
Two-photon calcium imaging was used to record individual cell activity in L2/3. A 16× lens was placed over the cranial window and water was filled in between. A 920 nm laser (Spectra-Physics) was used to excite the GCamp (∼15 mW) and the fluorescence signal was collected with a photomultiplier tube (H7422A-40, Hamamatsu) at 1.18 s per frame at 786 pixels/mm (Prairie View, Bruker Imaging). The field of view was ∼651 × 651 μm.
Zheng H.J., Meagher J.P., Xu D., Patel Y.A., O’Connor D.H, & Kwon H.B. (2021). Environmental Enrichment Sharpens Sensory Acuity by Enhancing Information Coding in Barrel Cortex and Premotor Cortex. eNeuro, 8(3), ENEURO.0309-20.2021.
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2

Optogenetic Probing of Visual Cortex

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Visual stimuli were generated by a custom-written Matlab software provided by M. Caudill, and displayed on a gamma-corrected LCD monitor (Dell, 48 × 30 cm, 60-Hz refresh rate, mean luminance 50 cd m−2) positioned 15 cm from the eye contralateral to the craniotomy. Full-field sinusoidal drifting gratings (50% and 100% contrast, spatial frequency of 0.04 and 0.08 cycles per degree, temporal frequency of 1 and 4 Hz) were displayed at 2 orthogonal orientations (0° and 90°) for 1.5 s, preceded and followed by the presentation of a grey screen of mean luminance for 1.5 s and 5 s, respectively.
To photostimulate iChloC, a blue LED (470 nm, Thorlabs) was coupled to a fiber optic (1.0 mm diameter, Thorlabs) placed over V1. The light was presented at 15 mW (corresponds to 19 mW/mm2 at the fiber tip) in pulses of 5 ms, 10 ms, 50 ms and 100 ms duration. Trials with visual stimulus only were interleaved with trials with visual stimulus and iChloC photoactivation.
Wietek J., Beltramo R., Scanziani M., Hegemann P., Oertner T.G, & Simon Wiegert J. (2015). An improved chloride-conducting channelrhodopsin for light-induced inhibition of neuronal activity in vivo. Scientific Reports, 5, 14807.
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3

Optogenetic Manipulation of VP Neurons

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VP neurons were visualized with a 40× water-immersion objective on an upright fluorescent microscope (BX51WI, Olympus, USA) equipped with gradient contrast infrared optics. Whole-cell voltage clamp recordingswere madefrom dorsal lateral VP neurons using an Axopatch-200B amplifier (Molecular Devices). GABA-A IPSCs were recorded with patch pipettes (2.0–3.5 MΩ) filled with an internal solution containing the following (in mM): 57.5 KCl, 57.5 K-methylsulfate, 20 NaCl, 1.5 MgCl2, 5 HEPES, 10 BAPTA, 2 ATP, 0.2 GTP, and 10 phosphocreatine, pH 7.35, 290 mOsM. To isolate GABA-A currents, excitatory synaptic blockers, NBQX (5 mM) and 3-((R)-2-carboxypi- perazin-4-yl)-propyl-1-phosphonic acid (CPP 5 mM) were added to the aCSF. All neurons were voltage clamped at —60 mV. Series resistance was monitored throughout the experiment (range, 3–15 MU). GABA-A IPSCs were evoked byapaired light stimulation (2 stimuli at 20 Hz; every30 s).A fiber optic (200 mm/0.22 NA) connected to a blue LED (470 nm; Thorlabs) was placed near the recording, and light stimulation (0.2–2 ms) was given to evoke GABA-A IPSCs. Data were acquired using pClamp 10 software, sampled at 50 kHz, and filtered at 1 kHz. Analysis was performed with AxoGraphX (Axograph Scientific). The peak amplitude of GABA-A IPSCs were averaged over the last 3 min of drug application and normalized to the average 5 min before drug application.
Matsui A, & Alvarez V.A. (2018). Cocaine Inhibition of Synaptic Transmission in the Ventral Pallidum Is Pathway-Specific and Mediated by Serotonin. Cell reports, 23(13), 3852-3863.
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4

Optogenetic Cardiac Defibrillation Protocol

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We employed local and global illumination to stimulate the heart, whereby only global illumination was used for cardioversion. Local illumination was achieved by positioning the tip of an optical fiber of ⌀ = 400 μm in contact with the left ventricle. On the other hand, in order to achieve a consistent optogenetic stimulation of the whole heart surface and therewith global illumination, the hearts were vertically arranged surrounded by three blue-light emitting diodes (blue-LED, Thorlabs) with their wavelengths centered at 460 nm and limited by a 470 ± 20 nm bandpass filter (ET470/40x, Chroma) (see Figure 1). Synchronous millisecond control of LED at different intensities was conducted via a function generator (Arbitrary Function Generator A2230, Agilent Instruments). Intensity measurements were done using the PM100D optical power meter and the S120VC photodiode power sensor (Thorlabs). Since the experimental setup consists of three blue-LED spaced at 120°, the intensity was measured directly facing each LED from the heart position and the calculated mean was considered the overall light intensity during global illumination.
To minimize effects of potential edema as well as metabolic changes during repeated arrhythmia periods on the defibrillation success rate, we limited the experimental time to 2 h and a maximum number of defibrillation attempts of 50.
Quiñonez Uribe R.A., Luther S., Diaz-Maue L, & Richter C. (2018). Energy-Reduced Arrhythmia Termination Using Global Photostimulation in Optogenetic Murine Hearts. Frontiers in Physiology, 9, 1651.
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5

Optogenetic Manipulation of VP Neurons

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VP neurons were visualized with a 40× water-immersion objective on an upright fluorescent microscope (BX51WI, Olympus, USA) equipped with gradient contrast infrared optics. Whole-cell voltage clamp recordingswere madefrom dorsal lateral VP neurons using an Axopatch-200B amplifier (Molecular Devices). GABA-A IPSCs were recorded with patch pipettes (2.0–3.5 MΩ) filled with an internal solution containing the following (in mM): 57.5 KCl, 57.5 K-methylsulfate, 20 NaCl, 1.5 MgCl2, 5 HEPES, 10 BAPTA, 2 ATP, 0.2 GTP, and 10 phosphocreatine, pH 7.35, 290 mOsM. To isolate GABA-A currents, excitatory synaptic blockers, NBQX (5 mM) and 3-((R)-2-carboxypi- perazin-4-yl)-propyl-1-phosphonic acid (CPP 5 mM) were added to the aCSF. All neurons were voltage clamped at —60 mV. Series resistance was monitored throughout the experiment (range, 3–15 MU). GABA-A IPSCs were evoked byapaired light stimulation (2 stimuli at 20 Hz; every30 s).A fiber optic (200 mm/0.22 NA) connected to a blue LED (470 nm; Thorlabs) was placed near the recording, and light stimulation (0.2–2 ms) was given to evoke GABA-A IPSCs. Data were acquired using pClamp 10 software, sampled at 50 kHz, and filtered at 1 kHz. Analysis was performed with AxoGraphX (Axograph Scientific). The peak amplitude of GABA-A IPSCs were averaged over the last 3 min of drug application and normalized to the average 5 min before drug application.
Matsui A, & Alvarez V.A. (2018). Cocaine Inhibition of Synaptic Transmission in the Ventral Pallidum Is Pathway-Specific and Mediated by Serotonin. Cell reports, 23(13), 3852-3863.
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6

Optogenetic Stimulation Mapping Protocol

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The optics were designed to minimize the spread of the laser in the x, y dimensions of the focal plane while accentuating the focus in z by underfilling the back aperture of the objective. Stimulation intensity was controlled by pulse duration (0.2–1 ms). Stimulation typically consisted of 9 × 9 and 10 × 14 maps of stimulation sites with independent stimuli being delivered in a pseudo-random (non-neighbor) sequence at an interstimulus interval of ≥150 ms and values reflect the average of 3–4 repetitions of the mapping experiment for each cell. Stimulation strength was modulated by gating the laser at maximal power (473 nm, AixiZ or 488 nm, BlueSky Research) with varying durations using timing signals from an external pulse controller (PrairieView software) and the internal power modulation circuitry of the laser or an external Pockels cell (Conoptics) with indistinguishable results. Wide-field activation of ChR2 was accomplished using blue LED (470 nm, ThorLabs) transmitted through the fluorescence light path of the BX51 microscope. LED intensity and timing were controlled through a variable current source (ThorLabs). Stimulus families (input/output curves) were delivered in a pseudorandom order and repeated 3–10 times per cell.
Brown J., Pan W.X, & Dudman J.T. (2014). The inhibitory microcircuit of the substantia nigra provides feedback gain control of the basal ganglia output. eLife, 3, e02397.
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7

Optogenetic Monitoring of Norepinephrine Release

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Carbon fiber microelectrodes (CFME, 75 μm in length) were lowered into 300 μM coronal slices and placed where the densest ChR2-eYFP expression was observed (CeA/BLA border) ThIRES-Cre::LC-BLA:ChR2 mice. To detect NE, the CFME was ramped from −0.4 V to 1.3 V versus a Ag/AgCl reference electrode (in the bath) at a rate of 400 V/s at 10 Hz. Slices were stimulated with 30 pulses of a blue LED (Thorlabs, 473 nm, 5 ms pulse width, 1 mW) via a 40X objective at 10 Hz every 5 min to release NE. Electrochemical data was collected and analyzed using a combination of Tar Heel CV (ESA, Chelmsford, MA) (Robinson and Wightman, 2007 ), HDCV (http://www.chem.unc.edu/facilities/electronics_software.html) (Bucher et al., 2013 (link)), and Labview (RRID:SCR_014325). Following collection, background subtracted cyclic voltammograms (CVs) were smoothed one time with a Fast Fourier Transformation (Bucher et al., 2013 (link)). CVs had characteristic oxidation and reduction peaks coinciding with catecholamine detection (ox: 600–700 mV red: −200–300 mV). Oxidative currents were analyzed at the peak of the oxidative potential for individual experiments. Clearance half-life (t1/2) was measured in Clampfit 10.2 (Molecular devices) as previously described (McElligott et al., 2013 (link)).
McCall J.G., Siuda E.R., Bhatti D.L., Lawson L.A., McElligott Z.A., Stuber G.D, & Bruchas M.R. (2017). Locus coeruleus to basolateral amygdala noradrenergic projections promote anxiety-like behavior. eLife, 6, e18247.
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8

Optogenetic Activation of SOM in V1

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ChR2-expressing SOM were activated via an optical fiber (core = 960 μm/ NA = 0.63) coupled to a blue LED (470 nm; Thorlabs) and placed above V1 such as to illuminate the entire surface of V1 (Power: 5-6 mW measured at the fiber tip). LED power was measured before each experiment with a digital power meter (PM100D, Thorlabs). The photo-tagging of the cells was performed before and after the block of head rotation trials.
Bouvier G., Senzai Y, & Scanziani M. (2020). Head movements Control the Activity of Primary Visual Cortex in a Luminance Dependent Manner. Neuron, 108(3), 500-511.e5.
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9

Optogenetic Glutamate Release in Prefrontal Cortex

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Glutamate release was triggered by activating channelrhodopsin-2 (ChR2) present in the presynaptic terminals of rBLA or cBLA inputs to the PFC (Little and Carter, 2012 (link); McGarry and Carter, 2016 (link)). ChR2 was activated with 2ms pulses of 473 nm light from a blue LED (473 nm; Thorlabs) through a 10 × 0.3 NA objective (Olympus) with a power range of 0.4–12 mW. LED power was adjusted until responses >100 pA were seen in at least one neuron in a recorded pair or triplet, with the same power used for all neurons in the slice. In some experiments, ChR2 was activated by 20-Hz stimulation with 2-ms pulses of light. Subcellular targeting recordings utilized a digital mirror device (Mightex Polygon 400 G) to stimulate a 10 × 10 grid of 75 µm squares at a power range of 0.05–0.2 mW per square at 1 Hz, with the first row aligned to the pia. For all other recordings, the objective was centered over the soma, unless noted otherwise. Intertrial interval was 10 s except for experiments involving trains of stimulation, in which it was 30 s.
Manoocheri K, & Carter A.G. (2022). Rostral and caudal basolateral amygdala engage distinct circuits in the prelimbic and infralimbic prefrontal cortex. eLife, 11, e82688.
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10

Optogenetic Silencing of Visual Cortex

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Visual cortex was silenced by illuminating the V1 craniotomy with a 1mm fiber optic coupled to a blue LED (470 nm; 20 mW total output, Doric) positioned several mm above the craniotomy or through the objective (20x) of a fluorescence microscope with a blue LED (470 nm, 2.3 mW total output, Thorlabs) coupled to the excitation port. The LED turned on 650 ms prior to the onset of a visual stimulus trial and lasted throughout the duration of the visual stimulus. Trials with cortical silencing were interleaved with trials without illumination in which cortical activity was intact. To validate the effectiveness of cortical silencing, spiking responses of V1 neurons in response to drifting gratings were recorded using loose-
Lien A.D, & Scanziani M. (2018). Cortical direction selectivity emerges at convergence of thalamic synapses. Nature, 558(7708).
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