We have observed the propagation of an approximately 35 ns long light pulse with a negative group velocity through a laser-cooled 85Rb atomic medium. The anomalous dispersion results from linear atom-light interaction, and is unrelated to long-lived ground state coherences often associated with fast light in atomic media. The observed negative group velocity (-c/360) in the Rb magneto-optical trap for a pulse attenuated by less than 50% is in good agreement with the value of dispersion measured independently by an RF heterodyne method. The spectral region of anomalous dispersion is between 15 and 40 MHz, which is an order of magnitude wider than that typically associated with ground-state coherences.
Infrared light can be used to modulate the activity of neuronal cells with broad generality and without any need for exogenous materials. The action potential response has been shown to be associated with heating due to the absorption of light by water in and around the illuminated tissues, which gives rise to at least two distinct processes: namely, the temperature pulses cause depolarizing capacitive currents due to an intramembrane thermo-mechanical effect, and in addition, temperature-sensitive TRPV ion channels (and likely, voltage-gated channels) drive additional membrane depolarization. However, substantial differences between the activation threshold of primary auditory neurons (<20 mJ/cm^2) and other neuronal types (>300 mJ/cm^2) in vivo have generated some controversy in the field. A temperature-dependent Hodgkin-Huxley type model, which combines capacitive currents and the experimentally-derived characteristics of voltage-gated potassium and sodium ion channels in primary auditory neurons, was used to accurately explain the in vitro response to 1870 nm infrared illumination. TRPV channels do not make a significant contribution in this case, suggesting that the detailed mechanism of the neuronal response to infrared light is dependent on the specific cell type. Furthermore, based on this detailed understanding of the cell behaviour, it is shown that action potentials cannot be generated at safe laser power levels. This suggests that the previously reported response of the auditory system to infrared stimulation in vivo might arise from a different mechanism, and calls into question the potential usefulness of the effect for auditory prostheses.
A simple interrogation technique is presented which relies on a characteristic specific to saturated fibre Bragg gratings (i.e. gratings where most of the energy at the Bragg wavelength has been reflected prior to the incident light reaching the far end of the grating). In this regime, when the grating is illuminated by a broadband source a change in pitch within a region of the grating will result in the emergence of reflected energy in other spectral regions without significant loss in power from the main Bragg peak. Hence there will be an increase in the overall integrated power reflected from the grating, which is a function of the degree of strain gradient experienced by the grating. This allows the degree of strain gradient to be directly converted to an intensity measurement without the need for an optical filter. Because environmental temperature effects would generally not be localised along the short physical length of the grating, any temperature changes will typically shift the reflection spectrum in the wavelength domain rather than alter the amount of reflected light, which renders the measurement effectively temperature-insensitive. Experimental data is presented demonstrating the application of this sensing approach to the detection of growth of cracks in metallic structures and disbonds in composite repairs. Some of these experiments were carried out during environmental thermal cycling to demonstrate the temperature independence of the measurement technique.
In infrared neural stimulation (INS), laser-evoked thermal transients are used to generate small depolarising currents in neurons. The laser exposure poses a moderate risk of thermal damage to the target neuron. Indeed, exogenous methods of neural stimulation often place the target neurons under stressful non-physiological conditions, which can hinder ordinary neuronal function and hasten cell death. Therefore, quantifying the exposure-dependent probability of neuronal damage is essential for identifying safe operating limits of INS and other interventions for therapeutic and prosthetic use. Using patch-clamp recordings in isolated spiral ganglion neurons, we describe a method for determining the dose-dependent damage probabilities of individual neurons in response to both acute and cumulative infrared exposure parameters based on changes in injection current. The results identify a local thermal damage threshold at approximately 60 ° C, which is in keeping with previous literature and supports the claim that damage during INS is a purely thermal phenomenon. In principle this method can be applied to any potentially injurious stimuli, allowing for the calculation of a wide range of dose-dependent neural damage probabilities. Unlike histological analyses, the technique is well-suited to quantifying gradual neuronal damage, and critical threshold behaviour is not required.
Abstract Objective. Infrared light can be used to modulate the activity of neuronal cells through thermally-evoked capacitive currents and thermosensitive ion channel modulation. The infrared power threshold for action potentials has previously been found to be far lower in the in vivo cochlea when compared with other neuronal targets, implicating spiral ganglion neurons (SGNs) as a potential target for infrared auditory prostheses. However, conflicting experimental evidence suggests that this low threshold may arise from an intermediary mechanism other than direct SGN stimulation, potentially involving residual hair cell activity. Approach. Patch-clamp recordings from cultured SGNs were used to explicitly quantify the capacitive and ion channel currents in an environment devoid of hair cells. Neurons were irradiated by a 1870 nm laser with pulse durations of 0.2–5.0 ms and powers up to 1.5 W. A Hodgkin-Huxley-type model was established by first characterising the voltage dependent currents, and then incorporating laser-evoked currents separated into temperature-dependent and temperature-gradient-dependent components. This model was found to accurately simulate neuronal responses and allowed the results to be extrapolated to stimulation parameter spaces not accessible during this study. Main results. The previously-reported low in vivo SGN stimulation threshold was not observed, and only subthreshold depolarisation was achieved, even at high light exposures. Extrapolating these results with our Hodgkin-Huxley-type model predicts an action potential threshold which does not deviate significantly from other neuronal types. Significance. This suggests that the low-threshold response that is commonly reported in vivo may arise from an alternative mechanism, and calls into question the potential usefulness of the effect for auditory prostheses. The step-wise approach to modelling optically-evoked currents described here may prove useful for analysing a wider range of cell types where capacitive currents and conductance modulation are dominant.
Neural stimulation plays an important role in achieving therapeutic interactions with both the central and peripheral nervous systems, and forms the basis of neural prostheses such as cochlear implants and pacemakers. The interactions are commonly based on electrical stimulation delivered by microelectrodes, which are implanted in the vicinity of the target tissue. Electrical stimulation has limited selectivity, as the resolution of the stimulus is degraded by current spread. Moreover, the implantation may cause injury to the target tissue and the host inflammatory response can reduce stability. In order to improve the performance of neural interfaces, optical stimulation is attracting increasing attention, based on techniques such as optogenetics, photoactive molecules, and infrared neural stimulation. However, optical techniques at present tend to rely on visible or infrared wavelengths that have a limited penetration in tissue. Alternatively, the near-infrared region, corresponding to the therapeutic window in tissue, can be accessed by two-photon stimulation with relatively expensive light sources, or by the introduction of extrinsic light absorbers. For the latter approach, gold nanorods have recently been shown to provide efficient stimulation in a range of cell types, when exposed to near infrared light. Given the wide range of surface functionalizations and relatively low toxicity of gold, this approach is expected to draw increasing interest in the field of neural stimulation. This Method describes experimental procedures that have been used to prepare primary auditory neurons with gold nanorods for near-infrared excitation. It is anticipated that these procedures could be adapted to a range of related neural stimulation studies.
Infrared stimulation offers an alternative to electrical stimulation of neuronal tissue, with potential for direct, non‐contact activation at high spatial resolution. Conventional methods of infrared neural stimulation (INS) rely on transient heating due to the absorption of relatively intense laser beams by water in the tissue. However, the water absorption also limits the depth of penetration of light in tissue. Therefore, the use of a near‐infrared laser at 780 nm to stimulate cultured rat primary auditory neurons that are incubated with silica‐coated gold nanorods (Au NRs) as an extrinsic absorber is investigated. The laser‐induced electrical behavior of the neurons is observed using whole‐cell patch clamp electrophysiology. The nanorod‐treated auditory neurons (NR‐ANs) show a significant increase in electrical activity compared with neurons that are incubated with non‐absorbing silica‐coated gold nanospheres and control neurons with no gold nanoparticles. The laser‐induced heating by the nanorods is confirmed by measuring the transient temperature increase near the surface of the NR‐ANs with an open pipette electrode. These findings demonstrate the potential to improve the efficiency and increase the penetration depth of INS by labeling nerves with Au NRs and then exposing them to infrared wavelengths in the water window of tissue.
It has been demonstrated in recent years that pulsed, infrared laser light can be used to elicit electrical responses in neural tissue, independent of any further modification of the target tissue. Infrared neural stimulation has been reported in a variety of peripheral and sensory neural tissue in vivo, with particular interest shown in stimulation of neurons in the auditory nerve. However, while INS has been shown to work in these settings, the mechanism (or mechanisms) by which infrared light causes neural excitation is currently not well understood. The protocol presented here describes a whole cell patch clamp method designed to facilitate the investigation of infrared neural stimulation in cultured primary auditory neurons. By thoroughly characterizing the response of these cells to infrared laser illumination in vitro under controlled conditions, it may be possible to gain an improved understanding of the fundamental physical and biochemical processes underlying infrared neural stimulation.
'/%3e%3c/defs%3e%3cpath fill='%23012169' d='M0 0h10080v5040H0z'/%3e%3cpath stroke='%23fff' stroke-width='.6' d='m0 0 6 3m0-3L0 3' clip-path='url(%23b)' transform='scale(840)'/%3e%3cpath stroke='%23e4002b' stroke-width='.4' d='m0 0 6 3m0-3L0 3' clip-path='url(%23c)' transform='scale(840)'/%3e%3cpath stroke='%23fff' stroke-width='840' d='M2520 0v2520M0 1260h5040'/%3e%3cpath stroke='%23e4002b' stroke-width='504' d='M2520 0v2520M0 1260h5040'/%3e%3cg fill='%23fff'%3e%3cuse xlink:href='%23d' x='2520' y='3780'/%3e%3cuse xlink:href='%23a' x='7560' y='4200'/%3e%3cuse xlink:href='%23a' x='6300' y='2205'/%3e%3cuse xlink:href='%23a' x='7560' y='840'/%3e%3cuse xlink:href='%23a' x='8680' y='1869'/%3e%3cuse xlink:href='%23e' x='8064' y='2730'/%3e%3c/g%3e%3c/svg%3e)