An assessment of ‘turtle-friendly' lights on the sea-finding behaviour of loggerhead turtle hatchlings (Caretta caretta)

Context It is well established that artificial light can disrupt the sea-finding ability of sea turtle hatchlings, and some manufactures are now marketing ‘turtle-friendly’ lights that are supposed to be minimally disruptive to this sea-finding behaviour. However, there have been no studies that have tested whether ‘turtle-friendly’ lights are benign to hatchling sea turtle sea-finding ability. Aims We tested two different types of ‘turtle-friendly’ lights (LED amber-light peak intensity 620 nm and LED red-light peak intensity 640 nm) to see whether they are disruptive to the sea-finding ability of eastern-coast Australian loggerhead turtle hatchlings. Methods Using standard circular-arena experiments, we assessed the directional preference of newly emerged loggerhead turtle hatchlings from the Woongarra Coast of Queensland, Australia, during different moon phases without artificial lighting and in the presence of ‘turtle-friendly’ lights. Key results Contrary to expectations, sea-finding ability of hatchlings was disrupted by the amber lights, particularly in the absence of a moon. The less intense red lights were less disruptive to hatchlings; however, misorientation and disorientation events still occurred when lights were within 4 m of hatchlings. The disruptive impact on sea-finding ability increased with the cumulative impact of multiple lights increasing light intensity. Conclusions The ‘turtle-friendly’ lights we used disrupted the sea-finding ability of eastern-coast Australian loggerhead turtle hatchlings, with the most pronounced disruption occurring under moonless conditions. Implications The use of amber and red LED lights adjacent to the nesting beaches of loggerhead sea turtles should be managed because this lighting has the potential to disrupt the sea-finding ability of sea turtle hatchlings.

Light alters nociceptive effects of magnetic field shielding in mice: intensity and wavelength considerations

Previous experiments with mice have shown that repeated 1 hour daily exposure to an ambient magnetic field-shielded environment induces analgesia (antinociception). The exposures were carried out in the dark (less than 2.0×10 16 photons s −1 m −2 ) during the mid-light phase of the diurnal cycle. However, if the mice were exposed in the presence of visible light (2.0×10 18 photons s −1 m −2 , 400–750 nm), then the analgesic effects of shielding were eliminated. Here, we show that this effect of light is intensity and wavelength dependent. Introduction of red light (peak at 635 nm) had little or no effect, presumably because mice do not have photoreceptors sensitive to red light above 600 nm in their eyes. By contrast, introduction of ultraviolet light (peak at 405 nm) abolished the effect, presumably because mice do have ultraviolet A receptors. Blue light exposures (peak at 465 nm) of different intensities demonstrate that the effect has an intensity threshold of approximately 12% of the blue light in the housing facility, corresponding to 5×10 16 photons s −1 m −2 (integral). This intensity is similar to that associated with photoreceptor-based magnetoreception in birds and in mice stimulates photopic/cone vision. Could the detection mechanism that senses ambient magnetic fields in mice be similar to that in bird navigation?

Voltage-Dependent Calcium Channel CaV1.3 Subunits Regulate the Light Peak of the Electroretinogram

In response to light, the mouse retinal pigment epithelium (RPE) generates a series of slow changes in potential that are referred to as the c-wave, fast oscillation (FO), and light peak (LP) of the electroretinogram (ERG). The LP is generated by a depolarization of the basolateral RPE plasma membrane by the activation of a calcium-sensitive chloride conductance. We have previously shown that the LP is reduced in both mice and rats by nimodipine, which blocks voltage-dependent calcium channels (VDCCs) and is abnormal in lethargic mice, carrying a null mutation in the calcium channel β4 subunit. To define the α1 subunit involved in this process, we examined mice lacking CaV1.3. In comparison with wild-type (WT) control littermates, LPs were reduced in CaV1.3−/− mice. This pattern matched closely with that previously noted in lethargic mice, confirming a role for VDCCs in regulating the signaling pathway that culminates in LP generation. These abnormalities do not reflect a defect in rod photoreceptor activity, which provides the input to the RPE to generate the c-wave, FO, and LP, because ERG a-waves were comparable in WT and CaV1.3−/− littermates. Our results identify CaV1.3 as the principal pore-forming subunit of VDCCs involved in stimulating the ERG LP.

The Light Peak of the Electroretinogram Is Dependent on Voltage-gated Calcium Channels and Antagonized by Bestrophin (Best-1)

Mutations in VMD2, encoding bestrophin (best-1), cause Best vitelliform macular dystrophy (BMD), adult-onset vitelliform macular dystrophy (AVMD), and autosomal dominant vitreoretinochoroidopathy (ADVIRC). BMD is distinguished from AVMD by a diminished electrooculogram light peak (LP) in the absence of changes in the flash electroretinogram. Although the LP is thought to be generated by best-1, we find enhanced LP luminance responsiveness with normal amplitude in Vmd2−/− mice and no differences in cellular Cl− currents in comparison to Vmd2+/+ littermates. The putative Ca2+ sensitivity of best-1, and our recent observation that best-1 alters the kinetics of voltage-dependent Ca2+ channels (VDCC), led us to examine the role of VDCCs in the LP. Nimodipine diminished the LP, leading us to survey VDCC β-subunit mutant mice. Lethargic mice, which harbor a loss of function mutation in the β4 subunit of VDCCs, exhibited a significant shift in LP luminance response, establishing a role for Ca2+ in LP generation. When stimulated with ATP, which increases [Ca++]I, retinal pigment epithelial cells derived from Vmd2−/− mice exhibited a fivefold greater response than Vmd2+/+ littermates, indicating that best-1 can suppress the rise in [Ca2+]I associated with the LP. We conclude that VDCCs regulated by a β4 subunit are required to generate the LP and that best-1 antagonizes the LP luminance response potentially via its ability to modulate VDCC function. Furthermore, we suggest that the loss of vision associated with BMD is not caused by the same pathologic process as the diminished LP, but rather is caused by as yet unidentified effects of best-1 on other cellular processes.

Possibility of using laser spectroscopy for the intraoperative detection of nonfluorescing brain tumors and the boundaries of brain tumor infiltrates

✓The response of nonfluorescing infiltrating tumors that had been exposed to 5–aminolevulinic acid and irradiated using a laser at a wavelength of 405 nm was analyzed intraoperatively using spectroscopy. Histological analyses demonstrated that neoplastic cells were present in the tissue region that displayed a peak at 636 nm, whereas no neoplastic cells were present in the region that exhibited only the excitation light peak. The authors conclude that the intraoperative use of laser spectroscopy can allow the diagnosis of infiltrating tumor and the detection of boundaries of the infiltrate when standard fluorescence techniques fail.