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If a brain is exposed to an intermittent light source, are specific areas going to fire? If yes, which of them? Is there a experimental data about this effect?

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    $\begingroup$ What do you mean? Cutting open a skull and shining light into it? Why would the brain's cells be able to sense light? Even if they did, how could we possibly answer your question without knowing which areas of the brain you were illuminating? $\endgroup$ – terdon Nov 13 '13 at 19:46
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    $\begingroup$ as @terdon said, just shining light on the brain wont make it sense it (unless of course it is a laser of sorts which causes a lesion :P) . You need photoreceptors for sensing light. In fact I have heard that brain doesnt have mechanoreceptors and nociceptors so someone wont feel that their brain is being cut <read and seen it in the Hannibal (by Thomas Harris): Not a very reliable source, though :P >. $\endgroup$ – WYSIWYG Nov 14 '13 at 11:34
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It is thought that there are no active optical receptors in the brain normally, its possible some effect might show up in the future, it would be minor at best.

Shining light into the brain is standard procedure in optogenetics experiments. A subpopulation of neurons is transformed to express an optical receptor to modulate genetic or signalling properties of the cell.

So the reason I say it would be small effect on a native brain is that these experiments do give good results and are run with controls which do not have the optical receptors added, which typically show no change in brain activity.

optogenetic modulation of activity in a rat prefrontal cortex

Channelrhodopsin-2 (ChR2) induces temporally precise blue light-driven activity in rat prelimbic prefrontal cortical neurons. a) In vitro schematic (left) showing blue light delivery and whole-cell patch-clamp recording of light-evoked activity from a fluorescent CaMKllα::ChR2-EYFP expressing pyramidal neuron (right) in an acute brain slice. b) In vivo schematic (left) showing blue light (473 nm) delivery and single-unit recording. (bottom left) Coronal brain slice showing expression of CaMKllα::ChR2-EYFP in the prelimbic region. Light blue arrow shows tip of the optical fiber; black arrow shows tip of the recording electrode (left). White bar, 100 µm. (bottom right) In vivo light recording of prefrontal cortical neuron in a transduced CaMKllα::ChR2-EYFP rat showing light-evoked spiking to 20 Hz delivery of blue light pulses (right). Inset, representative light-evoked single-unit response.

Image taken from the linked Wikipedia page and originally from Baratta et al..

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Short answer
Illumination of neurons with light of varying wavelengths can activate them, causing them to fire action potentials. It may, however, not be the photons that activate the neurons per se, but the resulting temperature changes.

Background
In contrast to the comments and original answer, it is possible to activate neurons, other than photoreceptors, with light.

Infrared laser light (~2000 nm) has been demonstrated to activate neurons in the periphery, including neurons in the sciatic and facial nerves and the spiral ganglion cells in the cochlea (Thompson et al., 2014). Interestingly, green laser light in the visible spectrum (532 nm) has also been shown to activate neurons (Wenzel et al., 2009). In the brain, laser light has been shown to activate neurons, including the primary visual cortex and somatosensory cortex. Typically, short (intermittent) bursts of stimulation are used, with exposure times in the millisecond range (Thompson et al., 2014).

The underlying mechanism of laser-activation of neurons is debated. The current evidence points to the possibility that focal illumination of neurons with light may increase the temperature of the cell, which may result in changes in membrane capacitance. Changes in membrane capacitance can cause voltage differences. Hence, lasers may induce action potentials by causing heat-induced depolarizations. Further, it is thought that temperature changes affects transmembrane ion channels and TRPV channels that in turn play a modulatory role in the laser-induced activation of neurons. TRPV channels, for example, include the heat-sensing TRPV1 receptor, that is thought to be activated by laser light-induced temperature changes (Thompson et al., 2014).

Why the fuzz about laser-induced neuron activation? Cochlear and retinal implants restore limited auditory and visual function in the deaf and blind, respectively. In both techniques, electrodes are used to activate spiral ganglion cells (in the inner ear) retinal ganglion cells (in the eye). Electric currents have the tendency to spread laterally through the tissue, preventing focused activation of specific localized regions of the cochlea and retina, respectively. Hence, both approaches suffer from channel-channel interactions, leading to crude stimulation profiles and reduced frequency resolution (cochlear implants) and low spatial-resolution (in case of retinal implants). Lasers, on the other hand, can be made into nearly infinitesimally small rays that have minimal scatter compared to electric current spread. Hence, laser-induced activation may be useful for specifically stimulating small populations of neurons in a certain tissue, opening up great possibilities in neural-prosthetics, such as auditory and visual prosthetics (Rettenmeijer, 2014).

References
- Thompson et al., Curr Mol Imaging (2014); 3(2): 162–77
- Rettenmeijer, Biomed Opt Express (2014) 5(4): 1014–25
- Wenzel et al., J Biomed Opt (2009); 14(4): 044007

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