Magnetic Fields Modulate Blue-Light-Dependent Regulation of Neuronal Firing by Cryptochrome
← Research streamIn electrophysiological recordings from Drosophila larval motoneurons with ectopic cryptochrome expression, blue-light-dependent depolarization and increased input resistance were markedly potentiated by an applied magnetic field (100 mT). This potentiation w…
Study snapshot
Abstract
Magnetic Fields Modulate Blue-Light-Dependent Regulation of Neuronal Firing by Cryptochrome Giachello CN, Scrutton NS, Jones AR, Baines RA. Magnetic Fields Modulate Blue-Light-Dependent Regulation of Neuronal Firing by Cryptochrome. J Neurosci. 2016 Oct 19;36(42):10742-10749. ncbi.nlm.nih.gov Abstract Many animals are able to sense the Earth's geomagnetic field to enable behaviors such as migration. It is proposed that the magnitude and direction of the geomagnetic field modulates the activity of cryptochrome (CRY) by influencing photochemical radical pair intermediates within the protein. However, this proposal will remain theoretical until a CRY-dependent effect on a receptor neuron is shown to be modified by an external magnetic field (MF). It is established that blue-light (BL) photoactivation of CRY is sufficient to depolarize and activate Drosophila neurons. Here, we show that this CRY-dependent effect is significantly potentiated in the presence of an applied MF (100 mT). We use electrophysiological recordings from larval identified motoneurons, in which CRY is ectopically expressed, to show that BL-dependent depolarization of membrane potential and increased input resistance are markedly potentiated by an MF. Analysis of membrane excitability shows that these effects of MF exposure evoke increased action potential firing. Almost nothing is known about the mechanism by which a magnetically induced change in CRY activity might produce a behavioral response. We further report that specific structural changes to the protein alter the impact of the MF in ways that are strikingly similar to those from recent behavioral studies into the magnetic sense of Drosophila These observations provide the first direct experimental evidence to support the hypothesis that MF modulation of CRY activity is capable of influencing neuron activity to allow animal magnetoreception. SIGNIFICANCE STATEMENT: The biophysical mechanism of animal magnetoreception is still unclear. The photoreceptor protein cryptochrome has risen to prominence as a candidate magnetoreceptor molecule based on multiple reports derived from behavioral studies. However, the role of cryptochrome as a magnetoreceptor remains controversial primarily because of a lack of direct experimental evidence linking magnetic field (MF) exposure to a change in neuronal activity. Here, we show that exposure to an MF (100 mT) is sufficient to potentiate the ability of light-activated cryptochrome to increase neuronal action potential firing. Our results provide critical missing evidence to show that the activity of cryptochrome is sensitive to an external MF that is capable of modifying animal behavior.
AI evidence extraction
Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.
Main findings
In electrophysiological recordings from Drosophila larval motoneurons with ectopic cryptochrome expression, blue-light-dependent depolarization and increased input resistance were markedly potentiated by an applied magnetic field (100 mT). This potentiation was associated with increased action potential firing, and specific cryptochrome structural changes altered the magnetic-field impact.
Outcomes measured
- Blue-light-dependent depolarization of membrane potential
- Input resistance
- Membrane excitability
- Action potential firing rate
- Cryptochrome structural changes affecting magnetic-field impact
Limitations
- Sample size not reported in the provided abstract/metadata
- Exposure duration and magnetic-field frequency characteristics not specified (only field strength given)
- Findings are in an animal/invertebrate neuronal preparation with ectopic cryptochrome expression, which may limit generalizability
View raw extracted JSON
{
"study_type": "animal",
"exposure": {
"band": "ELF",
"source": "applied magnetic field",
"frequency_mhz": null,
"sar_wkg": null,
"duration": null
},
"population": "Drosophila (larval identified motoneurons; cryptochrome ectopically expressed)",
"sample_size": null,
"outcomes": [
"Blue-light-dependent depolarization of membrane potential",
"Input resistance",
"Membrane excitability",
"Action potential firing rate",
"Cryptochrome structural changes affecting magnetic-field impact"
],
"main_findings": "In electrophysiological recordings from Drosophila larval motoneurons with ectopic cryptochrome expression, blue-light-dependent depolarization and increased input resistance were markedly potentiated by an applied magnetic field (100 mT). This potentiation was associated with increased action potential firing, and specific cryptochrome structural changes altered the magnetic-field impact.",
"effect_direction": "mixed",
"limitations": [
"Sample size not reported in the provided abstract/metadata",
"Exposure duration and magnetic-field frequency characteristics not specified (only field strength given)",
"Findings are in an animal/invertebrate neuronal preparation with ectopic cryptochrome expression, which may limit generalizability"
],
"evidence_strength": "low",
"confidence": 0.74,
"peer_reviewed_likely": "yes",
"keywords": [
"magnetic field",
"100 mT",
"blue light",
"cryptochrome",
"Drosophila",
"motoneuron",
"electrophysiology",
"membrane potential",
"input resistance",
"action potential firing",
"magnetoreception",
"radical pair"
],
"suggested_hubs": [
{
"slug": "mechanisms-cryptochrome-magnetoreception",
"weight": 0.9,
"reason": "Study tests magnetic-field modulation of cryptochrome-dependent neuronal firing relevant to magnetoreception mechanisms."
}
]
}AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.
Identifiers and source
DOI: Not supplied
PubMed: Not supplied
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