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Patton, A. P.

Publications and source records attributed to Patton, A. P..

2 recordsLinked to original sources

Magnetic Fields Influence Visual Responses in Mice

Many animals use the Earths magnetic field for the purposes of orientation and navigation, although the sensory mechanisms remain unclear. It has been proposed that retinal responses to light may be modulated by magnetic fields. However, to date, there is no evidence for a retinal response to magnetic fields in mammals. Here we show that magnetic fields affect expression of the neuronal activity marker c-Fos in the mouse retina in a light dependent manner. These retinal responses to magnetic fields are abolished in mice lacking the candidate magnetoreceptor cryptochrome. To characterise the signalling pathways involved, we then used RNAseq and cell-type mapping. We also show that magnetic fields increase exploratory behaviour in a visually dependent task and lengthen the period of the retinal circadian clock. Together, our data provide the first evidence for a mammalian retinal response to magnetic fields at a cellular, molecular and functional level, which may influence vision.

neuroscience↗

Astrocytic control of extra-cellular GABA drives circadian time-keeping in the suprachiasmatic nucleus

The hypothalamic suprachiasmatic nucleus (SCN) is the master mammalian circadian clock. Its cell-autonomous timing mechanism, a transcriptional/translational feedback loop (TTFL), drives daily peaks of neuronal electrical activity. Intercellular signals synchronize and amplify TTFL and electrical rhythms across the circuit. SCN neurons are GABAergic, but the role of GABA in circuit-level time-keeping is unclear. SCN slices expressing the GABA sensor iGABASnFR demonstrate a circadian oscillation of extracellular GABA ([GABA]e) that, counter-intuitively, runs in antiphase to neuronal activity, peaking in circadian night. Resolving this paradox, we found that [GABA]e is regulated by GABA transporters (GATs), uptake peaking during circadian day. This is mediated by the circadian-regulated, astrocytically expressed GAT3 (Slc6a11). Clearance of [GABA]e in circadian day facilitates neuronal firing, neuropeptide release and TTFL rhythmicity. Moreover, genetic complementation demonstrated that the astrocytic TTFL can alone drive [GABA]e rhythms. Thus, astrocytic clocks maintain SCN circadian time-keeping by temporally controlling GABAergic inhibition of SCN neurons.

neuroscience↗