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Updated: Jul 13, 2026

Optogenetic Manipulation of Neural Circuits During Monitoring Sleep/wakefulness States in Mice
Published on: June 19, 2019
[Effect of photostimulation on the wakefulness-sleep cycle in the common frog Rana temporaria]
Abstract:
Effect of daily 30-min photostimulation in the 10 s light: 10 s pause (the total of 5 days) on the time structure of the wakefulness--protosleep cycle (WPC) was studied in the common frog Rana temporaria. Changes were analyzed of EEG wave components in three immobility forms of the type of catalepsy (P-1), catatonia (P-2), and cataplexy (P-3) that form protosleep. The first three photostimulations promoted a gradual increase of the P-1 state to 84.16 +/- 11.6% [the initial value (IV) 22.9 +/- 9.1%] and a decrease of representation of wakefulness to 4.86 +/- 2/1% (IV 13.8 +/- 7.8%), of P-2 to 11.1 +/- 5.3 (IV 53.3 +/- 13.3%), and of P-3 to 2.21 +/- 1.0% (IV 11.1 +/- 5.6%). After 4-5 photostimulations and especially after their complete cessation the percentage of P-1 in the WPC was restored to initial values, whereas the percentage of the frog WPC P-3 considered to be a precursor of the homoiothermal sleep rose to 20 +/- 8.3% after 5 photostimulations and to 38.5 +/- 6.7% the next day. Changes in the frog EEG spectra appeared only after one photostimulation and were characterized by a brief increase of power of alpha-like waves and by inhibition of slow 6-waves. In P-2 the power of the slow delta-waves gradually rose. In P-3 the EEG parameters did not change. In all experimental animals a decrease of the relative thymus and adrenal masses was revealed, which indicates the photostimulation regime used in the work induces stress. The obtained data allow thinking that a certain neurohormonal response to stress has already been formed at the amphibian level and that an important role in this response realization is played by a coordinated interaction of the hypothalamic sleep-regulating system providing protosleep manifestations and of the hypothalamic neurosecretory system triggering the stress-reaction hormonal cascade.
