Short‐term exposure to constant light promotes strong circadian phase‐resetting responses to nonphotic stimuli in Syrian hamsters

Abstract

Behavioral (nonphotic) stimuli can shift circadian rhythms by serotonin (5-HT) and/or neuropeptide Y (NPY) inputs to the suprachiasmatic nucleus (SCN) circadian clock. Based on the idea that behavioral phase resetting is modulated by endogenous changes in postsynaptic sensitivity to such transmitters, hamsters were exposed to constant light (LL; approximately 250 lx) for 1-3 days, which suppresses locomotor activity and eliminates the daily rhythm of SCN 5-HT release measured by microdialysis. Groups subjected to brief LL or maintained under a light/dark cycle (LD) received phase-resetting treatments with the 5-HT(1A,7) agonist (+/-)-2-dipropyl-amino-8-hydroxyl-1,2,3,4-tetrahydronapthalene (8-OH-DPAT) or sleep deprivation (SD). Animals were released to constant darkness at the start of the treatments. Phase advances to 8-OH-DPAT and SD during the day were 11 and 3 h for LL vs. 2 and 1 h for LD, respectively. Phase delays during the night were -12 and -5 h for LL vs. no responses for LD, respectively. Phase-transition curves for both LL treatments had slopes approximating 0, indicative of Type 0 phase resetting. For all treatments, the degree of locomotor suppression by LL was not correlated with the phase shift magnitude. Re-establishing locomotor activity by overnight food deprivation did not prevent potentiated shifting to SD. However, re-establishing peak extracellular 5-HT levels by intra-SCN 5-HT reverse microdialysis perfusion in LL did significantly reduce potentiated 8-OH-DPAT phase advances. Constant light also enhanced intra-SCN NPY-induced phase advances during the day (6 vs. 2 h for LD). These results suggest that LL promotes Type 0 phase resetting by supersensitizing 5-HT and/or NPY postsynaptic responses and possibly by attenuating the amplitude of the circadian pacemaker, thus enhancing circadian clock resetting nonspecifically.

Chronic ethanol intake modulates photic and non-photic circadian phase responses in the Syrian hamster

“…5). Similar responses to other non-photic phase-shifting stimuli have been reported recently in animals pre-exposed to constant light for one or more cycles prior to phase-shift testing (Knoch et al, 2004(Knoch et al, , 2006Landry and Mistlberger, 2005). Thus, these responses may have been related to our decision to delay the onset of darkness from the normal ZT 12 until ZT 21 on the day of treatment in order to facilitate triazolam administration during the night phase of the LD cycle, resulting in exposure to 23 hours of continuous light.…”

“…These responses resemble the so-called "type-0" resetting that has been associated with very strong phase-shifting stimuli and/or with lowamplitude circadian pacemakers (cf., Knoch et al, 2004). In order to use the Aschoff type-II approach -in which potential phase-shift stimuli are delivered near the transition from LD entrainment to a DD free-run (Mistlberger, 1996;Mrosovsky, 1996a) -to test the response to triazolam at ZT 21, it was necessary to either inject the animals in darkness or to extend the light phase of the LD cycle from ZT 12 to ZT 21 on the day of the test.…”

Acute ethanol modulates glutamatergic and serotonergic phase shifts of the mouse circadian clock in vitro

“…Notably, we found further that co-application of either AP5 or L-NAME with ethanol did not produce an additive stimulation of DPAT-induced phase shifts. Serotonergic treatments can generate significantly larger phase shifts than those seen here (Knoch et al, 2004;Medanic and Gillette, 1992), so it is therefore unlikely that the lack of additivity seen in these experiments is attributable to a ceiling effect. Thus, these data are consistent with the conclusion that ethanol inhibits glutamate signaling in the SCN, and this inhibition produces the enhancement of serotonergic phase shifts.…”

Differential effects of constant light on circadian clock resetting by photic and nonphotic stimuli in Syrian hamsters

“…Hence, strong resetting is designated Type 0 and weak resetting is designated Type 1 (Winfree, 1980). Examples of Type 0 resetting in hamsters ,were described earlier (Knoch et a/., 2004). Type 0 resetting has also been observed in humans (Jewett eta/., 1991) as well as invertebrates and plants (Engelmann 8; Johnsson, 1978;Shaw & Brody, 2000;Winfree, 1973).…”

“…In addition, environmental light history, in particular the duration of the photic component of'the LD cycle, has been shown to modulate nonphotic phase shifts (Knoch et a/., 2004;Mistlberger et a/., 2002). Hamsters housed in L1-vs. LD, showed strongly poten~tiated phase advances to sleep deprivation (SD), novel wheel-induced activity, and in,jections of the 5HT1~,7 agonist, &OH-DPAT, during the mid-subjective day.…”