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H Illnerová

Publications and source records attributed to H Illnerová.

14 recordsLinked to original sources
PubMed1992

Entrainment of the rat circadian clock controlling the pineal N-acetyltransferase rhythm depends on photoperiod.

Entrainment of the circadian clock as a function of time when a light stimulus is presented has been studied in detail while little attention has been paid to a role photoperiod may play in the resetting. To find out whether and how photoperiod affects the entrainment, resetting of the rat circadian pacemaker by delays in the evening light offset and by advances in the morning light onset, respectively, was studied in rats maintained either under a short photoperiod, with 8 h of light and 16 h of darkness per day (LD 8:16) or under a long, LD 18:6 photoperiod. To assess phase shifts of the clock, the suprachiasmatic nucleus controlled rhythm in the pineal N-acetyltransferase (NAT), namely the time of the evening NAT rise and the time of the morning decline, were followed. One day after a delay in lights off, on LD 8:16 the NAT rhythm with a normal amplitude was retained following longer delays of the light offset and the maximum phase delay of the NAT rise was 3 times larger than on LD 18:6. One day after an advance in lights on, the NAT decline was phase advanced under both photoperiods; on LD 8:16 the maximum shift was 3 times as large as on LD 18:6. On LD 8:16, the NAT rise was not shifted after shorter advances in lights on and became phase delayed only when the light onset was brought forward to before midnight while on LD 18:6 the NAT rise was phase delayed after any, even a mere 1 h, advance in lights on. The data show that magnitude and direction of phase shifts of the NAT rhythm depend not only on the time of light presentation but on photoperiod as well. Difference in resetting of the rhythm under various photoperiods may reflect photoperiod-dependent changes of an underlying pacemaker.

Acetyltransferases↗
PubMed1992

Human circadian rhythm in serum melatonin in short winter days and in simulated artificial long days.

Serum melatonin rhythm was studied in 6 human subjects experiencing short winter days resembling light/dark (LD) 8:16 h and in 6 subjects exposed at the same time to a long, LD 16:8 h skeleton photoperiod, with 3 h of bright light in the evening and again in the morning; 4 out of the 6 subjects entrained to the simulated summer photoperiod within 3 days. In the synchronized subjects, the nocturnal melatonin signal was 3 h shorter than in those experiencing just winter days. The data indicate that humans are able to respond to environmental day length by forming a proper endogenous photoperiodic signal.

Adult↗
PubMed1992

Resetting of the rat circadian clock after a shift in the light/dark cycle depends on the photoperiod.

Adjustment of the circadian clock to shifts in the light/dark (LD) cycle was assessed from the rat pineal N-acetyltransferase (NAT) rhythm which is controlled by a pacemaker in the suprachiasmatic nucleus of the hypothalamus. Re-entrainment to an 8-h delay in the LD cycle took more than 3 days in rats maintained under a regime with 18 h of light and 6 h of darkness per day (LD 18:6) whereas it was completed within 3 days in those maintained under LD 12:12. Re-entrainment to an advance in the LD cycle proceeded through a transient diminution or almost disappearance of the NAT rhythm amplitude following a 5-h, 3-h and even a mere 2-h advance shift under LD 18:6, whereas no such diminution occurred under LD 12:12 even after a 5-h advance shift. Altogether, the data indicate that resetting of the circadian clock after shifts in the LD cycle depends on the photoperiod.

Animals↗
PubMed1992

Entrainment of the circadian rhythm in the rat pineal N-acetyltransferase activity by melatonin is photoperiod dependent.

Entraining effect of melatonin on the circadian rhythm in rat pineal N-acetyltransferase (NAT) activity was studied under various photoperiods. Melatonin administration prior to dark onset for 5 successive days phase-advanced the evening NAT rise under the light:dark (LD) cycle of either LD 10:14 or LD 8:16, but not under LD 12:12. It is assumed that under the latter regime, the end of a light period exhibited a phase-delaying effect on the NAT rise. The light exposure appeared to be a stronger Zeitgeber than melatonin itself. Data show that melatonin applied in the late light period advances the evening NAT rise under a short photoperiod only; under a longer photoperiod, the phase-advancing effect of melatonin may conflict with a phase-delaying effect of the end of a light period, and the effect of light exposure overrides that of melatonin.

Animals↗
PubMed1992

Resetting of the mammalian circadian clock through lowering of the amplitude: rat pineal N-acetyltransferase rhythm as a model.

During resetting of the mammalian circadian clock, not only phase of the clock is shifted, but amplitude of overt rhythms driven by the clock may be temporarily reduced or even abolished. The present paper is aimed to elucidate the mechanism of amplitude reduction of the overt circadian rhythm in the rat pineal N-acetyltransferase (NAT). The rhythm has two phase markers, namely the time of the evening NAT rise and that of the morning decline. When the phase relationship between both markers is compressed drastically, the NAT rise may occur just close to or at the time of the decline and consequently the NAT rhythm with a full amplitude cannot be expressed. Such a compression may occur in two ways: either animals are subjected to a considerable advance in the light onset which phase advances the morning NAT decline and at the same time phase delays the evening NAT rise, or they are subjected to a considerable delay in the light offset, which primarily phase delays more the NAT rise than the decline. While in the former case the phase markers move in opposite directions, in the latter case they move in the same direction, but to a different extent. The data suggest a complex structure of the underlying clock.

Animals↗
PubMed1976

Effect of dihydroxyphenylalanine, imipramine and coffeine on the light induced decrease in nocturnal serotonin N-acetyltransferase in the rat pineal gland.

The s.c. administration of 150mg L-dihydroxphyenylalaine/kg b.w. 15 min before the decapitation prevents the light induced decrease in nocturnal serotonin N-acetyltransferase activity in the rat pineal gland. The s.c. administration of 50mg imipramine/kg b.w., resp. 100mg/kg b.w., 15 min before the decapitation, slows down, or prevents the light induced fall in the activity. The maintenance of a sufficient level of active norepinephrine on beta-receptors, either by displacement of norepinephrine in the nerve endings by dopamine, or by the inhibition of norepinephrine reuptake by imipramine, thus slows down or prevents the decrease in serotonin N-acetyltransferase activity after exposure to light during the night. The i.p. administration of a phosphodiesterase inhibitor coffeine citrate in a dose 200mg/kg 90 min after switching off the light for the night stimulated serotonin N-acetyltransferase activity 270 min after the light and been switched off, but did not influence the abrupt decrease induced in nocturnal activity by exposure to light.

Acetyltransferases↗