Stimulation of Melatonin Receptors Decreases Calcium Levels in Xenopus Tectal Cells by Activating GABAC Receptors

2005 ◽  
Vol 94 (2) ◽  
pp. 968-978 ◽  
Author(s):  
Claudia Prada ◽  
Susan B. Udin ◽  
Allan F. Wiechmann ◽  
Irina V. Zhdanova

To investigate the physiological effects of melatonin receptors in the Xenopus tectum, we have used the fluorescent indicator Fluo-4 AM to monitor calcium dynamics of cells in tectal slices. Bath application of KCl elicited fluorescence increases that were reduced by melatonin. This effect was stronger at the end of the light period than at the end of the dark period. Melatonin increased γ-aminobutyric acid-C (GABAC)–receptor activity, as demonstrated by the ability of the GABAC-receptor antagonists, picrotoxin and TPMPA, to abolish the effects of melatonin. In contrast, neither the GABAA-receptor antagonist bicuculline nor the GABAB-receptor antagonist CGP 35348 diminished the effects of melatonin. RT-PCR analyses revealed expression of the 3 known melatonin receptors, MT1 (Mel1a), MT2 (Mel1b), and Mel1c. Because the effect of melatonin on tectal calcium increases was antagonized by an MT2-selective antagonist, 4-P-PDOT, we performed Western blot analyses with an antibody to the MT2 receptor; the data indicate that the MT2 receptor is expressed primarily as a dimeric complex and is glycosylated. The receptor is present in higher amounts at the end of the light period than at the end of the dark period, in a pattern complementary to the changes in melatonin levels, which are higher during the night than during the day. These results imply that melatonin, acting by MT2 receptors, modulates GABAC receptor activity in the optic tectum and that this effect is influenced by the light–dark cycle.

1982 ◽  
Vol 16 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Burghart Jilge

The circadian caecotrophy rhythm was synchronized with the light-dark cycle of 12 : 12 h. During this the rabbits practised caecotrophy regularly during the light period. While most rabbits manifested 1 caecotrophy per 24 h (monophasic caecotrophy), some had an additional caecotrophy during the dark period (diphasic caecotrophy). During continuous light the circadian caecotrophy rhythm ran free monophasically, even in those rabbits which were diphasic under the preceding 12 : 12 regime. The average period length amounted to 24·7 ± 0·3 h. Following restoration of the 12 : 12 routine animals reestablished their original caecotrophy pattern. In a further test the caecotrophy pattern remained constant during a constant 12 : 12 regimen, but changed in 7 of 16 animals when the photoperiod was reduced first to 60 min and then to 2 × 60 min light every 24 h. The reduction of the lit time resulted in an increased occurrence of diphasic animals. Details of synchronization of the caecotrophy rhythm with the different light-dark schedules are given. These results accord with data obtained in nocturnal rodent species.


Holzforschung ◽  
2003 ◽  
Vol 57 (6) ◽  
pp. 567-573 ◽  
Author(s):  
Y. Hosoo ◽  
M. Yoshida ◽  
T. Imai ◽  
T. Okuyama

Summary This paper describes the effect of light on the diurnal change in the innermost surface of developing secondary walls. Cryptomeria japonica D. Don saplings were grown in two growth chambers, in which temperature and relative humidity were kept constant and the light-dark phase of the photoperiod varied. One chamber reproduced the natural light-dark phase, while the other reversed it. Samples of differentiating xylem were collected during the dark period when the tangential strain, used as an index of volumetric changes in differentiating cells, was high, and during the light period when the tangential strain was low. The innermost surface of developing secondary walls in differentiating tracheids was observed by field emission scanning electron microscopy. In the specimens collected during the dark period, amorphous material was observed and the cell wall surface was immunogold-labeled with an anti-glucomannan antiserum. In the specimens collected during the light period, cellulose microfibrils were clearly evident, and amorphous material and immunogold labeling were rarely observed. These results demonstrate that the diurnal changes in the innermost surface of developing secondary walls correspond to the light-dark cycle over 24 h.


2015 ◽  
Vol 112 (48) ◽  
pp. E6691-E6698 ◽  
Author(s):  
Atish Mukherji ◽  
Ahmad Kobiita ◽  
Manohar Damara ◽  
Nisha Misra ◽  
Hamid Meziane ◽  
...  

The light-entrained master central circadian clock (CC) located in the suprachiasmatic nucleus (SCN) not only controls the diurnal alternance of the active phase (the light period of the human light-dark cycle, but the mouse dark period) and the rest phase (the human dark period, but the mouse light period), but also synchronizes the ubiquitous peripheral CCs (PCCs) with these phases to maintain homeostasis. We recently elucidated in mice the molecular signals through which metabolic alterations induced on an unusual feeding schedule, taking place during the rest phase [i.e., restricted feeding (RF)], creates a 12-h PCC shift. Importantly, a previous study showed that the SCN CC is unaltered during RF, which creates a misalignment between the RF-shifted PCCs and the SCN CC-controlled phases of activity and rest. However, the molecular basis of SCN CC insensitivity to RF and its possible pathological consequences are mostly unknown. Here we deciphered, at the molecular level, how RF creates this misalignment. We demonstrate that the PPARα and glucagon receptors, the two instrumental transducers in the RF-induced shift of PCCs, are not expressed in the SCN, thereby preventing on RF a shift of the master SCN CC and creating the misalignment. Most importantly, this RF-induced misalignment leads to a misexpression (with respect to their normal physiological phase of expression) of numerous CC-controlled homeostatic genes, which in the long term generates in RF mice a number of metabolic pathologies including diabetes, obesity, and metabolic syndrome, which have been reported in humans engaged in shift work schedules.


2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Chiung-Hsiang Cheng ◽  
Pei-Lu Yi ◽  
Jaung-Geng Lin ◽  
Fang-Chia Chang

Electroacupuncture (EA) possesses various therapeutic effects, including alleviation of pain, reduction of inflammation and improvement of sleep disturbance. The mechanisms of EA on sleep improvement, however, remain to be determined. It has been stated in ancient Chinese literature that the Anmian (EX17) acupoint is one of the trigger points that alleviates insomnia. We previously demonstrated that EA stimulation of Anmian acupoints in rats during the dark period enhances non-rapid eye movement (NREM) sleep, which involves the induction of cholinergic activity in the nucleus tractus solitarius (NTS). In addition to cholinergic activation of the NTS, activation of the endogenous opioidergic system may also be a mechanism by which acupuncture affects sleep. Therefore, this study was designed to investigate the involvement of the NTS opioidergic system in EA-induced alterations in sleep. Our present results indicate that EA of Anmian acupoints increased NREM sleep, but not rapid eye movement sleep, during the dark period in rats. This enhancement in NREM sleep was dose-dependently blocked by microinjection of opioid receptor antagonist, naloxone, and theμ-opioid receptor antagonist, naloxonazine, into the NTS; administrations ofδ-receptor antagonist, natrindole, and theκ-receptor antagonist,nor-binaltrophimine, however, did not affect EA-induced alterations in sleep. Furthermore,β-endorphin was significantly increased in both the brainstem and hippocampus after the EA stimuli, an effect blocked by administration of the muscarinic antagonist scopolamine into the NTS. Our findings suggest that mechanisms of EA-induced NREM sleep enhancement may be mediated, in part, by cholinergic activation, stimulation of the opiodergic neurons to increase the concentrations ofβ-endorphin and the involvement of theμ-opioid receptors.


2010 ◽  
pp. 581-590
Author(s):  
T Wu ◽  
Y Ni ◽  
F Zhuge ◽  
Z Fu

To investigate the effect of light cue on the resetting of the peripheral clocks, we examined the resetting processes of clock genes (Per1, Per2, Bmal1, Cry1, Dec1, and Rev-erbα) in the liver and heart of rats after the feeding and light-dark (LD) reversal via a 24-h light period transition. The liver clock was reset quickly within 3 days, while the heart clock needed a longer time course of 5-7 days to be completely re-entrained. Moreover, the reentrainment of Per1 and Per2 in the liver clock was more rapid than that of the other four clock genes, suggesting the important role of these two clock genes in initiating the circadian resetting of the hepatic clock. However, the resetting rates of these two clock genes were as similar as the others in the heart clock. Therefore, the resetting mechanisms underlining these two peripheral clocks may be totally distinct. Furthermore, the reentrainment of the liver and heart clocks were relatively lengthened after the feeding and LD reversal via a light period transition compared to a dark period transition, suggesting a simultaneous shift of feeding schedule and the LD cycle may facilitate the circadian resetting in rats.


1998 ◽  
Vol 275 (3) ◽  
pp. R793-R802 ◽  
Author(s):  
Fang-Chia Chang ◽  
Mark R. Opp

We have previously hypothesized that corticotropin-releasing hormone (CRH) is involved in the regulation of physiological waking. To further elucidate this role for CRH, we administered intracerebroventricularly into rats two specific CRH-receptor antagonists, α-helical CRH-(9—41) (α-hCRH) or astressin, and determined changes in electroencephalogram-defined waking and sleep. Our results indicate that both of these receptor antagonists reduce the amount of time spent awake in a dose-related manner when administered before the dark period of the light-dark cycle. However, the time courses for these effects differ between antagonists; effective doses of α-hCRH reduce waking during the first 2 h postinjection, whereas effective doses of astressin reduce waking during postinjection hours 7–12. In contrast to dark-onset administrations, the amount of waking is not altered by either CRH-receptor antagonist when administered before the light period. These results support our hypothesis that CRH contributes to the regulation of physiological waking, since interfering with the binding of CRH to its receptor reduces spontaneous waking.


Author(s):  
Tetsuaki Osafune ◽  
Shuji Sumida ◽  
Tomoko Ehara ◽  
Eiji Hase ◽  
Jerome A. Schiff

Changes in the morphology of pyrenoid and the distribution of RuBisCO in the chloroplast of Euglena gracilis were followed by immunoelectron microscopy during the cell cycle in a light (14 h)- dark (10 h) synchronized culture under photoautotrophic conditions. The imrnunoreactive proteins wereconcentrated in the pyrenoid, and less densely distributed in the stroma during the light period (growth phase, Fig. 1-2), but the pyrenoid disappeared during the dark period (division phase), and RuBisCO was dispersed throughout the stroma. Toward the end of the division phase, the pyrenoid began to form in the center of the stroma, and RuBisCO is again concentrated in that pyrenoid region. From a comparison of photosynthetic CO2-fixation with the total carboxylase activity of RuBisCO extracted from Euglena cells in the growth phase, it is suggested that the carboxylase in the pyrenoid functions in CO2-fixation in photosynthesis.


2019 ◽  
Vol 20 (10) ◽  
pp. 2452 ◽  
Author(s):  
Martha López-Canul ◽  
Seung Hyun Min ◽  
Luca Posa ◽  
Danilo De Gregorio ◽  
Annalida Bedini ◽  
...  

Melatonin (MLT) is a neurohormone that regulates many physiological functions including sleep, pain, thermoregulation, and circadian rhythms. MLT acts mainly through two G-protein-coupled receptors named MT1 and MT2, but also through an MLT type-3 receptor (MT3). However, the role of MLT receptor subtypes in thermoregulation is still unknown. We have thus investigated the effects of selective and non-selective MLT receptor agonists/antagonists on body temperature (Tb) in rats across the 12/12-h light–dark cycle. Rectal temperature was measured every 15 min from 4:00 a.m. to 9:30 a.m. and from 4:00 p.m. to 9:30 p.m., following subcutaneous injection of each compound at either 5:00 a.m. or 5:00 p.m. MLT (40 mg/kg) had no effect when injected at 5 a.m., whereas it decreased Tb during the light phase only when injected at 5:00 p.m. This effect was blocked by the selective MT2 receptor antagonist 4P-PDOT and the non-selective MT1/MT2 receptor antagonist, luzindole, but not by the α1/MT3 receptors antagonist prazosin. However, unlike MLT, neither the selective MT1 receptor partial agonist UCM871 (14 mg/kg) nor the selective MT2 partial agonist UCM924 (40 mg/kg) altered Tb during the light phase. In contrast, UCM871 injected at 5:00 p.m. increased Tb at the beginning of the dark phase, whereas UCM924 injected at 5:00 a.m. decreased Tb at the end of the dark phase. These effects were blocked by luzindole and 4P-PDOT, respectively. The MT3 receptor agonist GR135531 (10 mg/kg) did not affect Tb. These data suggest that the simultaneous activation of both MT1 and MT2 receptors is necessary to regulate Tb during the light phase, whereas in a complex but yet unknown manner, they regulate Tb differently during the dark phase. Overall, MT1 and MT2 receptors display complementary but also distinct roles in modulating circadian fluctuations of Tb.


1993 ◽  
Vol 265 (2) ◽  
pp. H770-H773 ◽  
Author(s):  
W. Zhang ◽  
S. W. Mifflin

The nucleus tractus solitarius (NTS) is the primary site of termination of arterial baroreceptor and chemoreceptor afferent fibers. Excitatory amino acid (EAA) receptors within NTS have been shown to play an important role in the mediation of arterial baroreceptor reflexes; however, the importance of EAA receptors within NTS in the mediation of arterial chemoreceptor reflexes remains controversial. Therefore, in chloralose-urethan-anesthetized, mechanically ventilated, paralyzed rats, 4 nmol of the broad-spectrum EAA receptor antagonist kynurenic acid (Kyn) was injected into the NTS to observe the effects of EAA receptor blockade on the pressor responses evoked by either activation of ipsilateral carotid body chemoreceptors (by close arterial injection of CO2-saturated bicarbonate) or electrical stimulation of ipsilateral carotid sinus nerve (CSN). Under control conditions, activation of carotid body chemoreceptors and CSN stimulation evoked increases in arterial pressure of 27 +/- 2 (n = 24 sites) and 28 +/- 3% (n = 8), respectively. Kyn microinjection into NTS significantly reduced the pressor responses evoked by activation of carotid body chemoreceptors and electrical stimulation of the CSN for 20 and 25 min, respectively. Attenuation of pressor responses evoked by chemoreceptor activation were maximal at 20 min post-Kyn injection (13 +/- 2%), whereas CSN-evoked pressor responses were maximally attenuated at 15 min (6 +/- 4%). Microinjection into NTS of 4 nmol of xanthurenic acid, a structural analogue of Kyn with no EAA receptor antagonist properties, had no effect on chemoreceptor reflexes. We conclude that EAA receptors within NTS play an important role in the mediation of arterial chemoreceptor reflexes.


2000 ◽  
Vol 84 (4) ◽  
pp. 1934-1941 ◽  
Author(s):  
Rainer Haberberger ◽  
Reas Scholz ◽  
Wolfgang Kummer ◽  
Michaela Kress

Multiple muscarinic receptor subtypes are present on sensory neurons that may be involved in the modulation of nociception. In this study we focused on the presence of the muscarinic receptor subtypes, M2 and M3 (M2R, M3R), in adult rat lumbar dorsal root ganglia (DRG) at the functional ([Ca2+]i measurement), transcriptional (RT-PCR), and translational level (immunohistochemistry). After 1 day in culture exposure of dissociated medium-sized neurons (20–35 μm diam) to muscarine was followed by rises in [Ca2+]i in 76% of the neurons. The [Ca2+]i increase was absent after removal of extracellular calcium and did not desensitize after repetitive application of the agonist. This rise in [Ca2+]i may be explained by the expression of M3R, which can induce release of calcium from internal stores via inositoltrisphospate. Indeed the effect was antagonized by the muscarinic receptor antagonist atropine as well as by the M3R antagonist, 4-diphenylacetoxy-N-(2 chloroethyl)-piperidine hydrochloride (4-DAMP). The pharmacological identification of M3R was corroborated by RT-PCR of total RNA and single-cell RT-PCR, which revealed the presence of mRNA for M3R in lumbar DRG and in single sensory neurons. In addition, RT-PCR also revealed the expression of M2R, which did not seem to contribute to the calcium changes since it was not prevented by the M2 receptor antagonist, gallamine. Immunohistochemistry demonstrated the presence of M2R and M3R in medium-sized lumbar DRG neurons that also coexpressed binding sites for the lectin I-B4, a marker for mainly cutaneous nociceptors. The occurrence of muscarinic receptors in putative nociceptive I-B4-positive neurons suggests the involvement of these acetylcholine receptors in the modulation of processing of nociceptive stimuli.


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