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PubMed2005

Melatonin plays a crucial role in the regulation of rhythmic clock gene expression in the mouse pars tuberalis.

Circadian rhythms in physiology and behavior are driven by a central clock residing within the hypothalamic suprachiasmatic nucleus (SCN). Molecularly, the biological clock is based on the transcriptional/translational feedback loop of clock genes (mPer, mCry, Clock, and Bmal1). Circadian expression of clock genes is not limited to the SCN, but is found in many peripheral tissues. Peripheral rhythms depend on neuroendocrine/neuronal output from the SCN. Melatonin, the hormone of darkness, represents an important neuroendocrine output of the circadian clock. The hypophyseal pars tuberalis (PT) is one of the main target regions for melatonin. The aim of the study was to test whether mPer, mCry, Clock, and Bmal1 are rhythmically expressed in the mouse PT and how the absence of melatonin receptors affects clock gene expression. We analyzed clock gene expression by in situ hybridization and compared wild-type (WT), melatonin 1 receptor knockout (MT1 ko), and melatonin 2 receptor knockout (MT2 ko) mice. mPer1, mCry1, Clock, and Bmal1, but not mPer2 and mCry2, were rhythmically expressed in the PT of WT and MT2 ko mice. In the PT of MT1 ko mice, expression of mPer1, mCry1, Clock, and Bmal1 was dramatically reduced. We conclude that melatonin, acting through the MT1 receptor, is an important regulator of rhythmic clock gene expression in the mouse PT.

Animals↗
PubMed2002

Clock genes in mammalian peripheral tissues.

For many years, neurons of the suprachiasmatic nucleus (SCN) in the hypothalamus were thought to contain the unique mammalian clock controlling circadian rhythmicity of peripheral tissues via neural and humoral signals. Surprisingly, the cloning and characterisation of mammalian clock genes have revealed that they are expressed in a circadian manner throughout the body. It is generally accepted now that peripheral cells contain a circadian clock which is similar to the one present in SCN neurons, although only the latter seems to be self-sustained. It is still unclear how these peripheral clocks are synchronised by the central SCN clock, albeit humoral signals appear to be crucial. Interestingly, peripheral clocks can be uncoupled from the central clock in particular conditions such as restricted-feeding, allowing peripheral tissues to adapt themselves to cues incompatible to other cues perceived by the SCN (mainly the photoperiod). Whereas circadian clocks have been intensively dissected, little is known about the mechanisms by which these clocks regulate the expression of clock-controlled genes. Direct regulation for some of them by the products of clock genes was recently documented, but this probably represents the exception rather than the rule. We should soon be able to describe complete circadian transcriptional cascades from clock genes to enzymes and structural proteins. In addition to circadian humoral and neural signals, these cascades should help us to understand how gene expression, physiology and behaviour are influenced by the rotation of the Earth around its axis.

Animals↗
PubMed2005

Molecular cloning of Clock cDNA from the prawn, Macrobrachium rosenbergii.

CLOCK, which belongs to the basic helix-loop-helix (bHLH)/PER-ARNT-SIM (PAS) superfamily of transcription factors, is one of the most essential proteins involved in circadian systems of animals. Clock genes have been cloned from several species, including mammals, insects, birds, fish, and amphibians. In the present study, we successfully isolated a Clock homolog (termed Mar-Clock) from the giant prawn, Macrobrachium rosenbergii. The 2949-bp cDNA contained a 2115 bp open reading frame that encoded a putative CLOCK protein of 704 amino acids (termed Mar-CLOCK) exhibiting high identities with CLOCK homologs in other species (30-35%). This is the first report of a circadian clock gene from crustaceans. Mar-CLOCK possessed an exceptionally long glutamine-rich domain (140 amino acids) in its C-terminus, which usually ranges from 14 to 57 amino acids in other known CLOCKs and is supposed to function in transcriptional activation. Using RT-PCR, we observed that Mar-Clock was expressed in all tested tissues. Semiquantitative RT-PCR was performed to investigate the gene expression profile during the light-dark cycle. The results indicated that the expression of the Mar-Clock gene had no significant rhythmicity in central nervous tissues (thoracic ganglia and eyestalk) or peripheral tissues (gill, ovary, hepatopancreas, and muscle). Furthermore, gene expression tended to increase in the central nervous system (brain, thoracic, and abdominal ganglia) of eyestalk-ablated or constant dark (DD) prawns, and in the eyestalk-ablated gill. No expression change was found under constant light (LL) or in heart and muscle.

Amino Acid Sequence↗
PubMed2004

Resetting mechanism of central and peripheral circadian clocks in mammals.

Almost all organisms on earth exhibit diurnal rhythms in physiology and behavior under the control of autonomous time-measuring system called circadian clock. The circadian clock is generally reset by environmental time cues, such as light, in order to synchronize with the external 24-h cycles. In mammals, the core oscillator of the circadian clock is composed of transcription/translation-based negative feedback loops regulating the cyclic expression of a limited number of clock genes (such as Per, Cry, Bmal1, etc.) and hundreds of output genes in a well-concerted manner. The central clock controlling the behavioral rhythm is localized in the hypothalamic suprachiasmatic nucleus (SCN), and peripheral clocks are present in other various tissues. The phase of the central clock is amenable to ambient light signal captured by the visual rod-cone photoreceptors and non-visual melanopsin in the retina. These light signals are transmitted to the SCN through the retinohypothalamic tract, and transduced therein by mitogen-activated protein kinase and other signaling molecules to induce Per gene expression, which eventually elicits phase-dependent phase shifts of the clock. The central clock controls peripheral clocks directly and indirectly by virtue of neural, humoral, and other signals in a coordinated manner. The change in feeding time resets the peripheral clocks in a SCN-independent manner, possibly by food metabolites and body temperature rhythms. In this article, we will provide an overview of recent molecular and genetic studies on the resetting mechanism of the central and peripheral circadian clocks in mammals.

Animals↗
PubMed2006

Circadian rhythms and different photoresponses of Clock gene transcription in the rat suprachiasmatic nucleus and pineal gland.

The aim of this study was to observe and compare the endogenous circadian rhythm and photoresponse of Clock gene transcription in the suprachiasmatic nucleus (SCN) and pineal gland (PG) of rats. With free access to food and water in special darkrooms, Sprague-Dawley rats were housed under the light regime of constant darkness (DD) for 8 weeks (n=36) or 12 hour-light: 12 hour-dark cycle (LD) for 4 weeks (n=36), respectively. Then, their SCN and PG were dissected out every 4 h in a circadian day, 6 rats at each time (n=6). All animal treatments and sampling during the dark phases were conducted under red dim light (<0.1 lux). The total RNA was extracted from each sample and the semi-quantitative RT-PCR was used to determine the temporal mRNA changes of Clock gene in the SCN and PG at different circadian times (CT) or zeitgeber times (ZT). The grayness ratio of Clock/H3.3 bands was served as the relative estimation of Clock gene expression. The experimental data were analyzed by the Cosine method and the Clock Lab software to fit original results measured at 6 time points and to simulate a circadian rhythmic curve which was then examined for statistical difference by the amplitude F test. The main results are as follows: (1) The mRNA levels of Clock gene in the SCN under DD regime displayed the circadian oscillation (P<0.05). The endogenous rhythmic profiles of Clock gene transcription in the PG were similar to those in the SCN (P>0.05) throughout the day with the peak at the subjective night (CT15 in the SCN or CT18 in the PG) and the trough during the subjective day (CT3 in the SCN or CT6 in the PG). (2) Clock gene transcription in the SCN under LD cycle also showed the circadian oscillation (P<0.05), and the rhythmic profile was anti-phasic to that under DD condition (P<0.05). The amplitude and the mRNA level at the peak of Clock gene transcription in the SCN under LD were significantly increased compared with that under DD (P<0.05), while the value of corresponding rhythmic parameters in the PG under LD were remarkably decreased (P<0.05). (3) Under LD cycle, the circadian profiles of Clock gene transcription induced by light in the PG were quite different from those in the SCN (P<0.05). Their Clock transcription rhythms were anti-phasic, i.e., showing peaks at the light phase ZT10 in the SCN or at the dark time ZT17 in the PG and troughs during the dark time ZT22 in the SCN or during the light phase ZT5 in the PG. The findings of the present study indicate a synchronous endogenous nature of the Clock gene circadian transcriptions in the SCN and PG, and different roles of light regime in modulating the circadian transcriptions of Clock gene in these two central nuclei.

Animals↗
PubMed1979

Effects of response-contingent clock stimuli on behavior maintained by intravenous codeine in the rhesus monkey.

Response-contingent brief presentations of clock stimuli differentially correlated with food availability altered rates of codeine-maintained lever pressing. Rhesus monkeys performed under a two lever multiple schedule: Multiple fixed interval clock 5 min variable interval 2 min. Different colored lights were presented during successive 75 sec period of the fixed-interval clock component. Lever pressing under the FI Clock schedule was maintained by presentation of 1 g Noyes pellets, and lever pressing under the VI schedule by 0.05 mg/kg infusions of codeine PO4. Characteristic schedule-controlled performance developed in both schedule components. When the clock stimulus from the first or the final period of the FI Clock schedule was presented contingent upon completion of a short fixed ratio of responses during the variable-interval schedule component, the first clock stimulus decreased and the final clock stimulus increased rates of codeine-maintained lever pressing. Neither the first nor the final clock stimulus altered the frequency of codeine injection. The effect of each clock stimulus was accentuated by increasing the duration of stimulus presentation and by decreasing the response requirement for stimulus illumination. These rate-altering effects of the clock stimuli were most pronounced when different reinforcers were presented in the two components of the multiple schedule when either food or intravenous codeine injection was available under both components of the multiple schedule, response-contingent clock stimulus presentation did not alter response rates under the VI schedule.

Animals↗
PubMed1990

Use of time clocks for employees in health-care institutions.

The reasons for time clock use in health-care institutions, the categories of workers required to use a time clock and other timekeeping methods, and the incidence of time-clock-related conflicts were studied. A questionnaire was mailed to a random sample of 565 hospitals in October 1989. Usable responses were received from 340 (60.0%) of the institutions. Reasons given for time clock use included payroll tabulation, overtime calculation, and ensuring fair payment. Thirty-four institutions (10.0%) required all employees to clock in, and 179 (52.6%) required some employees to do so. A written time card completed by the employee was the method used most frequently if a time clock was not used. Clinical pharmacists were required to clock in at 51 institutions (15.0%), staff pharmacists at 62 (18.2%), and pharmacy technicians at 144 (42.9%). Clinical nurse specialists and registered nurses clocked in at 88 (25.9%) and 169 (49.7%) hospitals, respectively, and licensed practical nurses and nurse's aides each clocked in at 176 hospitals (51.8%). Less than 6% of the hospitals required salaried pharmacists or nurses to use a time clock. Of the respondents, 152 (44.7%) reported that they were not aware of any conflicts or that no conflicts had been experienced. Inconvenience and inaccurate clocking were the most common sources of conflict cited. Most hospitals use time clocks for nonsalaried employees for bookkeeping purposes; dissatisfaction with this method of tracking hours worked does not appear to be widespread.

Labor Unions↗
PubMed1999

Molecular cloning and characterization of the human CLOCK gene: expression in the suprachiasmatic nuclei.

The Clock gene is an essential regulator of circadian rhythms. It encodes a member of the basic helix-loop-helix/PER-ARNT-SIM family of transcription factors known to play a central role in the control of diverse cellular events. Previously we described the functional identification and molecular isolation of the Clock gene in the mouse, its interaction with the BMAL1 protein, and the role of this complex as a transcriptional activator in the circadian pacemaker. Here, we report the cloning, exon organization, chromosomal location, and mRNA expression of the human CLOCK gene. The coding sequence of human CLOCK extends for 2538 bp and is 89% identical to its mouse ortholog; its deduced amino acid sequence is 846 residues long and is 96% identical to mouse CLOCK. Radiation hybrid mapping localized human CLOCK to the long arm of human chromosome 4 (4q12). Direct sequencing of a genomic CLOCK clone indicated that the coding sequence of human CLOCK extends over 20 exons and that its intron/exon organization is identical to that of the mouse ortholog. Northern blot analysis indicated widespread expression of two major transcripts of 8 and 10 kb, and in situ hybridization of human brain tissue revealed elevated expression of CLOCK mRNA in the suprachiasmatic nuclei, the locus of circadian control in mammals, and in the cerebellum. Comparison of cDNA clones revealed two single nucleotide polymorphisms in noncoding sequence flanking the CLOCK open reading frame. The central role of Clock in the organization of circadian rhythms suggests that it will be a useful candidate gene for genetic analyses of disorders associated with dysfunction of the circadian system.

Alleles↗
PubMedDate not supplied

Clock genes of Mammalian cells: practical implications in tissue culture.

The clock genes family is expressed by all the somatic cells driving central and peripheral circadian rhythms through transcription/translation feedback loops. The circadian clock provides a local time for a cell and a way to integrate the normal environmental changes to smoothly adapt the cellular machinery to new conditions. The central circadian rhythm is retained in primary cultures by neurons of the suprachiasmatic nuclei. The peripheral circadian rhythms of the other somatic cells are progressively dampened down up to loss unless neuronal signals of the central clock are provided for re-entrainment. Under typical culture conditions (obscurity, 37 +/- 1 degrees C, 5-7% CO(2)), freshly explanted peripheral cells harbor chaotic expression of clock genes for 12-14 h and loose, coordinated oscillating patterns of clock components. Cells of normal or cancerous phenotypes established in culture harbor low levels of clock genes idling up to the re-occurrence of new synchronizer signals. Synchronizers are physicochemical cues (like thermic oscillations, short-term exposure to high concentrations of serum or single medium exchange) able to re-induce molecular oscillations of clock genes. The environmental synchronizers are integrated by response elements located in the promoter region of period genes that drive the central oscillator complex (CLOCK:BMAL1 and NPAS2:BMAL1 heterodimers). Only a few cell lines from different species and lineages have been tested for the existence or the functioning of a circadian clockwork. The best characterized cell lines are the immortalized SCN2.2 neurons of rat suprachiasmatic nuclei for the central clock and the Rat-1 fibroblasts or the NIH/3T3 cells for peripheral clocks. Isolation methods of fragile cell phenotypes may benefit from research on the biological clocks to design improved tissue culture media and new bioassays to diagnose pernicious consequences for health of circadian rhythm alterations.

Animals↗
PubMed2006

Circadian regulator CLOCK is a histone acetyltransferase.

The molecular machinery that governs circadian rhythmicity comprises proteins whose interplay generates time-specific transcription of clock genes. The role of chromatin remodeling in a physiological setting such as the circadian clock is yet unclear. We show that the protein CLOCK, a central component of the circadian pacemaker, has histone acetyltransferase (HAT) activity. CLOCK shares homology with acetyl-coenzyme A binding motifs within the MYST family of HATs. CLOCK displays high sequence similarity to ACTR, a member of SRC family of HATs, with which it shares also enzymatic specificity for histones H3 and H4. BMAL1, the heterodimerization partner of CLOCK, enhances HAT function. The HAT activity of CLOCK is essential to rescue circadian rhythmicity and activation of clock genes in Clock mutant cells. Identification of CLOCK as a novel type of DNA binding HAT reveals that chromatin remodeling is crucial for the core clock mechanism and identifies unforeseen links between histone acetylation and cellular physiology.

ARNTL Transcription Factors↗
PubMed2004

Reproductive performance in female Clock Delta19 mutant mice.

The relationship between circadian rhythmicity and rodent reproductive cyclicity is well established, but the impact of disrupted clock gene function on reproduction has not been well established. The present study evaluated the reproductive performance of mice carrying the Clock(Delta19) mutation that were either melatonin deficient (Clock(Delta19/Delta19)) or had the capacity to synthesise melatonin reinstated (Clock(Delta19/Delta19)+MEL). The Clock(Delta19/Delta19) mice took 2-3 days longer to mate, and to subsequently deliver pups, than their control line. The melatonin-competent mutants had a smaller, but still significant (P < 0.05), delay. The Clock(Delta19) mutation resulted in smaller median litter sizes compared with control lines (seven v. eight pups; P < 0.05), whereas melatonin proficiency reversed this difference. Survival to weaning was 84% and 80% for the Clock(Delta19/Delta19) and Clock(Delta19/Delta19)+MEL lines, respectively, compared with 94-96% for the two control lines. The Clock(Delta19/Delta19) mutants became behaviourally arrhythmic in constant darkness but, despite this, seven of seven became pregnant when paired with males after at least 14 days of constant darkness (five of seven within 4 days of pairing). In the Clock(Delta19/Delta19)+MEL mice, seven of 15 became arrhythmic in constant darkness but still became pregnant. The seven mice that free ran for at least 14 days in constant darkness with a period of 27.1 h also became pregnant. The present study has demonstrated that the Clock(Delta19) mutation has significant, but subtle, effects on reproductive performance. The reintroduction of melatonin competency and/or other genes as a result of crosses with CBA mice reduced the impact of the mutation further. It would appear that redundancy in genes in the circadian system allows the reproductive cyclicity to persist in mice, albeit at a suboptimal level.

Animals↗
PubMed2002

Human clock genes.

Rhythmic variations in physiological and behavioural processes are mediated by both endogenous and exogenous factors. Endogenous factors include self-sustaining biological pacemakers or clocks which in the absence of strong external influences self-sustain periodic rhythms in such diverse physiological and psychological processes as core body temperature, food intake, cognitive performance and mood. Clocks with endogenous periods near or at 24 h (called circadian clocks from the Latin, circa dies, meaning about one day) have been documented from prokaryotes to single cell eukaryotes to multi-cellular, complex animals such as flies, rodents and humans. Over the past few years, a revolution in the understanding of the molecular basis of these clocks has led to the identification of a number of core clock genes and their proteins, and the development of elegant feedback models to explain the molecular gears of circadian clocks. At least eight human orthologs of mouse core clock genes have been identified, and polymorphisms in two of these, hClock and hPer2, have been implicated in human sleep disorders. Remarkably, knowledge of these core clock genes and the development of sophisticated reporter systems to monitor clock gene promoter activity have led to the astonishing observation that our body is actually composed of millions of cellular clocks and oscillators whose co-ordinated activity gives rise to pronounced daily, monthly, and seasonal rhythms in physiology and behaviour. An idea that is gaining favour is that our physical and mental well-being is probably determined by the appropriate phasing of these millions of cellular clocks with recurring, meaningful events in the environment.

Animals↗
PubMed2003

Circadian gene expression of clock genes and plasminogen activator inhibitor-1 in heart and aorta of spontaneously hypertensive and Wistar-Kyoto rats.

OBJECTIVE: Heart and aorta possess biologic clocks, but their involvement in genetic hypertension has been unknown. Plasminogen activator inhibitor-1 (PAI-1) expression is directly regulated by clock genes, while angiotensin II modulates both PAI-1 and clock gene expression. We therefore examined circadian expression of PAI-1 and clock genes, and effects of angiotensin type 1 (AT1) receptor antagonism, in heart and aorta of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. METHODS: We examined cardiac and aortic mRNA expression for PAI-1 and clock genes (Per2, Bmal1, Clock, and Dbp) every 4 h throughout the day by quantitative reverse transcription-polymerase chain reaction, and intervention with the AT1 receptor antagonist candesartan and equihypotensive hydralazine. RESULTS: Cardiac PAI-1 expression was high in the dark, while aortic PAI-1 expression was high in the light. Both cardiac and aortic PAI-1 expression were greater in SHR than in WKY rats. Candesartan treatment decreased cardiac PAI-1 expression only in the dark in WKY rats but throughout the day in SHR. Candesartan but not hydralazine strongly attenuated circadian fluctuation of aortic PAI-1 mRNA in SHR and WKY rats. Clock genes oscillated synchronously in heart and aorta of SHR and WKY rats. Clock gene expression was increased in heart but not aorta of SHR. Candesartan did not affect clock gene expression. CONCLUSIONS: Enhanced expression of clock genes may increase PAI-1 expression in concert with activated renin-angiotensin system in SHR heart. Rather than clock genes, the renin-angiotensin system induces daily fluctuation and increased expression of aortic PAI-1 mRNA in SHR.

ARNTL Transcription Factors↗
PubMed2006

Functional central rhythmicity and light entrainment, but not liver and muscle rhythmicity, are Clock independent.

The circadian rhythmicity of hormone secretion, body temperature, and sleep/wakefulness results from an endogenous rhythm of neural activity generated by clock genes in the suprachiasmatic nucleus (SCN). One of these genes, Clock, has been considered essential for the generation of cellular rhythmicity centrally and in the periphery; however, melatonin-proficient Clock(Delta19) + MEL mutant mice retain melatonin rhythmicity, suggesting that their central rhythmicity is intact. Here we show that melatonin production in these mutants was rhythmic in constant darkness and could be entrained by brief single daily light pulses. Under normal light-dark conditions, per2 and prokineticin2 (PK2) mRNA expression was rhythmic in the SCN of Clock(Delta19) + MEL mice. Expression of Bmal1 and npas2 was not altered, whereas per1 expression was arrhythmic. In contrast to the SCN, per1 and per2 expression, as well as Bmal1 expression in liver and skeletal muscle, together with plasma corticosterone, was arrhythmic in Clock(Delta19) + MEL mutant mice in normal light-dark conditions. npas2 mRNA was also arrhythmic in liver but rhythmic in muscle. The Clock(Delta19) mutation does not abolish central rhythmicity and light entrainment, suggesting that a functional Clock homolog, possibly npas2, exists in the SCN. Nevertheless, the SCN of Clock(Delta19) + MEL mutant mice cannot maintain liver and muscle rhythmicity through rhythmic outputs, including melatonin secretion, in the absence of functional Clock expression in the tissues. Therefore, liver and muscle, but not SCN, have an absolute requirement for CLOCK, with as yet unknown Clock-independent factors able to generate the latter.

ARNTL Transcription Factors↗
PubMed2005

The thymus is similar to the testis in its pattern of circadian clock gene expression.

The molecular basis for the circadian clock in mammals consists of a number of genes and proteins that form transcription-translation feedback loops. These loops result in a 24-h rhythm in the expression of mRNA and protein levels. Although the anatomical site of the central circadian clock is the SCN of the hypothalamus, all of the circadian clock genes are expressed in tissues other than the brain. Moreover, cyclic gene and protein expression occurs in most of these tissues. The best known exception to this rule is the testis, which shows constant rather than cyclic expression of circadian clock genes. Indeed, the testis of multiple animal species displays constant circadian clock gene expression. In recent work, the authors showed that the thymus is similar to the testis in that expression of circadian clock genes is either constant over a 24-h period or cycles with a dampened amplitude, depending on which gene is examined. In the current study, they extend and confirm their findings regarding noncyclic circadian clock gene and protein expression in the testis and the thymus. More important, they also show that expression of these genes in both testis and thymus does not depend on the transcriptional activator, CLOCK, which is necessary for cyclic gene expression in the SCN and in other tissues. These results extend the molecular similarities between the thymus and the testis and suggest that similar mechanisms are at work for regulating expression of circadian clock genes in both tissues. One commonality between these 2 organs is that they are composed primarily of differentiating cells. The authors hypothesize that the circadian clock is not operational in immature, differentiating cells. Possibly, the clock starts in mature cells upon receipt of an initiating signal.

Animals↗
PubMed2005

A behavior systems view of the organization of multiple responses during a partially or continuously reinforced interfood clock.

We examined how a 50% Pavlovian partial reinforcement (PRF) schedule, versus a 100% continuous reinforcement (CRF) schedule, altered the asymptotic amount and distribution of focal and general search behavior in rats during 48-sec trials with and without a four-segment interfood clock (S1-S2-S3-S4-US). Under CRF, but not PRF, average asymptotic focal search (nosing in the feeder) increased across the last two clock segments (S3 and S4), and more for the clock group than the no-clock group. Locomotor general search peaked in the second clock segment (S2) for the CRF-clock and CRF-no-clock groups and in S3 for the PRF-clock groups. Furthermore, the ratio of general search to maximum focal search was higher for the PRF-clock group than for the CRF-clock group. This pattern of results supports the view that predictable reward presentations temporally organize search states and related responses between food presentations. The relative expression of these responses varies with the predictability and proximity of reward and is more sharply defined in the presence of a clock.

Animals↗
PubMed1999

[Comparative study of 230 women to determine the maximum closure pressure and functional length of the urethra at 0, 3, 6 and 9 o'clock].

OBJECTIVE: The maximum closure pressure (MCP) of the urethra, measured by the urethral profile, constitutes an index of urinary continence. The objective of this study, in a large population of women, was to evaluate the possible variations of MCP and functional length (FL) of the urethra, according to the position of a urodynamic probe designed to perform lateral sectorial measurements. MATERIAL AND METHODS: Measurements were performed between July and December 1998, in 230 patients with a mean age of 55 years, using a probe perfused with water and equipped with an urethral side orifice. We compared, by analysis of variance for repeated measures, MCP and mean FL at 0 o'clock (MCPm0, LFm0), 3 o'clock (MCPm3, LFm3), 6 o'clock (MCPm6, LFm6) and 9 o'clock (MCPm9, LFm9). RESULTS: The values for MCPm and LFm obtained according to the rotation of the probe were as follows: MCPm0 = 65.68 +/- 12.46 cmH20, MPCm3 = 55.44 +/- 16.97 cmH20, MCPm6 = 58.07 +/- 15.85 cmH20, and MCPm9 = 53.85 +/- 16.89 cmH20, LFm0 = 28.92 +/- 5.32 mm, LFm3 = 30.18 +/- 6.82 mm, LFm6 = 32.40 +/- 6.82 mm and LFm9 = 30.83 +/- 6.07 mm. CONCLUSION: LCP may variable considerably in the same subject according to rotation of the probe. In our series, MCPm at 0 o'clock was significantly higher than MCPm at 3 o'clock, 6 o'clock and 9 o'clock. This difference appears to increase with age. The lowest values for MCPm were observed at 3 o'clock and 9 o'clock. The MCPm at 6 o'clock was intermediate and the closest value to the mean pressure calculated from MCPm in the four positions. On the other hand, FL varied only slightly according to the position of the probe.

Adolescent↗
PubMed2000

Expression of clock gene in the brain of rainbow trout: comparison with the distribution of melatonin receptors.

To identify brain structures potentially acting as biological clocks in rainbow trout (Oncorhynchus mykiss), the expression sites of a trout homolog of the mouse clock gene were studied and compared with that of melatonin receptors (Mel-R). For this purpose, a partial sequence of the trout clock gene, including a PAS domain, was obtained by reverse transcription-polymerase chain reaction and used to perform in situ hybridization. The highest density of clock transcripts was observed in the periventricular layer (SPV) of the optic tectum, but a weaker expression was detected in some pretectal nuclei, such as the posterior pretectal nucleus (PO) and the periventricular regions of the diencephalon. Comparison of the hybridization signal in fish sacrificed at 08:00 and 17:00 did not indicate major changes in clock expression levels. Comparison of adjacent sections alternatively treated with clock and Mel-R probes suggests that both messengers are probably expressed in the same cells in the SPV and PO. In addition, in situ hybridization with a glutamate decarboxylase 65 probe, demonstrates that cells expressing clock and Mel-R in the optic tectum are gamma-aminobutyric acid neurons. The tight overlapping between the expression of Mel-R and clock transcripts in cells of the PO and SPV suggests a functional link between these two factors. These results indicate that the optic tectum and the pretectal area of the rainbow trout are major sites of integration of the melatonin signal, express the clock gene, and may act as biological clocks to influence behavioral and endocrine responses in trout.

Amino Acid Sequence↗