Internal interactions within the human circadian system: the masking effect

Summary In the realm of human circadian rhythms, the masking effect is defined as the change in the course of deep body temperature induced by changes in the degree of physical activity, or by the alteration between sleep and wake. This effect is particularly obvious during internal desynchronization where the rhythms of deep body temperature, and the sleep-wake sleep-wake sleep cycle — i.e. one of the masking factors — run with different periods.Every sleep onset is accompanied by a rapid drop, and wake onset by a rapid rise in deep body temperature, each one with an overshoot of about 50% of the steady state variations. When rhythms are calculated, with the dominant temperature period as the screening period, exclusively from data obtained during sleep episodes, on the one hand, and from those obtained exclusively during wake, on the other, two average cycles emerge: the sleep temperature curve and the wake temperature curve. Both run in parallel but are separated by the masking effcct. As derived from many experiments, the mean masking effect amounts to 0.28±0.06°C. The masking effect also depends to some extent on the phase of the temperature rhtthm; it is larger than average around the temperature maximum and during the descending phase of the temperature cycle, where the alertness commonly is highest and the probability to sleep, in general, and the REM sleep propensity, in particular, are smaller than average. This also can be interpreted to indicate that the sleep temperature curve is phase advanced relative to the wake temperature curve; this, on the average, by 0.9±0.3 h.If the individually determined amount of masking is added to the temperature data obtained during sleep, or substracted from the temperature data obtained during wake, a temperature curve emerges that can be though of as being purified of the masking effect. Analyses of this artificial curve allow estimation of that part of the internal interactions uninfluenced by the masking effect. On the average, about half of the amount of interaction between the rhythm of sleep-wake and that of deep body temperature is explained by the masking effect, whereas the other half is oscillatory interaction. Both types of interaction are inherent and inseparable parts of the circadian clock mechanism, as can be deduced from model considerations.     

Bicuculline and picrotoxin block γ-aminobutryic acid-gated Cl− conductance by different mechanisms

Summary Using isolated, internally perfused bullfrog dorsal root ganglion cells we have studied the dose-response curves for -aminobutyric acid (GABA) in the presence of internally or externally applied GABA antagonists. With external application of antagonists the inhibition of the GABA current by bicuculline was competitive and that by picrotoxin was noncompetitive. Picrotoxin but not bicuculline blocked when internally perfused.To whom reprint requests should be addressed.Acknowledgments. We thank Drs S. Minakami and S. Yasui for helpful discussions and comments.     

Ecdysteroids: possible candidates for the hormone which triggers salivary gland degeneration in the ixodid tickAmblyomma hebraeum

Summary Following engorgement, female ixodid ticks secrete a tick salivary gland degeneration factor (TSGDF) into the hemolymph. Here we show that the arthropod ecdysteroid hormones, ecdysome and 20-hydroxyecdysone, induce degeneration of tick salivary glands maintained in organ culture. The effective dose range in vitro is 30–300 ng/ml, a range reported to be physiological for this species following repletion. In addition, infusion of 20-hydroxyecdysome in vivo induces salivary gland degeneration. We therefore propose that TSGDF may be an ecdysteroid.Acknowledgments. Some of the data reported here were presented to the annual meeting of the Canadian Society of Zoologists, 15–18 May 1983; Program of abstracts, page 53. Financial support of the Canadian National Sportsmen's Fund and NSERC Canada to W.R.K. is gratefully acknowledged.     

Juvenile hormone titre and regulation in the cockroachDiploptera punctata

Summary Titres of juvenile hormone (JH) have been determined in both hemolymph and whole body extracts of femaleDiploptera punctata during the first gonotrophic cycle using a method employing gas chromatography/mass spectrometry for qualitative and quantitative analysis. JH III is the sole JH found in both adult and last instarD. punctata. Maximum values of 1500 ng/ml (6M) were observed at the middle of the gonotrophic cycle, when basal oocyte growth rate was greatest. Changes in rates of JH release in vitro by corpora allata paralleled closely the changes in JH titre, suggesting that biosynthesis is a major regulator of titre. JH levels per animal were calculated from observed JH titres, and at certain time points in the gonotrophic cycle JH levels obtained from analysis of whole bodies were significantly greater than those predicted from hemolymph titres. These results suggest the existence of a nonhemolymph JH pool inD. punctata. Decay in JH titre after allatectomy of 5 day females has also been studied. Following a rapid initial decline, the rate of decay slowed appreciably 4 h post-operation. Thus, use of a first-order rate constant to estimate half-life of JH significantly underestimated the longevity of the hormone. The apparent persistence of JH following allatectomy may be due to the existence of a nonhemolymph JH pool.     

The susceptibility to exercise-induced muscle damage increases as rats grow larger

Summary Glucose-6-phosphate dehydrogenase and N-acetyl--glucosaminidase activities were both elevated after eccentric exercise indicating that this type of exercise causes muscle damage. Muscle damage as measured by glucose-6-phosphate dehydrogenase activity in the vastus intermedius was greater and occurred later in larger rats indicating that the susceptibility to muscle damage is increased and the repair process delayed in older and larger animals.     

In vitro mutagenicity testing of a potent,new, benzoyl urea insect growth regulator

Summary Bacterial mutagenicity assay to detect potential chronic toxicity of a potent, new, benzoyl urea insect growth regulator (CGA-112913 or IKI-7899, formerly UC-62644) was conducted using 5 histidine auxotrophs ofSalmonella typhimurium. Tests within the concentration range of 0.9–500 g (saturating)/plate of the compound with and without the 5–9 mammalian metabolic activation system showed no mutagenic effects clearing the way for long-term chronic toxicology studies.The authors thank Professor Bruce N. Ames for supplying the tester strains together with all the relevant information for conducting the bioassays and Ms. Norma Charlebois for her meticulous technical assistance.     

Adrenocortical metabolism and plasma corticosterone in soman intoxicated rabbits

Summary The organophosphate neurotoxin soman produced impairments in adrenocortical RNA and protein metabolism. Fasciculate and reticular cell RNA and protein contents were supporessed with sublethal to acutely lethal dosages (20, 30 and 40 g/kg, s.c.) during the acute excitatory phase of intoxication and at 6–8 h post injection. All three dosages produced ca 90% inactivation of plasma cholinesterase. A transient elevation of plasma corticosterone occurred with 20 g/kg soman whereas there was a protracted increase with 30 g/kg. Corticosterone was not significantly elevated with 40 g/kg, but death occurred at 13±4 min. Thus, the magnitude and/or nature of soman-induced metabolic impairments does not appear to prevent adrenal activation.Supported by US Army Medical Research and Development Command Contract DAMD 17-81-C-1202.     

Quantitative genetic models of sexual selection

Summary Quantitative genetic models of sexual selection have disporven some of the central tenets of both the handicap mechanism and the sexy son hypothesis. These results suggest that the good genes approach to sexual selection may generally lead to erroneous results.Runaway sexual selection seems possible under a wide variety of circumstances. Quantittive genetic models have revealed runaway processes for sexually selected attributes expressed in both sexes and for attributes of parental care. Furthermore, the runaway could occur simultaneously in a series of populations that straddle an environmental gradient. While the models support the feasibility of runaway processes, empirical studies are needed to evaluate whether runaways actually happen. Estimates of critical genetic parameters are particularly needed, as well as measures of natural and sexual selection acting on the same population.The models also show that sexual selection has tremendous potential to produce population differentiation, particularly in epigamic traits. Differentiation is promoted by indeterminancy of evolutionary outcome, transient differences among populations during the final slow approach to equilibrium, sampling drift among equilibrium populations, and the tendency of sexual selection to amplify geographic variation arising from spatial differences in natural selection. Recent work with two- and three-locus models of sexual selection has produced results that parallel the results of the polygenic models^36–38,58. Thus the feature of indeterminate equilibria (outcome dependent on initial conditions) is common to both types of model.     

Endorcine cells producing regulatory peptides

Summary Recent data on the immunologication of regulatory peptides and related propeptide sequences in endocrine cells and tumours of the gastrointestinal tract pancreas, lung, thyroid, pituitary (ACTH and opioids), adrenals and paraganglia have been revised and discussed. Gastrin, xenopsin, cholecystokinin (CCK), somatostatin, motilin, secretin, GIP (gastric inhibitory beenrevised and discussed. Gastrin, xenopsin, cholecystokinin (CCK), somatostatin, motilin, secretin, GIP (gastric inhibitory polypeptide), neurotensin, glicentin/glucagon-37 and PYY (peptide tyrosine tyrosine) are the main products of gastrointestinal endocrine cells; glucagon, CRF (corticotropin releasing factor), somatostatin, PP (pancreatic polypeptide) and GRF (growth hormone releasing factor), in addition to insulin, are produced in pancreatic islet cells; bombesin-related peptidesare the main markers of pulmonary endocrine cells; calcitonin and CGRP (calcitonin gene-related peptide) occur in thyroid and extrathyroid C cells; ACTH and endorphins in anterior and intermediate lobe pituitary cells, -MSH and CLIP (corticotropoin-like intermediate lobe peptide) in intermediate lobe cells; met- and leu-enkephalins and related peptides in adrenal medullary and paraganglionic cells as well as in some gut (enterochromaffin) cells; NPY (neuropeptide Y) in adrenalin-type adrenal medullary cells, etc.. Both tissue-appropriate and tissue-inappropriate regulatory peptides are produced by endocrine tumours, with inappropriate peptides mostly produced by malignant tumours.