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During spaceflight, the homeostasis of the living body is threatened with cosmic environment including microgravity and irradiation. Traditional Chinese medicine could ameliorate the internal imbalance during spaceflight, but its mechanism is still unclear. In this article, we compared the difference of neuroendocrine-immune balance between simulated microgravity (S) and simulated microgravity and irradiation (SAI) environment. We also observed the antagonistic effect of SAI using a traditional Chinese medicine formula (TCMF). Wistar rats were, respectively, exposed under S using tail suspending and SAI using tail suspending and 60 Co-gama irradiation exposure. The SAI rats were intervened with TCMF. The changes of hypothalamic-pituitary-adrenal (HPA) axis, splenic T-cell, celiac macrophages, and related cytokines were observed after 21 days. Compared with the normal group, the hyperfunction of HPA axis and celiac macrophages, as well as the hypofunction of splenic T-cells, was observed in both the S and SAI group. Compared with the S group, the levels of plasmatic corticotropin-releasing hormone (CRH), macrophage activity, and serous interleukin-6 (IL-6) in the SAI group were significantly reduced. The dysfunctional targets were mostly reversed in the TCMF group. Both S and SAI could lead to NEI imbalance. Irradiation could aggravate the negative feedback inhibition of HPA axis and macrophages caused by S. TCMF could ameliorate the NEI dysfunction caused by SAI., Competing Interests: The authors declare that there is no conflict of interest regarding the publication of this paper., (Copyright © 2020 Haoru Zhu et al.)

Prolonged or repeated activation of the stress response can have negative psychological and physical consequences. The prefrontal cortex (PFC) is thought to exert an inhibitory influence on the activity of autonomic and neuroendocrine stress response systems. In this study, we further investigated this hypothesis by increasing PFC excitability using transcranial direct current stimulation (tDCS). Healthy male participants were randomized to receive either anodal (excitatory) tDCS ( n  = 15) or sham stimulation ( n  = 15) over the left dorsolateral prefrontal cortex (DLPFC) immediately before and during the exposure to a psychosocial stress test. Autonomic (heart rate (HR) and its variability) and neuroendocrine (salivary cortisol) parameters were assessed. One single session of excitatory tDCS over the left DLPFC (i) reduced HR and favored a larger vagal prevalence prior to stress exposure, (ii) moderated stress-induced HR acceleration and sympathetic activation/vagal withdrawal, but (iii) had no effect on stress-induced cortisol release. However, anodal tDCS over the left DLPFC prevented stress-induced changes in the cortisol awakening response. Finally, participants receiving excitatory tDCS reported a reduction in their levels of state anxiety upon completion of the psychosocial stress test. In conclusion, this study provides first insights into the efficacy of one single session of excitatory tDCS over the left DLPFC in attenuating autonomic and neuroendocrine effects of psychosocial stress exposure. These findings might be indicative of the important role of the left DLPFC, which is a cortical target for noninvasive brain stimulation treatment of depression, for successful coping with stressful stimuli.

Background: Patients with low-grade gliomas (LGG) can survive years with their illness. Proton radiotherapy (PRT) can reduce off-target dose and decrease the risk of treatment-related morbidity. We examined long-term morbidity following proton therapy in this updated prospective cohort of patients with LGG., Methods: Twenty patients with LGG were enrolled prospectively and received PRT to 54 Gy(RBE) in 30 fractions. Comprehensive baseline and longitudinal assessments of toxicity, neurocognitive and neuroendocrine function, quality of life, and survival outcomes were performed up to 5 years following treatment., Results: Six patients died (all of disease) and six had progression of disease. Median follow-up was 6.8 years for the 14 patients alive at time of reporting. Median progression-free survival (PFS) was 4.5 years. Of tumors tested for molecular markers, 71% carried the IDH1-R132H mutation and 29% had 1p/19q co-deletion. There was no overall decline in neurocognitive function; however, a subset of five patients with reported cognitive symptoms after radiation therapy had progressively worse function by neurocognitive testing. Six patients developed neuroendocrine deficiencies, five of which received Dmax ≥20 Gy(RBE) to the hypothalamus-pituitary axis (HPA). Most long-term toxicities developed within 2 years after radiation therapy., Conclusions: The majority of patients with LGG who received proton therapy retained stable cognitive and neuroendocrine function. The IDH1-R132H mutation was present in the majority, while 1p/19q loss was present in a minority. A subset of patients developed neuroendocrine deficiencies and was more common in those with higher dose to the HPA., (Copyright © 2019 Elsevier B.V. All rights reserved.)

The skin, a self-regulating protective barrier organ, is empowered with sensory and computing capabilities to counteract the environmental stressors to maintain and restore disrupted cutaneous homeostasis. These complex functions are coordinated by a cutaneous neuro-endocrine system that also communicates in a bidirectional fashion with the central nervous, endocrine, and immune systems, all acting in concert to control body homeostasis. Although UV energy has played an important role in the origin and evolution of life, UV absorption by the skin not only triggers mechanisms that defend skin integrity and regulate global homeostasis but also induces skin pathology (e.g., cancer, aging, autoimmune responses). These effects are secondary to the transduction of UV electromagnetic energy into chemical, hormonal, and neural signals, defined by the nature of the chromophores and tissue compartments receiving specific UV wavelength. UV radiation can upregulate local neuroendocrine axes, with UVB being markedly more efficient than UVA. The locally induced cytokines, corticotropin-releasing hormone, urocortins, proopiomelanocortin-peptides, enkephalins, or others can be released into circulation to exert systemic effects, including activation of the central hypothalamic-pituitary-adrenal axis, opioidogenic effects, and immunosuppression, independent of vitamin D synthesis. Similar effects are seen after exposure of the eyes and skin to UV, through which UVB activates hypothalamic paraventricular and arcuate nuclei and exerts very rapid stimulatory effects on the brain. Thus, UV touches the brain and central neuroendocrine system to reset body homeostasis. This invites multiple therapeutic applications of UV radiation, for example, in the management of autoimmune and mood disorders, addiction, and obesity.

Purpose: To evaluate neuroendocrine late effects in paediatric patients with low grade glioma (LGG) who underwent radiotherapy., Methods and Material: We performed a retrospective evaluation of 40 children with LGG treated from July 2002 to January 2015 with external radiotherapy. Tumour locations were cerebral hemisphere (n=2); posterior fossa (n=15); hypothalamic-pituitary axis (HPA, n=15); spine (n=5). Three patients presented a diffuse disease. We looked for a correlation between endocrine toxicity and tumour and treatment parameters. The impact of some clinical and demographic factors on endocrinal and neuro toxicity was evaluated using the log-rank test., Results: The median follow-up was 52months (range: 2-151). Median age at irradiation was 6. The dose to the HPA was significantly associated with endocrine toxicity (P value=0.0190). Patients who received chemotherapy before radiotherapy and younger patients, showed worse performance status and lower IQ. The 5-year overall survival (OS) and progression free survival (PFS) rates were 94% and 73.7%, respectively., Conclusion: Radiotherapy showed excellent OS and PFS rates and acceptable late neuroendocrine toxicity profile in this population of LGG patients treated over a period of 13years. In our experience, the dose to the HPA was predictive of the risk of late endocrine toxicity., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Lower vertebrates use rapid light-regulated changes in skin colour for camouflage (background adaptation) or during circadian variation in irradiance levels. Two neuroendocrine systems, the eye/alpha-melanocyte-stimulating hormone (α-MSH) and the pineal complex/melatonin circuits, regulate the process through their respective dispersion and aggregation of pigment granules (melanosomes) in skin melanophores. During development, Xenopus laevis tadpoles raised on a black background or in the dark perceive less light sensed by the eye and darken in response to increased α-MSH secretion. As embryogenesis proceeds, the pineal complex/melatonin circuit becomes the dominant regulator in the dark and induces lightening of the skin of larvae. The eye/α-MSH circuit continues to mediate darkening of embryos on a black background, but we propose the circuit is shut down in complete darkness in part by melatonin acting on receptors expressed by pituitary cells to inhibit the expression of pomc, the precursor of α-MSH., (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Two biological processes regulate light-induced skin colour change. A fast 'physiological pigmentation change' (i.e. circadian variations or camouflage) involves alterations in the distribution of pigment containing granules in the cytoplasm of chromatophores, while a slower 'morphological pigmentation change' (i.e. seasonal variations) entails changes in the number of pigment cells or pigment type. Although linked processes, the neuroendocrine coordination triggering each response remains largely obscure. By evaluating both events in Xenopus laevis embryos, we show that morphological pigmentation initiates by inhibiting the activity of the classical retinal ganglion cells. Morphological pigmentation is always accompanied by physiological pigmentation, and a melatonin receptor antagonist prevents both responses. Physiological pigmentation also initiates in the eye, but with repression of melanopsin-expressing retinal ganglion cell activity that leads to secretion of alpha-melanocyte-stimulating hormone (α-MSH). Our findings suggest a model in which eye photoperception links physiological and morphological pigmentation by altering α-MSH and melatonin production, respectively., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

In the eyes of mammals, specialized photoreceptors called intrinsically photosensitive retinal ganglion cells (ipRGC) have been identified that sense photoperiodic or daylight exposure, providing them over time with seasonal information. Detectors of photoperiods are critical in vertebrates, particularly for timing the onset of reproduction each year. In birds, the eyes do not appear to monitor photoperiodic information; rather, neurons within at least 4 different brain structures have been proposed to function in this capacity. Specialized neurons, called deep brain photoreceptors (DBP), have been found in the septum and 3 hypothalamic areas. Within each of the 4 brain loci, one or more of 3 unique photopigments, including melanopsin, neuropsin, and vertebrate ancient opsin, have been identified. An experiment was designed to characterize electrophysiological responses of neurons proposed to be avian DBP following light stimulation. A second study used immature chicks raised under short-day photoperiods and transferred to long day lengths. Gene expression of photopigments was then determined in 3 septal-hypothalamic regions. Preliminary electrophysiological data obtained from patch-clamping neurons in brain slices have shown that bipolar neurons in the lateral septal organ responded to photostimulation comparable with mammalian ipRGC, particularly by showing depolarization and a delayed, slow response to directed light stimulation. Utilizing real-time reverse-transcription PCR, it was found that all 3 photopigments showed significantly increased gene expression in the septal-hypothalamic regions in chicks on the third day after being transferred to long-day photoperiods. Each dissected region contained structures previously proposed to have DBP. The highly significant increased gene expression for all 3 photopigments on the third, long-day photoperiod in brain regions proposed to contain 4 structures with DBP suggests that all 3 types of DBP (melanopsin, neuropsin, and vertebrate ancient opsin) in more than one neural site in the septal-hypothalamic area are involved in reproductive function. The neural response to light of at least 2 of the proposed DBP in the septal/hypothalamic region resembles the primitive, functional, sensory ipRGC well characterized in mammals., (©2015 Poultry Science Association Inc.)

Animal seasonal reproduction involves complicated neuroendocrine processes of the hypothalamo-pituitary-gonadal axis. It is dominantly regulated by photoperiod, a crucial environmental cue. Melatonin, as internal photoperiod signal, regulates seasonal reproduction of animals. In recent years, it has been found that Kiss1/GPR54 system, which may influence GnRH secretion evidently, is regulated by both melatonin and feedback action of gonadal steroid hormones. Consequently, Kiss1/GPR54 system may play a key role in seasonal reproduction. Additionally, there exists another potential retrograde control pathway of seasonal breeding, which involves TSH-DIO2/DIO3 system. TSH-DIO2/ DIO3 system affects synthesis and secretion of GnRH and is regulated by melatonin, as well as Kiss1/GPR54 system. In this article, melatonin signal, especially the research advances of Kissl/GPR54 system and TSH-DIO2/DIO3 system were reviewed.

Purpose: The morphometric characteristics of A1 and A2 protocerebral neurosecretory neurons (cell and nuclei size, number of nucleoli in the nuclei); corpora allata size, nuclei size, cell number, were investigated in the pupae of yellow mealworm, Tenebrio molitor (L.), exposed to a strong static magnetic field of 320 mT maximum induction (10,000 times higher than the Earth's)., Materials and Methods: The experimental groups of Tenebrio molitor pupae were: A control group exposed only to natural magnetic field and sacrificed at the eighth day of pupal development (C); and pupae kept in a strong static magnetic field for eight days and then sacrificed (MF). Serial brain cross-sections were stained using the Alcian Blue Floxin technique. All the parameters were analyzed and measurements were performed using an image processing and analysis system (Leica, Cambridge, UK) linked to a Leica DMLB light microscope (program is QWin - Leica's Quantimet Windows-based image analysis tool kit)., Results: The values of morphometric parameters of neurosecretory neurons and corpora allata were significantly increased after exposure of the pupae to the strong magnetic field., Conclusions: The strong magnetic field influence characteristics of protocerebral neurosecretory neurons and corpora allata in the late Tenebrio molitor pupae.

Light and electron microscopic methods were used to analyze changes in secretory neurons in the supraoptic (SON) and paraventricular (PVN) nuclei in the hypothalamus in 100 adult male rats at time points from the first minutes to 180 days after 48 hours of full-time exposure to bright light. At the early time points after exposure, the cellular formulae of the SON and PVN shifted towards functionally active neurons with minimal quantities of secretory granules, large nuclei and nucleoli, low RNA contents, small numbers of rough endoplasmic reticulum cisterns, vacuoles, and lysosomes in the perikarya. The number of cells depositing secretion was greater than in controls at 24 h in the SON and PVN and at 10 days in the SON. Normalization of the cellular formula and the structural organization of the protein-synthesizing apparatus of PVN neurons occurred at 10-30 days, with normalization in the SON at 30-180 days. These data provide evidence that the range of plasticity of neurons in the PVN on exposure to full-time bright light was more significant than that in the SON.

The activity of large dorsomedial protocerebral A2' neurosecretory neurons were investigated in late pupae of Tenebrio molitor L, which were exposed to a static magnetic field of 320 mT. Experimental groups were C: the control group which was kept at 5 meters from the magnet; CMF: pupae which were reared in control conditions and sacrificed on the eighth day of pupal stage (parents were kept in a magnetic field); and MF: pupae kept in a permanent magnetic field for eight days. Our results indicate the effects of a static magnetic field on the cytological characteristics and activity of large A2' neurosecretory neurons of Tenebrio molitor pupae.

The structural changes of neurons of the rat hypothalamic supraoptic (SON) and of paraventricular (PVN) nucleus after 48 h of bright light exposure, of 5 Gy whole-body X-irradiation and of their combination subjected to the analysis by means of light-optic and of electron microscopy for the estimation of radimodificated effect of light exposure lasted 24 h a day and plasticity of neuroendocrine transducers interacted with the optic sensory system. The structural changes of neurons of the SON after combined action are less considerable and more prolonged in comparison with the PVN that loas defermined by their direct connection with the optic sensory system via the retinohypothalamic tract.

Day length regulates the effects of gonadal steroids on gonadotropin secretion and behavior in seasonal breeders. To determine whether this influence of photoperiod results from changes in androgen receptor expression in Siberian hamster brain regions that regulate neuroendocrine function, androgen receptor immunostaining was examined in castrated animals given either no androgen replacement or one of three doses of testosterone (T) resulting in physiological serum concentrations. Half of the animals were housed under inhibitory photoperiod conditions, and immunostaining was quantified 11 days later. Measurement of serum gonadotropin and prolactin concentrations confirmed that androgen exerted graded effects on pituitary function but that the animals were killed before photoperiodic influences had fully developed. T significantly increased the numbers of androgen receptor-immunoreactive cells in every brain region examined. Photoperiod exerted no significant influence on androgen receptor-immunoreactive cell number in the arcuate nucleus, bed nucleus of the stria terminalis (BNST), medial preoptic nucleus, or in medial amygdala. An interaction between T and photoperiod was observed in the BNST and in the rostral and middle portions of the arcuate nucleus. Although increasing concentrations of T resulted in more intense cellular immunostaining in the BNST and arcuate, this effect was not influenced by day length. These results indicate that relatively short-duration (11 days) exposure to inhibitory photoperiod triggers localized and regionally specific changes in androgen receptor expression.

The suppression of melatonin by exposure to low frequency electromagnetic fields (EMFs) 'the melatonin hypothesis'. has been invoked as a possible mechanism through which exposure to these fields may result in an increased incidence of cancer. While the effect of light on melatonin is well established, data showing a similar effect due to EMF exposure are sparse and, where present, are often poorly controlled. The current review focuses on the complexities associated with using melatonin as a marker and the dynamic nature of normal melatonin regulation by the circadian neuroendocrine axis. These are issues which the authors believe contribute significantly to the lack of consistency of results in the current literature. Recommendations on protocol design are also made which, if followed, should enable researchers to eliminate or control for many of the confounding factors associated with melatonin being an output from the circadian clock.

During American and Russian short and long-term space flights neuroimmune dysregulations have been observed in man and rats for up to three months after the return. During Extra-Vehicular Activity, radiation exposure risk is greater to elicit short and/or long-term deleterious effects on the functional capacity of the neuroimmune system. In order to assess the effects of high LET events on neuroimmune networks, our preliminary ground-based study was to investigate brain inflammatory responses in mouse after low dose radiation exposure with high LET particles (12C, 95MeV/u, 42 mGy). Plasma corticosterone levels were rapidly (6 hours) increased by two-fold, then decreased 24 hours post-irradiation. At 3 days plasma corticosterone and ACTH concentrations were also two- to three-fold increased. Plasma ACTH levels were still elevated up to seven days to two months. Furthermore immune functions are under current assessment. The results of this study should allow a greater understanding of the effects of high LET particles on neuroimmune system., (c2002 COSPAR. Published by Elsevier Science Ltd. All rights reserved.)

Disturbed growth in the child surviving cancer is multifactorial. This chapter examines the evidence for, and the difficulties in determining, individual drug treatment or disease effects at multiple endocrine levels influencing growth and against a changing baseline of adjuvant cancer therapies with potentially additive toxicity. The evolutionary pattern and potential aetiology of the neuro-endocrine deficit and growth-plate disturbance, the (unrandomized) effects of hormone replacement therapy and areas which require further study are also addressed. The reasons why growth hormone (GH) secretion is so exquisitely sensitive to disturbance, even though deficiencies soon after lesser cranial insults can be difficult to detect, are explored with evidence cited from the few existing prospective and interventional studies. The extent and nature of the hypothalamo-pituitary disturbance needs further prospective interventional study and disease-site- and treatment-specific comparisons. Practical treatment and surveillance strategies to optimize growth potential, age-appropriate development, peak bone mineral accretion, hair re-growth and future health and well-being are also suggested. Health-related outcomes resulting from today's newer therapies and enhanced surveillance need documenting in future (inter)national cancer trials, where randomized studies of hormonal intervention may also become possible.

Transcranial magnetic stimulation (TMS) is a technology that allows for non-invasive modulation of the excitability and function of discrete brain cortical areas. TMS uses alternating magnetic fields to induce electric currents in cortical tissue. In psychiatry, TMS has been studied primarily as a potential treatment for major depression. Most studies indicate that slow-frequency repetitive TMS (rTMS) and higher frequency rTMS have antidepressant properties. A meta-analysis of controlled studies indicates that this effect is fairly robust from a statistical viewpoint. However, effect sizes are heterogeneous, and few studies have shown that rTMS results in substantial rates of clinical response or remission, and the durability of antidepressant effects is largely unknown. We review in detail rTMS studies in the treatment of depression, as well as summarize treatment studies of mania, obsessive-compulsive disorder, post-traumatic stress disorder, and schizophrenia. We also review the application of TMS in the study of the pathophysiology of psychiatric disorders and summarize studies of the safety of TMS in human subjects.

The neuroendocrine and behavioral effects of repetitive transcranial magnetic stimulation (rTMS) were investigated in two rat lines selectively bred for high and low anxiety-related behavior. The stimulation parameters were adjusted according to the results of accurate computer-assisted and magnetic resonance imaging-based reconstructions of the current density distributions induced by rTMS in the rat and human brain, ensuring comparable stimulation patterns in both cases. Adult male rats were treated in two 3-day series under halothane anesthesia. In the forced swim test, rTMS-treatment induced a more active coping strategy in the high anxiety-related behavior rats only (time spent struggling; 332% vs. controls), allowing these animals to reach the performance of low anxiety-related behavior rats. In contrast, rTMS-treated low anxiety-related behavior rats did not change their swimming behavior. The development of active coping strategies in high anxiety-related behavior rats was accompanied by a significantly attenuated stress-induced elevation of plasma corticotropin and corticosterone concentrations. In summary, the behavioral and neuroendocrine effects of rTMS of frontal brain regions in high anxiety-related behavior rats are comparable to the effects of antidepressant drug treatment. Interestingly, in the psychopathological animal model repetitive transcranial magnetic stimulation induced changes in stress coping abilities in the high-anxiety line only.

Background: Cranial irradiation for children with brain tumors frequently leads to neuroendocrine deficiencies. In this controlled study, the authors investigated risk factors for cardiovascular disease (CVD) for long term survivors of childhood brain cancer. They also tested whether the presence of these risk factors was related to endocrine status., Methods: In 26 survivors of childhood brain cancer (mean age, 25.8 years; mean posttreatment interval, 16 years) and 29 healthy controls (mean age, 27.7 years), the blood pressure, smoking habits, body mass index (BMI), and waist/hip (W/H) ratio were determined. Lipids and lipoproteins were measured and endocrine function was assessed. Carotid intima-media thickness (IMT) measurements were performed by high resolution ultrasonography., Results: In the survivors of childhood brain cancer, systolic blood pressure and W/H ratio were elevated compared with controls. The cholesterol/high density lipoprotein ratio (4.7 +/- 1.7 vs. 3.4 +/- 0.8 mmol/L, P = 0.0005), low density lipoprotein cholesterol level (3.3 +/- 0.9 vs. 2.8 +/- 0.6 mmol/L, P = 0.027), and apolipoprotein B level (P = 0.001) were higher in survivors of childhood brain cancer, whereas HDL cholesterol was lower (P = 0.005). The IMT was increased in the survivor group, but only in the carotid bulb (0.63 mm +/- 1.6 vs. 0.53 mm +/- 1.1, P = 0.02), not in the internal or common carotid artery. In the absolute growth hormone deficient (GHD) population (n = 9), LDL cholesterol and apolipoprotein B levels were elevated and the W/H ratio was particularly increased compared with the other survivors of childhood brain cancer., Conclusions: For long term survivors of brain cancer, the risk for CVD is strongly increased due to dyslipidemia, central obesity, and elevated systolic blood pressure, particularly for those with GHD. The first effects of this increased risk for CVD were observed in the carotic bulb, as assessed by IMT measurements. Efforts should be directed at CVD prevention by risk factor control.

Ultraviolet (UV) irradiation of the skin causes both inflammation and alterations in the skin immune system. There is increasing experimental evidence that UV-induced skin inflammation is influenced by the sensory nervous system and the neuroendocrine system in the skin. The resulting complex network of cytokines, chemokines, neuropeptides, neuropeptide-degrading enzymes, neurohormones, and other inflammatory mediators mediate photodermatitis and cutaneous inflammation. Neuropeptides such as substance P (SP) and calcitonin gene-related peptide (CGRP) are released from sensory nerves innervating the skin upon UV exposure. In addition, a variety of cells in the skin produce increased neuroendocrine hormones such as proopiomelanocortin (POMC) peptides and their receptors as well as neurotrophins after UV exposure. Neuropeptides and neurohormones are capable of directly or indirectly mediating UV-induced cutaneous neurogenic inflammation by the induction of vasodilatation, plasma extravasation, and augmentation of UV-induced cytokine, chemokine, or cellular adhesion molecule expression required for activation and trafficking of inflammatory cells into the inflamed tissue. Neuropeptides and neurotrophins may also play a role in the repair of cutaneous UV injury. In addition to proinflammatory effects, UV-induced neuropeptides and neurohormones such as CGRP and alpha-melanocyte-stimulating hormone may have immunosuppressive effects in the skin. This review will focus on the role that SP, CGRP, POMC peptides, and their receptors may play in modulating UV-induced inflammation in the skin.

Light can induce an acute suppression and/or circadian phase shift of plasma melatonin levels in subjects with normal color vision. It is not known whether this photic suppression requires an integrated response from all photoreceptors or from a specialized subset of photoreceptors. To determine whether normal cone photoreceptor systems are necessary for light-induced melatonin suppression, we tested whether color vision-dificient human subjects experience light-induced melatonin suppression. In 1 study, 14 red-green color vision-deficient subjects and 7 normal controls were exposed to a 90-min, 200-lux, white light stimulus from 0200-0330 h. Melatonin suppression was observed in the controls (t = -7.04; P < 0.001), all color vision-deficient subjects (t = -4.76; P < 0.001), protanopic observers (t = -6.23; P < 0.005), and deuteranopic observers (t = -3.48; P < 0.05), with no significant difference in the magnitude of suppression between groups. In a second study, 6 red/green color vision-deficient males and 6 controls were exposed to a broad band green light stimulus (120 nm with lambda max 507 nm; mean +/- SEM, 305 +/- 10 lux) or darkness from 0030-0100 h. Hourly melatonin profiles (2000-1000 h) were not significantly different in onset, offset, or duration between the two groups. Melatonin suppression was also observed after exposure to the green light source at 0100 h (color vision deficient: t = -2.3; df = 5; P < 0.05; controls: t = -3.61; df = 5; P < 0.01) and 0115 h (color vision deficient: t = -2.74; df = 5; P < 0.05; controls: t = -3.57; df = 5; P < 0.01). These findings suggest that a normal trichromatic visual system is not necessary for light-mediated neuroendocrine regulation.

Temperate zone birds terminate reproduction when they become photorefractory. In many species, refractoriness is "absolute" in that gonadal regression occurs before day length declines, and individuals are reproductively unresponsive even to continuous light. Based on studies of a few species, this form of refractoriness appears to be associated with a reduction (compared with breeding and/or photosensitive birds) in numbers of hypothalamic cells and fibers that are immunoreactive for gonadotropin releasing hormone (GnRH). Some species display "relative" refractoriness, in that day length must decline before gonadal regression occurs, and individuals never lose the capacity to respond to very long days. A few reports suggest that GnRH levels in the brain do not change in relatively refractory birds. House sparrows (Passer domesticus) regress their gonads sooner when day length declines during summer than they do if photoperiod is not permitted to decline after the summer solstice (i.e., they appear to be "relatively" refractory). However, if held on long days they eventually regress the gonads despite no decline in photoperiod (they appear to be "absolutely" refractory). In this experiment, we tested whether gonadal regression was associated with changes in hypothalamic GnRH in adult male house sparrows. We used immunocytochemistry (primary antibody sensitive to both forms of avian GnRH) to compare the distribution and number of GnRH-immunoreactive cells and fibers among reproductively active individuals on long days, "absolutely" refractory individuals on long days, and presumably "relatively" refractory individuals induced to regress by shortened days. Similar reductions in ir-GnRH cell number and cell size occurred in both groups of refractory birds compared with birds still in breeding condition. Gonadal regression also was correlated with reduced staining intensity of cell bodies and reduced fiber staining, but these reductions were somewhat more pronounced in the "absolutely" than the "relatively" refractory birds. We discuss these results in light of other studies of avian GnRH changes with reproductive stage. Our results are consistent with the idea that house sparrows become absolutely refractory, regardless of whether exposed to a decline in photoperiod. However, the results also suggest that relative refractoriness may induce gonadal regression through a cessation of GnRH secretion, whereas absolute refractoriness involves down-regulation of peptide production as well.

The biological effects of relative low level internal irradiation were introduced. 1. Life span studies on carcinogenesis. Pacific Northwest Laboratory observed 3782 rats given a single inhalation of 239Pu O2 at initial lung burden ranging from 0.25 to 180 nCi. Significant life span shortening was found at lung dose > 8 Gy and it was indicated that the presence of a "possible" threshold of about 1 Gy for lung tumor formation. 2. Health effects of radon and its progeny. Both experimental and epidemiological survey were studied. The nominal probability coefficient (fatality) for the public and workers are 7.90 x 10(5) per mJhm-3 (2.77 x 10(-4) per working level month, WLM). 3. Health effects on 3H on postnatal brain development and neurobehavior, genetic effects, carcinogenic effects and adaptive effects of 3H were investigated. 4. Study on the effects of neuroendocrine system under low level irradiation of 75Se (Auger electron emitter) and 35S (beta-particles emitter). The results showed that the neuroendocrine system is very sensitive to small dose of internal irradiation.

A controlled trial entered 343 patients with virus hepatitis A, B and associated forms. In addition to standard treatment the patients' adrenals and thyroid were exposed to electromagnetic waves (460 MHz) in alternative daily regimens and under minimal power. As shown by clinical, rheohepatographic, hormonal, immunological and follow-up evidence, positive results were achieved in 69% of the patients.

It has been found that in 2 hours after the total gamma irradiation of rats at doses of 20 and 100 Gy the ACTH and glucagon levels in plasma increased by 5-6 and 10-12 times correspondingly. No significant changes in levels of plasma insulin and glucose have been revealed.

Thymomodulin and Thymolymphotropin, biologically active thymus derivative peptides exert recovery effects on the functionality of some membrane bound, mitochondrial and lysosomal enzymes (monoamine oxidase, ATPase, phosphatases, cytochrome oxidase, succinate oxidase) affected by gamma-irradiation. These drugs exert antistress effect by re-establishing the function of hypothalamus-pituitary-adrenal axis and that of lymphoid organs.

The light/dark cycle to which animals, and possibly humans, are exposed has a major impact on their physiology. The mechanisms whereby specific tissues respond to the light/dark cycle involve the pineal hormone melatonin. The pineal gland, an end organ of the visual system in mammals, produces the hormone melatonin only at night, at which time it is released into the blood. The duration of elevated nightly melatonin provides every tissue with information about the time of day and time of year (in animals that are kept under naturally changing photoperiods). Besides its release in a circadian mode, melatonin is also discharged in a pulsatile manner; the physiological significance, if any, of pulsatile melatonin release remains unknown. The exposure of animals including man to light at night rapidly depresses pineal melatonin synthesis and, therefore, blood melatonin levels drop precipitously. The brightness of light at night required to depress melatonin production is highly species specific. In general, the pineal gland of nocturnally active mammals, which possess rod-dominated retinas, is more sensitive to inhibition by light than is the pineal gland of diurnally active animals (with cone-dominated retinas). Because of the ability of the light/dark cycle to determine melatonin production, the photoperiod is capable of influencing the function of a variety of endocrine and non-endocrine organs. Indeed, melatonin is a ubiquitously acting pineal hormone with its effects on the neuroendocrine system having been most thoroughly investigated. Thus, in nonhuman photoperiodic mammals melatonin regulates seasonal reproduction; in humans also, the indole has been implicated in the control of reproductive physiology.

Damage to bowel often complicates radiotherapy for abdominal and pelvic malignancy. The symptoms of chronic irradiation enteropathy, which often include intractable diarrhoea, are generally attributed to vascular injury. We have examined specimens of bowel resected from patients who had been therapeutically irradiated to assess the extent of injury to the enteric nerve plexuses. To facilitate visualisation of nerve fibres and cells of neural or neuroendocrine origin, sections were immunostained with antibodies to neuron-specific enolase or PGP 9.5, widely used markers of nerves and neurons. Electron microscopy was performed in selected cases. In 27 out of 33 specimens the number of nerve fibres in the lamina propria was obviously increased compared to that in control material. Scattered cells with the histological, immunohistochemical and ultrastructural features of ganglion cells were noted within the lamina propria in 23 of the specimens, and in 18 cases so-called neuroendocrine cells, not normally seen in this location, were also present. These radiation-induced changes in the innervation of the bowel may contribute to the symptoms of chronic radiation enteropathy.

A single whole-body X-irradiation of pregnant Wistar rats at a dose of 1.05 Gy at 10.30, 12.30 and 14.30 h respectively, of gestational day 10 resulted in significantly high incidences of hydrocephalic offspring. No hydrocephalic offspring resulted from X-irradiation of pregnant rats with 1.05 Gy at 16.30 h, whereas a dose of 1.22 Gy at 16.30 h resulted in a low but statistically significant incidence of hydrocephalus. Neither 1.05 Gy nor 1.22 Gy X-irradiation of pregnant rats at 18.30 h resulted in any hydrocephalic offspring. Dysplasia of the subcommissural organ was noticed in all the hydrocephalic brains histologically examined.

The literature on taste aversion learning is reviewed and discussed, with particular emphasis on those studies that have used exposure to ionizing radiation as an unconditioned stimulus to produce a conditioned taste aversion. The primary aim of the review is to attempt to define the mechanisms that lead to the initiation of the taste aversion response following exposure to ionizing radiation. Studies using drug treatments to produce a taste aversion have been included to the extent that they are relevant to understanding the mechanisms by which exposure to ionizing radiation can affect the behavior of the organism.

The role of the area postrema in radiation-induced emesis and taste aversion learning and the relationship between these behaviors were studied in cats. The potential involvement of neural factors which might be independent of the area postrema was minimized by using low levels of ionizing radiation (100 rads at a dose rate of 40 rads/min) to elicit a taste aversion, and by using body-only exposures (4500 and 6000 rads at 450 rads/min) to produce emesis. Lesions of the area postrema disrupted both taste aversion learning and emesis following irradiation. These results, which indicate that the area postrema is involved in the mediation of both radiation-induced emesis and taste aversion learning in cats under these experimental conditions, are interpreted as being consistent with the hypotheses that similar mechanisms mediate both responses to exposure to ionizing radiation, and that the taste aversion learning paradigm can therefore serve as a model system for studying radiation-induced emesis.

The effect of spinal anesthesia, dilatation and curettage plus the first intracavitary radiotherapy or only that of intracavitary radiotherapy on growth hormone (HGH = the response of anterior pituitary) and arginine vasopressin (AVP = the response of posterior pituitary) levels was studied in 10 patients suffering from cervical or endometrial uterine cancer. Differing from earlier animal studies, irradiation had no effect on GH or AVP secretion, nor was there any change in the hormone levels following spinal anesthesia and dilatation and curettage. The neurosecretory response of hypothalamic-hypophyseal axis to spinal anesthesia and minor gynecological surgery appears to be minimal.

Studies carried out in several mammalian species during the 1950's led to the concept of a 'vomiting center' located in the dorsolateral reticular formation and a 'chemoreceptor trigger zone' (CTZ) within or near the area postrema (AP). This early work suggested that the AP was essential for vomiting induced by a variety of chemical emetics and by ionizing radiation. However, the lesion techniques used often produced significant damage to neural tissue underlying the AP, as well as to the AP itself, making localization of function very difficult. In the present study, electrolytic lesions confined to the AP abolished both radiation- and apomorphine-induced emesis in dogs. Thus, in addition to its postulated function in osmoreception and central cardiovascular regulation, the AP also appears to have a key role in vomiting initiated by chemical emetics and by ionizing irradiation.

An experimental study in pregnant rats has demonstrated an obvious effect of endonasal, vaginal and epigastric application of the helium-neon laser on histophysiologic characteristics of the hypothalamo-neuropituitary neurosecretory system, the epiphysis and the myometrium. Therefore, the exposure to the laser beam, particularly the endonasal one may enhance the cervical-hypothalamic reflex.

Exposure of the general public and in particular certain occupational groups to radiofrequency radiation (RFR) is ubiquitous and of growing concern. No clear and widely accepted understanding of the biological effects and health implications of such RFR exposure has emerged. This paper reviews the data available, including reports of RFR effects on single cells or cell components, on genetic composition or development, on developed organs, tissues, or cell systems, and on integrative and regulatory biological systems. Reports of RFR effects on the immunological system, with consideration of the influence of neuroendocrine responses, are critically reviewed in greater detail to illustrate important points regarding data acquisition and assessment, and understanding and application of the RFR bioeffects literature in general. Factors affecting RFR bioeffects research are reviewed, and recommendations for future studies are provided.

Electrical activity was recorded intracellularly from neurosecretory cells in the crayfish eyestalk identified by lucifer yellow injection. The activity is most commonly enhanced by illumination of retinal fields. Increments in spontaneous activity as well as bursts in otherwise silent cells were the most common type of response. Occasionally light-induced inhibitory responses were recorded. At neuropil level, light pulses result in EPSPs with amplitudes dependent on intensity of light and the previous adaptation to darkness.