A kilonova as the electromagnetic counterpart to a gravitational-wave source.

Gravitational waves were discovered with the detection of binary black-hole mergers and they should also be detectable from lower-mass neutron-star mergers. These are predicted to eject material rich in heavy radioactive isotopes that can power an electromagnetic signal. This signal is luminous at optical and infrared wavelengths and is called a kilonova. The gravitational-wave source GW170817 arose from a binary neutron-star merger in the nearby Universe with a relatively well confined sky position and distance estimate. Here we report observations and physical modelling of a rapidly fading electromagnetic transient in the galaxy NGC 4993, which is spatially coincident with GW170817 and with a weak, short γ-ray burst. The transient has physical parameters that broadly match the theoretical predictions of blue kilonovae from neutron-star mergers. The emitted electromagnetic radiation can be explained with an ejected mass of 0.04 ± 0.01 solar masses, with an opacity of less than 0.5 square centimetres per gram, at a velocity of 0.2 ± 0.1 times light speed. The power source is constrained to have a power-law slope of -1.2 ± 0.3, consistent with radioactive powering from r-process nuclides. (The r-process is a series of neutron capture reactions that synthesise many of the elements heavier than iron.) We identify line features in the spectra that are consistent with light r-process elements (atomic masses of 90-140). As it fades, the transient rapidly becomes red, and a higher-opacity, lanthanide-rich ejecta component may contribute to the emission. This indicates that neutron-star mergers produce gravitational waves and radioactively powered kilonovae, and are a nucleosynthetic source of the r-process elements.

An ultraviolet-optical flare from the tidal disruption of a helium-rich stellar core.

The flare of radiation from the tidal disruption and accretion of a star can be used as a marker for supermassive black holes that otherwise lie dormant and undetected in the centres of distant galaxies. Previous candidate flares have had declining light curves in good agreement with expectations, but with poor constraints on the time of disruption and the type of star disrupted, because the rising emission was not observed. Recently, two 'relativistic' candidate tidal disruption events were discovered, each of whose extreme X-ray luminosity and synchrotron radio emission were interpreted as the onset of emission from a relativistic jet. Here we report a luminous ultraviolet-optical flare from the nuclear region of an inactive galaxy at a redshift of 0.1696. The observed continuum is cooler than expected for a simple accreting debris disk, but the well-sampled rise and decay of the light curve follow the predicted mass accretion rate and can be modelled to determine the time of disruption to an accuracy of two days. The black hole has a mass of about two million solar masses, modulo a factor dependent on the mass and radius of the star disrupted. On the basis of the spectroscopic signature of ionized helium from the unbound debris, we determine that the disrupted star was a helium-rich stellar core.

The role of the dura in conditioned taste avoidance induced by cooling the area postrema of male rats.

Experiments were designed to assess the contribution of the dura mater to the formation of conditioned taste avoidance induced by cooling the area postrema. The results of the first experiment verified that the temperature of the dura showed a temperature gradient at various distances from the tip of the cold probe. In the second and third experiments, a circle of dura was cut away so that different amounts of the area postrema could be cooled without cooling the overlying dura. Cooling the dura plus the area postrema did not produce a stronger avoidance than just cooling the area postrema. In the fourth experiment, the cerebellar cortex was cooled with and without cooling the dura. Cooling the cerebellar cortex produced conditioned taste avoidance, and cooling the dura plus the cerebellar cortex did not produce a stronger avoidance. Taken together, these results suggest that cooling the dura mater does not contribute to the conditioned taste avoidance induced by cooling the area postrema. The results of the fifth experiment showed that cooling the area postrema produced a stronger conditioned taste avoidance than cooling the cerebellar cortex. It is suggested that the avoidance induced by cooling both of these structures is the result of physiological changes occurring when neurons in these structures are inactivated and when the subdural meninges are cooled. Furthermore, these changes are more severe when the area postrema is cooled.

Estradiol accelerates extinction of lithium chloride-induced conditioned taste aversions through its illness-associated properties.

Estradiol accelerates extinction of LiCl-induced conditioned taste aversions when it is present during a period that starts 2-3 days after acquisition and extends throughout extinction (before and during extinction). It has been suggested that estradiol acts before, not during, extinction and that its effect on extinction is associated with its illness-inducing properties. This hypothesis is based on previous work which shows an attenuation of conditioned taste aversion learning when rats are exposed to illness-inducing agents during a period that starts 2 days after acquisition and ends 2 days before extinction trials are initiated. Four experiments were designed to test elements of this hypothesis. The first two experiments demonstrated that if an estradiol-filled Silastic capsule is implanted before extinction of a LiCl-induced aversion, when the conditioned taste is not present, it accelerates extinction, but if it is implanted during extinction, when the conditioned taste is present, it prolongs extinction. The third experiment showed that the same dose of estradiol that accelerates extinction of a LiCl-induced aversion was effective in producing a conditioned taste aversion when it was present for 18 h after consumption of a novel sucrose solution. The fourth experiment indicated that serum levels of estradiol were elevated during the 18 h. These results are consistent with the hypothesis that the acceleration of extinction by estradiol is associated with its illness-inducing properties. It is suggested that estradiol acts on neural areas that mediate illness information and that one of these areas, the area postrema is necessary for estradiol to accelerate extinction of a LiCl-induced aversion.

Estradiol accelerates extinction of a conditioned taste aversion in female and male rats.

Exogenous testosterone treatment prolongs extinction of conditioned taste aversions and estradiol treatment prevents testosterone from prolonging extinction in both gonadectomized males and females. Estradiol could require the presence of testosterone for its effect or its action alone could accelerate extinction. The first series of experiments were designed to test the hypothesis that estradiol accelerates extinction when it is given in the absence of testosterone. The results showed that estradiol accelerates extinction of conditioned taste aversions in the absence of testosterone in gonadectomized Sprague-Dawley females and Fischer 344 females and males. The second series of experiments were designed to determine whether estradiol and testosterone differ in the temporal requirements for their opposite effects on extinction. The results showed that estradiol can accelerate extinction when it is present before and during acquisition (from 8 days before until 3 days after acquisition) or when it is present before and during extinction (from 2 days after acquisition, which was 23 days before extinction, until extinction trials were terminated). This is in contrast to a previous finding that testosterone prolongs extinction only when it is present before and during extinction. The following two hypotheses were suggested to account for the temporal effects of estradiol on extinction of conditioned taste aversions: (1) the presence of estradiol during acquisition reduces the effectiveness of LiCl through its action on the opioid system, and the presence of estradiol during extinction activates a neural pathway, such as that associated with activity levels, that accelerates extinction of passive avoidance tasks in general or (2) the presence of estradiol before, not during, acquisition or extinction accelerates extinction because of its illness-inducing properties. Most of the evidence supports the second hypothesis.

Cooling the area postrema induces conditioned taste aversions in male rats and blocks acquisition of LiCl-induced aversions.

The experiments presented in this article were designed to examine whether area postrema (AP) lesions attenuate LiCl-induced conditioned taste aversions (CTAs) by disruption of information about the illness-producing properties of LiCl or by a lesion-induced malaise. Reversible lesioning of the AP caused by cooling induced a CTA in male rats. The cooling-induced CTA could be blocked if males were exposed to cooling for several days before acquisition day. Acquisition of a LiCl-induced CTA was blocked in males if they were exposed to cooling before acquisition day and during LiCl administration on acquisition day was attenuated but not blocked in males if they were exposed to cooling only before acquisition day, and was unchanged in males if they were exposed to cooling only during LiCl administration. Taken together these results indicate that the AP is important for acquisition of LiCl-induced CTAs but that inactivation of this area is so aversive it will induce CTAs that can obscure the attenuation of LiCl-induced aversions.

The effects of cooling the area postrema of male rats on conditioned taste aversions induced by LiC1 and apomorphine.

Although permanent lesion studies have demonstrated that the area postrema (AP), a chemoreceptor trigger zone, is part of the neural mechanism for conditioned taste aversions (CTAs), its exact role remains questionable. It has been suggested that the attenuated acquisition of a CTA after permanent lesions of the AP is the result of an inability to recognize the conditioned taste as novel. The present series of experiments was designed to test the hypothesis that lesions of the AP interfered with LiCl processing and not recognition of taste novelty. This was accomplished by using the reversible lesioning procedure, cooling, only during administration of the illness-inducing agent. In Expt. 1, measurement of thermal lines around the tip of the cold probe in the AP indicated that our cooling procedures allowed the majority of the AP to be cooled to temperatures that suppress neuronal activity and transsynaptic transmission, but not axonal transmission. In Expts. 2 and 3, rats were injected with either LiCl or apomorphine after consumption of a 10% sucrose solution. Cooling of the AP was initiated 5 min before administration of one of the illness-inducing agents and was continued for 55 min after injection. The rats were tested later for acquisition while the neural function of the AP was preserved. Our experimental results demonstrated that cooling the AP could attenuate the CTA induced by LiCl, but had no effect on the CTA induced by apomorphine. Since the AP was functional when the rats encountered the novel sucrose solution both before and after conditioning, but not functional when LiCl was given, these results do not support the recognition of taste novelty hypothesis.

The role of serum testosterone in the accelerated extinction of a conditioned taste aversion in fluid deprived male rats.

Fluid deprivation decreases serum testosterone (T) levels and increases the rate of extinction of a conditioned taste aversion in Sprague-Dawley male rats. It has been suggested that the decreased serum levels may be the primary factor responsible for the accelerated extinction rates during fluid deprivation. To test the generality of this hypothesis, the effect of fluid deprivation on T levels and extinction rate was investigated in Fischer 344 male rats. Extinction rates were accelerated in Fischer 344 rats but T levels were not decreased. In a second study, the behavioral and hormonal responses of Fischer 344 and Sprague-Dawley males to fluid deprivation were compared. Extinction rates were increased in both strains of rat by fluid deprivation, but serum T levels were decreased in fluid-deprived Sprague-Dawley males and not Fischer 344 males. It was suggested that the accelerated extinction in fluid-deprived Sprague-Dawley males was primarily due to decreases in serum T levels, while the faster extinction in deprived Fisher 344 males could be accounted for by decreases in sensitivity to T.

Decreased testosterone levels and accelerated extinction of a conditioned taste aversion in fluid-deprived male rats.

The hypothesis that fluid deprivation accelerates extinction of a conditioned taste aversion in male Sprague-Dawley-derived rats by reducing serum testosterone levels was tested. Serum testosterone levels were found to be lower in fluid-deprived males than in nondeprived males (Experiments 1 and 2). Exogenous testosterone treatment that results in high physiological levels of serum testosterone slowed the extinction of fluid-deprived gonadectomized males to rates comparable with those of nondeprived sham males (Experiment 3). It was noted, however, that testosterone treatment was less effective in slowing extinction in fluid-deprived gonadectomized males than in nondeprived gonadectomized males even though the serum testosterone levels were the same (Experiments 3 and 4). These results provide strong support for the original hypothesis, but they suggest that fluid deprivation also reduces sensitivity to testosterone.

Age-related deficits in brain estrogen receptors and sexual behavior of male rats.

Neural estrogen receptors (ER), serum testosterone (T), estradiol (E2) and luteinizing hormone (LH), and masculine sexual behavior were measured in young (5 months) and old (24 1/2 months) Fischer 344 male rats. We found that old intact males, which displayed significantly lower levels of sexual behavior, T, and LH than young intact males, also had lower levels of nuclear ER (ERn) in the amygdala (AMG). The age difference in ER binding did not appear to be a consequence of altered blood E2 levels because circulating E2 did not differ between the two age groups. Gonadectomy eliminated ejaculatory behavior and significantly reduced ERn in young males. When we administered exogenous T to gonadectomized males in doses that approximated levels found in young intact males, we found that sexual performance of old males was stimulated to precastration levels but not to levels found in young males. Moreover, such treatment failed to increase ERn in the AMG of old males to the levels measured in the AMG of young males. These results suggest that there is an association between the inability of T to increase ERn concentration in the AMG and the deficits in sexual performance that are characteristic of old males. Thus, the capacity of neural tissue to bind estrogen, presumably derived from circulating T, may be a limiting factor in the determination of androgen responsiveness in aging males.

Sexual behavior and serum levels of prolactin, testosterone, and estradiol in young and old rhesus males.

It has been suggested that increased prolactin levels may contribute to decreased libido in aging male primates. To test this hypothesis, the association of sexual performance and serum prolactin levels was determined in young (10 year) and old (25.7 year) male rhesus macaques. Old males displayed significantly lower levels of sexual behavior than young males but their serum prolactin levels were not significantly higher. The correlation between prolactin levels and different measures of sexual behavior also were not significant for either old or young males. These data suggest that elevations in prolactin levels do not significantly contribute to the age-related decline in sexual performance in rhesus males.

Age-related deficits in brain androgen binding and metabolism, testosterone, and sexual behavior of male rats.

Brain androgen binding and metabolism, serum testosterone (T), and sexual behavior were measured in old and young male Fischer 344 rats. After completion of sexual behavior tests, blood was collected for T assay and brains were removed for simultaneous measurements of cytosolic (ARc) and nuclear (ARn) androgen receptors and aromatase activity (AA) in the preoptic area (POA), hypothalamus (HYP) and amygdala (AMG). In Experiment 1, old and young intact males were examined. None of the old males ejaculated in any of the tests of sexual behavior whereas all of the young males ejaculated. The old males had lower levels of serum T, lower levels of ARn in the POA and HYP and lower levels of AA in the POA. The ARc levels of the old and young males did not differ. Experiment 2 was designed to determine if the deficits in brain androgen binding and metabolism were due to low levels of T. Old and young T-treated gonadectomized (GX-T) males and young intact (I) males were examined. T levels were comparable in the young and old GX-T males and were higher in each of these groups than in the young I males. In sexual behavior tests, all of the young but only 25% of the old GX-T males ejaculated. Although ARn levels in the old GX-T males were lower than in the young GX-T males, they were comparable to the young I male levels. No age-related differences in T induction of AA were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Sensitivity of male, female, and androgenized female rats to testosterone during extinction of a conditioned taste aversion.

Experiment 1 tested the hypothesis that male and female rats differ in the amount of testosterone (T) required to prolong extinction of a conditioned taste aversion. Gonadectomized male and female rats were implanted with empty or 30-, 60-, or 120-mm T-filled capsules. The males had slower extinction rates than females when both were implanted with 30-mm and 60-mm capsules but not when implanted with 120-mm capsules. The dimorphic sensitivity was not due to differences in plasma T levels: the levels for males and females were not different. Experiment 2 tested the hypothesis that the presence of T during the perinatal period results in a greater sensitivity to T in adulthood. Females exposed to T during the perinatal period showed prolonged extinction when given a 30-mm T-filled capsule as an adult, whereas unexposed females did not. These results support the hypothesis that the amount of T required to activate the prolonged extinction in an adult depends on perinatal exposure to T.

Blockage of the effects of testosterone on extinction of a conditioned taste aversion by estradiol: time of action.

Testosterone (T) prolongs the extinction of a conditioned taste aversion only if it is present during extinction. Experiments were conducted to determine whether estradiol (E) blocks the effects of T by acting during acquisition or extinction. In the first experiment, gonadectomized male and female rats injected with estradiol dipropionate (EP) and testosterone propionate (TP) during extinction had significantly faster extinction rates than those only injected with TP. Treating gonadectomized rats with TP prior to as well as during extinction did not prevent EP from blocking the effects of T. In Experiment 2, E was equally effective in preventing T from prolonging extinction when it was implanted in gonadectomized males during acquisition, extinction, or both acquisition and extinction. Thus, E does not have to be present concurrently with T during extinction to be effective. This suggests that E does not act on a T-related mechanism but rather acts independently of T.

Sexual performance of old and young male rhesus macaques following treatment with GnRH.

GnRH has been reported to facilitate sexual performance in a number of species. To determine whether the same was true for rhesus monkeys we measured sexual behavior and serum levels of testosterone (T) and luteinizing hormone (LH) following control tests and after treatment with two doses of GnRH. In the first experiment, old intact (N = 11) and old T-implanted, castrated (N = 4) rhesus macaques were examined. Mean intromission rate of old intact males was significantly lower following treatment with 100 micrograms of GnRH than following control injections. Other measures of sexual behavior did not differ across treatments. There were no significant treatment effects among the old castrated males. The failure to facilitate sexual performance may have been due to the age of the males and not to the species under study. Thus, in a second experiment the effects of GnRH were examined in young rhesus males. Again, there was no facilitation of sexual performance. This cannot be accounted for by a failure of GnRH to produce a physiological response. For both old and young intact males serum levels of LH and T increased significantly after treatment with both doses of GnRH. LH but not T levels increased significantly in the T-implanted males.

The effect of human chorionic gonadotropin on serum levels of testosterone, estradiol, and sexual behavior in young and old rhesus males.

Sexual behavior and serum levels of testosterone (T) and estradiol (E) were examined in five young and six old rhesus males (Macaca mulatta) before and after the injection of 500 and 1000 IU of HCG. The serum levels of T and E increased in both young and old males after injection of either dose of HCG. Serum levels of T were significantly higher in young than in old males in the period following the last injection of 1000 IU of HCG. Old males had significantly higher levels of serum E during treatment with 1000 IU of HCG, but serum E levels in the two groups did not differ before or after treatment. Serum levels of T and E did not differ between the young and old males when injected with 500 IU of HCG. HCG had no effect on sexual performance and the differences in levels of sexual performance between the young and old males were not eliminated.

Apomorphine, deprenyl, and yohimbine fail to increase sexual behavior in rhesus males.

Various doses of apomorphine, deprenyl, and yohimbine were administered to old (20-26 years) rhesus males that had been sexually active when younger and to younger (6-17 years) males that were characteristically sexually sluggish. These neuropharmacological agents have been reported to increase sexual behavior in male rats. In Experiment 1, 10 old intact rhesus males were tested after injection of vehicle and apomorphine, and 6 old testosterone-treated castrated males were tested after treatment with deprenyl and yohimbine and the vehicles for each drug. In experiment 2, the 5 younger males were tested after treatment with each of the drugs and with the vehicles for each drug. There were a few minor changes in behavior associated with certain doses of each of the drugs and as many depressive as facilitative effects on sexual behavior. This suggests that there are basic differences between rats and rhesus macaques in the systems mediating sexual behavior.

Change of female partner and postejaculatory performance of young and old rhesus males.

This study was undertaken to determine whether a change of female partner following ejaculation would reduce the postejaculatory interval (PEI). The male subjects were seven old (mean age 22.4 years) and five young (mean age 12.2 years) rhesus males (Macaca mulatta). The female subjects were four ovariectomized females rendered sexually receptive by treatment with estradiol benzoate. Introduction of a different female following ejaculation significantly reduced the PEI and latency to a second ejaculation in both young and old males. However, a different female did not reduce latencies to preejaculatory levels. The potential for enhanced sexual performance was retained in old rhesus males.

Old age and sexual exhaustion in male rhesus macaques.

The capacity for multiple ejaculations was measured in three groups of rhesus macaques whose ages ranged from 9 to 30 years. Each male was given a test of sexual exhaustion with each of five ovariectomized, estrogen treated females. Sexual exhaustion was defined as a 45-min period without a mount when the males were paired with a female. None of the very old males (25-30 years, N = 4) achieved more than two ejaculations before reaching sexual exhaustion. Old males (19-20 years, N = 5) displayed as many as six ejaculations and fully adult (9-15 years, N = 5) males achieved a maximum of five ejaculations before meeting the criterion of sexual exhaustion. Although very old males mounted as often as younger males they achieved fewer intromissions and the latency to intromission and ejaculation was longer. Mean mount and ejaculation latencies and the postejaculatory interval increased after ejaculation in all age groups. The females were not equally attractive sexually to the males and very old males were especially selective, copulating with only three of the females.