Spatial and temporal genetic structure at the fourth trophic level in a fragmented landscape.

A fragmented habitat becomes increasingly fragmented for species at higher trophic levels, such as parasitoids. To persist, these species are expected to possess life-history traits, such as high dispersal, that facilitate their ability to use resources that become scarce in fragmented landscapes. If a specialized parasitoid disperses widely to take advantage of a sparse host, then the parasitoid population should have lower genetic structure than the host. We investigated the temporal and spatial genetic structure of a hyperparasitoid (fourth trophic level) in a fragmented landscape over 50 × 70 km, using microsatellite markers, and compared it with the known structures of its host parasitoid, and the butterfly host which lives as a classic metapopulation. We found that population genetic structure decreases with increasing trophic level. The hyperparasitoid has fewer genetic clusters (K = 4), than its host parasitoid (K = 15), which in turn is less structured than the host butterfly (K = 27). The genetic structure of the hyperparasitoid also shows temporal variation, with genetic differentiation increasing due to reduction of the population size, which reduces the effective population size. Overall, our study confirms the idea that specialized species must be dispersive to use a fragmented host resource, but that this adaptation has limits.

Extracellular glutamate and GABA in the ventral tegmental area of alcohol-preferring AA and alcohol-avoiding ANA rats treated repeatedly with morphine.

Glutamate and gamma-amino-butyric acid (GABA) have been implicated in neuronal plasticity related to behavioral sensitization. In the present study, we examined morphine-induced changes in the extracellular concentrations of glutamate and GABA in the ventral tegmental area in alcohol-preferring Alko Alcohol (AA) and alcohol-avoiding Alko Non-Alcohol (ANA) rats that have previously been shown to differ in morphine-induced sensitization. The rats were given escalating doses (5-20 mg/kg) of morphine every other day for five days. This treatment produced behavioral sensitization to locomotor effects of morphine in AA, but not in ANA rats, when challenged with an additional injection of morphine (10 mg/kg) 10 days later. Morphine also increased the levels of glutamate in the ventral tegmental area only in AA rats, while no significant changes were found in the extracellular concentrations of GABA between the lines. Challenging the morphine-treated AA rats with ethanol (1.5 g/kg) did not modify the levels of glutamate or GABA. No changes in the concentrations of glutamate or GABA were seen in saline-treated AA and ANA rats after morphine challenge. These results render increased glutamate transmission in the ventral tegmental area a potential contributor to the higher susceptibility of AA rats to morphine-induced behavioral and neurochemical effects relative to ANA rats.

Ecological and genetic basis of metapopulation persistence of the Glanville fritillary butterfly in fragmented landscapes.

Ecologists are challenged to construct models of the biological consequences of habitat loss and fragmentation. Here, we use a metapopulation model to predict the distribution of the Glanville fritillary butterfly during 22 years across a large heterogeneous landscape with 4,415 small dry meadows. The majority (74%) of the 125 networks into which the meadows were clustered are below the extinction threshold for long-term persistence. Among the 33 networks above the threshold, spatial configuration and habitat quality rather than the pooled habitat area predict metapopulation size and persistence, but additionally allelic variation in a SNP in the gene Phosphoglucose isomerase (Pgi) explains 30% of variation in metapopulation size. The Pgi genotypes are associated with dispersal rate and hence with colonizations and extinctions. Associations between Pgi genotypes, population turnover and metapopulation size reflect eco-evolutionary dynamics, which may be a common feature in species inhabiting patch networks with unstable local dynamics.

Behavioral sensitization and voluntary ethanol drinking in alcohol-preferring AA rats exposed to different regimens of morphine treatment.

The purpose of the study was to investigate the effects of three different regimens of morphine treatment on subsequent voluntary ethanol drinking in alcohol-preferring AA (Alko Alcohol) rats. The rats were given morphine subcutaneously either intermittently on alternating days (15 x 10 mg/kg or 5 x 5-20 mg/kg in escalating doses) or subchronically on four consecutive days (3-20 mg/kg/d). Horizontal locomotor activity was monitored after challenges with additional morphine injections (3 mg/kg) ten days and six weeks after termination of the pretreatment to test if behavioral sensitization was induced by repeated morphine administration. Both intermittent pretreatments induced sensitized locomotor response after the first challenge, whereas subchronic injections did not. After the challenge the rats were given a free choice between tap water and 10% (v/v) ethanol solution for four weeks. The rats pretreated and challenged with morphine did not differ significantly in the acquisition of ethanol drinking from the saline-treated controls. In contrast, ethanol drinking was impaired during the first week of ethanol access in the saline-treated rats given a single morphine injection. The second morphine challenge given after the ethanol-drinking phase did not reveal sensitization in any of the groups. The results suggest that pattern of morphine administration rather than the dose or number of exposures to the drug is the most important factor in induction of behavioral sensitization, and that exposure to ethanol may interfere with this process. They also support earlier findings showing that acute morphine may suppress voluntary ethanol drinking, but failed to provide clear evidence for behavioral sensitization to morphine contributing to predilection towards ethanol in AA rats.

The Glanville fritillary genome retains an ancient karyotype and reveals selective chromosomal fusions in Lepidoptera.

Previous studies have reported that chromosome synteny in Lepidoptera has been well conserved, yet the number of haploid chromosomes varies widely from 5 to 223. Here we report the genome (393 Mb) of the Glanville fritillary butterfly (Melitaea cinxia; Nymphalidae), a widely recognized model species in metapopulation biology and eco-evolutionary research, which has the putative ancestral karyotype of n=31. Using a phylogenetic analyses of Nymphalidae and of other Lepidoptera, combined with orthologue-level comparisons of chromosomes, we conclude that the ancestral lepidopteran karyotype has been n=31 for at least 140 My. We show that fusion chromosomes have retained the ancestral chromosome segments and very few rearrangements have occurred across the fusion sites. The same, shortest ancestral chromosomes have independently participated in fusion events in species with smaller karyotypes. The short chromosomes have higher rearrangement rate than long ones. These characteristics highlight distinctive features of the evolutionary dynamics of butterflies and moths.

Long-term metapopulation study of the Glanville fritillary butterfly (Melitaea cinxia): survey methods, data management, and long-term population trends.

Long-term observational studies conducted at large (regional) spatial scales contribute to better understanding of landscape effects on population and evolutionary dynamics, including the conditions that affect long-term viability of species, but large-scale studies are expensive and logistically challenging to keep running for a long time. Here, we describe the long-term metapopulation study of the Glanville fritillary butterfly (Melitaea cinxia) that has been conducted since 1991 in a large network of 4000 habitat patches (dry meadows) within a study area of 50 by 70 km in the Åland Islands in Finland. We explain how the landscape structure has been described, including definition, delimitation, and mapping of the habitat patches; methods of field survey, including the logistics, cost, and reliability of the survey; and data management using the EarthCape biodiversity platform. We describe the long-term metapopulation dynamics of the Glanville fritillary based on the survey. There has been no long-term change in the overall size of the metapopulation, but the level of spatial synchrony and hence the amplitude of fluctuations in year-to-year metapopulation dynamics have increased over the years, possibly due to increasing frequency of exceptional weather conditions. We discuss the added value of large-scale and long-term population studies, but also emphasize the need to integrate more targeted experimental studies in the context of long-term observational studies. For instance, in the case of the Glanville fritillary project, the long-term study has produced an opportunity to sample individuals for experiments from local populations with a known demographic history. These studies have demonstrated striking differences in dispersal rate and other life-history traits of individuals from newly established local populations (the offspring of colonizers) versus individuals from old, established local populations. The long-term observational study has stimulated the development of metapopulation models and provided an opportunity to test model predictions. This combination of empirical studies and modeling has facilitated the study of key phenomena in spatial dynamics, such as extinction threshold and extinction debt.

Enhanced morphine-induced ethanol drinking in alcohol-preferring alko alcohol rats sensitized to morphine.

BACKGROUND: Alcohol-preferring alko alcohol (AA) rats are more susceptible to morphine-induced behavioral and neurochemical sensitization than alcohol nonpreferring alko nonalcohol (ANA) rats. Alko alcohol rats sensitized to morphine, however, do not show enhanced acquisition of ethanol drinking. The purpose of the present study was to clarify further interactions between morphine-induced behavioral sensitization and voluntary ethanol drinking in the AA rats. METHODS: Alko alcohol rats drinking ethanol in a limited 6-hour access paradigm were sensitized to morphine with repeated injections of morphine (5-15 mg/kg). Injection days alternated with days of ethanol access. Controls had access only to water and/or were given injections of saline. After a 5-day washout period from ethanol and morphine, the rats were challenged with morphine or saline and subsequent ethanol drinking or locomotor activity was recorded. RESULTS: Ethanol intake was suppressed during the repeated treatment with morphine, and the morphine-treated rats did not differ in ethanol intake from the controls when given access to ethanol after the washout. Intake of ethanol was, however, increased when the rats were challenged with morphine [1 or 10 mg/kg, subcutaneously (s.c.)], while in the controls an increase in ethanol intake was seen only after 1 mg/kg morphine. Sensitization to the locomotor stimulating effects of morphine was revealed in the morphine-treated rats after a challenge with morphine (3 or 10 mg/kg, s.c.). The controls that had been drinking ethanol also showed a sensitized response after morphine (3 mg/kg). CONCLUSIONS: Ethanol did not interfere with the development of sensitization to morphine. Furthermore, the neuroadaptations induced by repeated exposure to ethanol were sufficient to cause behavioral cross-sensitization to morphine. Sensitization to the behavioral effects of morphine alone, however, neither enhances the reinforcing properties of voluntarily consumed ethanol nor contributes to increase in its intake. The increase in ethanol intake found after an acute dose of morphine was augmented in rats withdrawn from repeated treatment with morphine. The data suggest that the neuronal mechanisms underlying behavioral sensitization to morphine probably are distinct from those mediating reinforcement from ethanol and that the morphine-induced neuroadaptations contribute to the enhancement of increase in ethanol intake by morphine.