Host tree traits in pasture areas affect forest and pasture specialist epiphyte species differently.

PREMISE: Epiphytes have commensal relationships with their host trees. Besides the influence of tree traits, little has been discussed concerning the ecology of epiphytes in disturbed habitats (e.g., pasture). We herein tested whether the occurrences of pasture and forest specialist epiphytes in pastures are affected differently by tree traits. We hypothesized that (H1) the richness and abundance of generalist epiphytes would be positively associated with area availability; (H2) the richness and abundance of forest epiphyte species would be associated both with (H2.a) area availability and (H2.b) tree traits related to higher seed adherence, and/or (H2.c) less severe habitat (e.g., high humidity and more shade). METHODS: We sampled 9567 epiphyte individuals from 16 species on 759 scattered remnant trees. The epiphyte species were divided into two ecological groups: forest specialists and pasture specialists. We evaluated four host tree traits: two related to tree size (crown area and trunk diameter) and two related to habitat type (crown leaf density and bark rugosity). RESULTS: The richness and abundance of both pasture and forest specialists were positively related with tree size. However, the abundance of pasture specialists was negatively related with crown leaf density, whereas richness of forest epiphytes was positively related with bark rugosity. CONCLUSIONS: Large scattered trees tend to present higher richness and abundance of both pasture and forest specialist epiphytes compared to the smaller trees. However, high crown leaf density limits abundance of pasture specialist epiphytes, whereas rugose bark increases the richness of forest epiphytes.

Prenatal exposure to nicotine in mice is associated with alterations in development and cellular and synaptic effects of alcohol in a brainstem arousal nucleus.

Using drugs of abuse while pregnant has tremendous negative consequences for the offspring, including an enhanced risk for substance use disorder (SUD). This vulnerability suggests that gestational exposure to drugs alters the developmental trajectory of neurons important in SUD processes, which could lead to later life changes in responsiveness to motivationally salient stimuli. The laterodorsal tegmentum (LDT) gates the behaviorally relevant firing pattern signaling stimuli saliency in mesoaccumbal circuits. Accordingly, any alterations in LDT functionality could alter output, and play a role in negative outcomes on motivated behavior associated with early-life nicotine exposure. Therefore, we investigated whether prenatal exposure to nicotine (PNE), which is a known teratogen, altered responsiveness of LDT neurons to alcohol by conducting electrophysiology in brain slices. Alcohol induced an outward current in control LDT cells, which was not seen in PNE LDT neurons. The frequency of mEPSCs was significantly decreased by alcohol in LDT PNE cells and accompanied by a decrease in action potential frequency, which were actions not seen in controls. Changes in baseline activity of PNE LDT cells were also observed. In summary, PNE LDT neurons showed alterations in baseline activity and membrane and synaptic responses to postnatal exposures to alcohol. The differences in PNE baseline activity and alcohol responses likely lead to differential output from the LDT to mesoaccumbal targets that could play a role in biasing coding of relevant stimuli, which could participate in the enhanced proclivity for development of SUD in those exposed during gestation to nicotine.

Sex- and age-dependent differences in nicotine susceptibility evoked by developmental exposure to tobacco smoke and/or ethanol in mice.

Either tobacco smoking or alcohol consumption during pregnancy sex-selectively increases susceptibility to drugs of abuse later in life. Considering that pregnant smoking women are frequently intermittent consumers of alcoholic beverages, here, we investigated whether a short-term ethanol exposure restricted to the brain growth spurt period when combined with chronic developmental exposure to tobacco smoke aggravates susceptibility to nicotine in adolescent and adult mice. Swiss male and female mice were exposed to tobacco smoke (SMK; research cigarettes 3R4F, whole-body exposure, 8 h/daily) or ambient air during the gestational period and until the tenth postnatal day (PN). Ethanol (ETOH, 2 g/Kg, 25%, i.p.) or saline was injected in the pups every other day from PN2 to PN10. There were no significant differences in cotinine (nicotine metabolite) and ethanol serum levels among SMK, ETOH and SMK + ETOH groups. During adolescence (PN30) and adulthood (PN90), nicotine (NIC, 0.5 mg/Kg) susceptibility was evaluated in the conditioned place preference and open field tests. NIC impact was more evident in females: SMK, ETOH and SMK + ETOH adolescent females were equally more susceptible to nicotine-induced place preference than control animals. At adulthood, SMK and SMK + ETOH adult females exhibited a nicotine-evoked hyperlocomotor profile in the open field, with a stronger effect in the SMK + ETOH group. Our results indicate that ethanol exposure during the brain growth spurt, when combined to developmental exposure to tobacco smoke, increases nicotine susceptibility with stronger effects in adult females. This result represents a worsened outcome from the early developmental dual exposure and may predispose nicotine use/abuse later in life.

Mood-related behavioral and neurochemical alterations in mice exposed to low chlorpyrifos levels during the brain growth spurt.

Organophosphates are among the most used pesticides. Particularly, chlorpyrifos (CPF) is responsible for a number of deleterious effects on brain development, which may program behavioral changes later in life. Here, we investigated whether a regimen of early low level CPF exposure that did not result in a significant inhibition of acetylcholinesterase (AChE) had deleterious effects on mood-related behaviors, as well as on cholinergic and serotonergic biomarkers in the mice brain. From the 3rd to 9th postnatal day (PN), male and female Swiss mice were subcutaneously injected with CPF. Mice were submitted to a battery of behavioral tests from PN60 to PN63: open field, elevated plus maze and forced swimming tests. The cholinergic and serotonergic biomarkers were assessed at PN10 and PN63. Our data indicated that early CPF exposure increased anxiety-like behavior in females and altered decision-making behavior in both sexes. Most biochemical alterations were sex-dependent and restricted to females. At PN10, CPF female mice showed increased serotonin and choline transporter binding in cerebral cortex. Distinctively, in adult females, the effects indicated a hypoactive state: CPF exposure reduced 5-HT1a receptor binding in cerebral cortex, as well as serotonin transporter binding and choline acetyltransferase activity in brainstem. Our results indicate that CPF exposure during the brain growth spurt deregulates serotonergic and cholinergic biomarkers. The effects are consistent with impaired synaptic function, may be related to long-term mood disorders and point out to higher female susceptibility.

Ethanol exposure during the brain growth spurt affects social behavior and increases susceptibility to acute ethanol effects during adolescence in male mice.

The brain is particularly vulnerable to ethanol effects during its growth spurt. Outcomes of early ethanol exposure such as hyperactivity have been extensively investigated; however, persons with fetal alcohol spectrum disorder frequently have social impairments and are heavy drinkers. Despite that, scant information is available regarding the neurobiological basis of these latter behavioral issues. Here, Swiss mice exposed to ethanol (Etoh, 5 g/kg i.p., alternate days) or saline during the brain growth spurt [postnatal day (PN) 2 to 8] were used to assess social behavior after an ethanol challenging during adolescence. At PN39, animals were administered with a single ethanol dose (1 g/Kg) or water by gavage and were then evaluated in the three-chamber sociability test. We also evaluated corticosterone serum levels and the frontal cerebral cortex serotoninergic system. Etoh males showed reductions in sociability. Ethanol challenging reverted these alterations in social behavior, reduced corticosterone levels, and increased the 5-HT2 receptor binding of male Etoh mice. No alterations were observed in 5-HT and 5-HIAA contents. These data support the idea that ethanol exposure during the brain growth spurt impacts social abilities during adolescence, alters ethanol reexposure effects, and suggests that stress response and serotoninergic system play roles in this phenomenon.

Forest fragmentation and impacts of intensive agriculture: Responses from different tree functional groups.

Agricultural landscapes are seen as areas of extreme importance for studying and developing strategies which integrate biodiversity conservation and ecosystem services with food production. The main strategies for intensifying agriculture are based on conventional agricultural practices of frequently using inputs for fertilization and correcting soil pH. Some studies show that these practices generate impacts on nearby forest fragments through soil contamination and increasing nutrient content. The objective of this study was to identify the impacts on the functional groups of sciophilous (late successional/shade-tolerant species) and heliophilous (pioneer/sun-loving) species of a tree community of 14 forest fragments near pasture areas and agricultural areas under conventional practices, raising the hypothesis that higher-fertility forest fragments adjacent to intensive agriculture modify the floristic composition of the tree community. Consequently, this study is based on the following questions: i) Do forest fragments within intensive farming environments present differences in floristic composition of species?; ii) Does the soil fertility influence the tree species composition?; iii) Which variables influence species abundance and richness in the forest fragments with different types of use around their environment? The floristic composition of fragments close to agricultural areas are more similar to each other than the composition of fragments close to pasture areas. Furthermore, the General Linear Model (GLM) results show a clear influence of the intensive farming environment on the richness and abundance of the two functional groups in the forest fragments, directly benefiting the abundance of heliophilous species, which are also benefited by the greater declivity and smaller fragment area, while the abundance of sciophytes is negatively correlated with these last two variables. The increase of calcium content is beneficial for the richness of heliophilous species, while the increase in phosphorus content influences a reduction in the richness of sciophyte species, which also strongly respond to the isolation between fragments. The results indicate a dominance trend of pioneer species in fragments with nutritionally enriched soils, providing evidence that the intense adoption of inputs in cultivated areas causes concrete impacts on the diversity of the tree community.

ATLANTIC EPIPHYTES: a data set of vascular and non-vascular epiphyte plants and lichens from the Atlantic Forest.

Epiphytes are hyper-diverse and one of the frequently undervalued life forms in plant surveys and biodiversity inventories. Epiphytes of the Atlantic Forest, one of the most endangered ecosystems in the world, have high endemism and radiated recently in the Pliocene. We aimed to (1) compile an extensive Atlantic Forest data set on vascular, non-vascular plants (including hemiepiphytes), and lichen epiphyte species occurrence and abundance; (2) describe the epiphyte distribution in the Atlantic Forest, in order to indicate future sampling efforts. Our work presents the first epiphyte data set with information on abundance and occurrence of epiphyte phorophyte species. All data compiled here come from three main sources provided by the authors: published sources (comprising peer-reviewed articles, books, and theses), unpublished data, and herbarium data. We compiled a data set composed of 2,095 species, from 89,270 holo/hemiepiphyte records, in the Atlantic Forest of Brazil, Argentina, Paraguay, and Uruguay, recorded from 1824 to early 2018. Most of the records were from qualitative data (occurrence only, 88%), well distributed throughout the Atlantic Forest. For quantitative records, the most common sampling method was individual trees (71%), followed by plot sampling (19%), and transect sampling (10%). Angiosperms (81%) were the most frequently registered group, and Bromeliaceae and Orchidaceae were the families with the greatest number of records (27,272 and 21,945, respectively). Ferns and Lycophytes presented fewer records than Angiosperms, and Polypodiaceae were the most recorded family, and more concentrated in the Southern and Southeastern regions. Data on non-vascular plants and lichens were scarce, with a few disjunct records concentrated in the Northeastern region of the Atlantic Forest. For all non-vascular plant records, Lejeuneaceae, a family of liverworts, was the most recorded family. We hope that our effort to organize scattered epiphyte data help advance the knowledge of epiphyte ecology, as well as our understanding of macroecological and biogeographical patterns in the Atlantic Forest. No copyright restrictions are associated with the data set. Please cite this Ecology Data Paper if the data are used in publication and teaching events.

Tobacco smoke and ethanol during adolescence: Both combined- and single-drug exposures lead to short- and long-term disruption of the serotonergic system in the mouse brain.

The impairment of the serotonergic system contributes to nicotine and ethanol effects on mood, suggesting that this system is targeted by each of these drugs and that co-exposure possibly worsens the disruption. Here, we tested this hypothesis in an adolescent mice model of tobacco smoke and/or ethanol exposure. From postnatal day (PN) 30-45, Swiss mice were exposed to one of the following: 1) tobacco smoke (SMK; research cigarettes 2R1F, whole-body exposure, 8 h/daily); 2) ethanol (ETOH; 2 g/kg i.p., every other day); 3) SMK + ETOH; 4) Control (VEH). At PN45 (end-of-exposure), hippocampal serotonin transporter (5 H TT) binding was increased in SMK and decreased in ETOH male mice. At PN50 (short-term deprivation), cortical 5 H TT was reduced in all drug-exposed mice. In the hippocampus, similar deficits were identified in females. In both brain regions, the effects of SMK + ETOH deprivation on 5 H TT were equivalent to the damage caused by either drug. At PN50, hippocampal 5 H T1A receptor binding was reduced in ETOH and SMK + ETOH mice. Similar results were observed in the male cortex. In females, deficits were identified in SMK mice. In both brain regions, SMK + ETOH 5 H T1A deficits reflected the summation of SMK and ETOH outcomes. At PN75 (long-term deprivation), there was a late-emergent increase in cortical 5 H T1A binding in SMK mice, while cortical 5 H T2 receptor binding was similarly increased in SMK and SMK + ETOH groups. Adolescent SMK and/or ETOH serotonergic impairment is sex-dependent and most evident during short-term deprivation. SMK + ETOH deprivation evokes serotonergic disruption that is at least equivalent to that caused by either drug alone.

Maternal undernutrition during lactation alters nicotine reward and DOPAC/dopamine ratio in cerebral cortex in adolescent mice, but does not affect nicotine-induced nAChRs upregulation.

Early undernutrition causes long lasting alterations that affect the response to psychoactive drugs. Particularly, undernutrition during lactation affects the acute locomotor response to nicotine during adolescence, but the reward effect of continued exposure to nicotine remains unknown. The goal of this study was to investigate the effects of undernutrition during lactation on the nicotine susceptibility indexed via conditioned place preference (CPP), on dopamine content and turnover and on nicotine-induced nicotinic cholinergic receptor (nAChR) upregulation in the cerebral cortex, midbrain and hippocampus of adolescent mice. The impact of undernutrition and nicotine exposure on stress-related hormones and leptin was also investigated. From postnatal day 2 (PN2) to weaning (PN21), dams were randomly assigned to one of the following groups: Control (C) - free access to standard laboratory diet (23% protein); Protein Restricted (PR) - free access to isoenergenetic diet (8% protein); Calorie Restricted (CR) - access to standard laboratory diet in restricted quantities (mean ingestion of PR). PR and CR groups showed less mass gain and less visceral fat mass. While C and CR were equally susceptible to nicotine-induced place preference conditioning, PR failed to show a conditioning pattern. In contrast, all groups presented a nicotine-evoked nAChR upregulation in the cerebral cortex. While dopamine and DOPAC levels did not differ between groups, the DOPAC/dopamine ratio was increased in CR animals. No differences in endocrine parameters were observed. Taken together, our results indicate that undernutrition during lactation programs for brain alterations later in life. Our data also suggest that early undernutrition does not affect the rewarding associative properties of nicotine at adolescence.

A ten fold reduction of nicotine yield in tobacco smoke does not spare the central cholinergic system in adolescent mice.

The tobacco industry has gradually decreased nicotine content in cigarette smoke but the impact of this reduction on health is still controversial. Since the central cholinergic system is the primary site of action of nicotine, here, we investigated the effects of exposure of adolescent mice to tobacco smoke containing either high or low levels of nicotine on the central cholinergic system and the effects associated with cessation of exposure. From postnatal day (PN) 30 to 45, male and female Swiss mice were exposed to tobacco smoke (whole body exposure, 8h/day, 7 days/week) generated from 2R1F (HighNic group: 1.74mg nicotine/cigarette) or 4A1 (LowNic group: 0.14mg nicotine/cigarette) research cigarettes, whereas control mice were exposed to ambient air. Cholinergic biomarkers were assessed in the cerebral cortex and midbrain by the end of exposure (PN45), at short- (PN50) and long-term (PN75) deprivation. In the cortex, nicotinic cholinergic receptor upregulation was observed with either type of cigarette. In the midbrain, upregulation was detected only in HighNic mice and remained significant in females at short-term deprivation. The high-affinity choline transporter was reduced in the cortex: of HighNic mice by the end of exposure; of both HighNic and LowNic females at short-term deprivation; of LowNic mice at long-term deprivation. These decrements were separable from effects on choline acetyltransferase and acetylcholinesterase activities, suggesting cholinergic synaptic impairment. Here, we demonstrated central cholinergic alterations in an animal model of tobacco smoke exposure during adolescence. This system was sensitive even to tobacco smoke with very low nicotine content.

Locomotor response to acute nicotine in adolescent mice is altered by maternal undernutrition during lactation.

Undernutrition during brain development causes long lasting alterations in different neurotransmitter systems that may alter responses to psychoactive drugs. Despite the recognized effects of early undernutrition on the cholinergic system, no evidence that demonstrates the influence of this insult on nicotine susceptibility has been reported. We investigated the effects of protein/calorie restriction during lactation on the susceptibility to nicotine in adolescent mice. Dams were randomly assigned to one of the following groups: Control (C, 20 litters)--free access to standard laboratory diet (23% protein); Protein Restricted (PR, 12 litters)--free access to a isoenergetic, 8% protein diet; Calorie Restricted (CR, 12 litters)--access to standard laboratory diet in restricted quantities (mean ingestion of PR: pair-fed group). Undernutrition extended from postnatal day 2 (PN2) to weaning (PN21). At PN30, animals either received an i.p. injection of nicotine (0.5mg/Kg) or saline and were immediately placed in open field (OF). After the OF, adrenal glands and serum were collected for the analyses of stress-related endocrine parameters and leptin concentration. PR and CR offspring showed less body mass gain and visceral fat mass. PR offspring presented reduced serum leptin concentration. In the OF, nicotine increased locomotor activity of C and PR, but not of CR. CR and PR offspring showed decreased adrenal catecholamine content, which was not dependent on nicotine exposure. Our results indicate that early undernutrition interferes with nicotine-elicited locomotor effects in adolescent mice and suggest that endocrine parameters alterations in malnourished animals do not influence the behavioral response to nicotine.

Effect of tobacco smoke exposure during pregnancy and preschool age on growth from birth to adolescence: a cohort study.

BACKGROUND: There is strong evidence of an association between maternal smoking during pregnancy and restriction of intrauterine growth, but the effects of this exposure on postnatal linear growth are not well defined. Furthermore, few studies have investigated the role of tobacco smoke exposure also after pregnancy on linear growth until adolescence. In this study we investigated the effect of maternal smoking exposure during pregnancy and preschool age on linear growth from birth to adolescence. METHODS: We evaluated a cohort of children born between 1994 and 1999 in Cuiabá, Brazil, who attended primary health clinics for vaccination between the years 1999 and 2000 (at preschool age) and followed-up after approximately ten years. Individuals were located in public and private schools throughout the country using the national school census. Height/length was measured, and length at birth was collected at maternity departments. Stature in childhood and adolescence was assessed using the height-for-age index sex-specific expressed as z-score from curves published by the World Health Organization. Linear mixed effects models were used to estimate the association between exposure to maternal smoking, during pregnancy and preschool age, and height of children assessed at birth, preschool and school age, adjusted for age of the children. RESULTS: We evaluated 2405 children in 1999-2000, length at birth was obtained from 2394 (99.5%), and 1716 at follow-up (71.4% of baseline), 50.7% of the adolescents were male. The z-score of height-for-age was lower among adolescents exposed to maternal smoking both during pregnancy and childhood (p < 0.01). Adjusting for age, sex, maternal height, maternal schooling, socioeconomic position at preschool age, and breastfeeding, children exposed to maternal smoking both during pregnancy and preschool age showed persistent lower height-for-age since birth to adolescence (coefficient: -0.32, p < 0.001) compared to non-exposed. Paternal smoking at preschool age was not associated with growth after adjustment for confounders. CONCLUSION: Exposure to maternal smoking not only during pregnancy, but also at early childhood, showed long-term negative effect on height of children until adolescence.

Methamidophos exposure during the early postnatal period of mice: immediate and late-emergent effects on the cholinergic and serotonergic systems and behavior.

Organophosphates (OPs) are among the most used pesticides. Although some OPs have had their use progressively more restricted, other OPs are being used without sufficient investigation of their effects. Here, we investigated the immediate neurochemical and delayed neurochemical and behavioral actions of the OP methamidophos to verify whether there are concerns regarding exposure during early postnatal development. From the third to the nineth postnatal day (PN), Swiss mice were sc injected with methamidophos (1mg/kg). At PN10, we assessed cholinergic and serotonergic biomarkers in the cerebral cortex and brainstem. From PN60 to PN63, mice were submitted to a battery of behavioral tests and subsequently to biochemical analyses. At PN10, the effects were restricted to females and to the cholinergic system: Methamidophos promoted increased choline transporter binding in the brainstem. At PN63, in the brainstem, there was a decrease in choline transporter, a female-only decrease in 5HT1A and a male-only increase in 5HT2 receptor binding. In the cortex, choline acetyltransferase activity was decreased and 5HT2 receptor binding was increased both in males and females. Methamidophos elicited behavioral alterations, suggestive of increased depressive-like behavior and impaired decision making. There were no significant alterations on anxiety-related measures and on memory/learning. Methamidophos elicited cholinergic and serotonergic alterations that depended on brain region, sex, and age of the animals. These outcomes, together with the behavioral effects, indicate that this OP is deleterious to the developing brain and that alterations are indeed identified long after the end of exposure.

Exposure to methamidophos at adulthood adversely affects serotonergic biomarkers in the mouse brain.

Epidemiologic studies describe a potential risk of depression and suicide in farm workers exposed to organophosphates (OPs). In a previous study we observed an increase in depressive-like behavior in adult mice exposed to the OP pesticide methamidophos. Considering the association between depression and the serotonergic (5HT) system, in the present study we investigated whether a subchronic exposure to methamidophos affects the serotonergic system of adult mice. From postnatal day 60 to 89 (PN60 to PN89), one of two concentrations of methamidophos (higher dose: 5.25 µg/ml; lower dose: 1.31 µg/ml) or vehicle was administered in the drinking water of male Swiss mice. We evaluated three serotonergic biomarkers during (PN89) and after (PN100) the exposure period: 5HT(1A) receptor binding with [(3)H]OH-DPAT, 5HT(2) receptor binding with [(3)H]ketanserin and 5HT transporter binding with [(3)H]paroxetine. Methamidophos elicited robust decreases in binding for all 5HT markers. These decreases were evident in brain regions containing 5HT cell bodies and dendritic arbors (midbrain, brainstem) as well as in the cerebral cortex, which contains 5HT projections. In the cerebral cortex, effects were identified in mice exposed to the higher dose of methamidophos while in the midbrain and brainstem, both doses elicited significant effects. Overall, effects were present both during and after exposure, even though there were some regional disparities regarding the persistence of effects. Our results indicate that exposure to methamidophos affects synaptic transmission promoting decreases of specific serotonergic biomarkers. These data suggest a mechanism of action of this pesticide that might explain the increased depressive-like behavior in adult mice.

Nicotine exposure during the third trimester equivalent of human gestation: time course of effects on the central cholinergic system of rats.

Up to 22% of pregnant women smoke, which constitutes a major health concern. Nicotine, a cholinergic agonist, causes deleterious effects on brain development. However, most studies investigate its effects during rodents' gestation, which corresponds, in terms of neural development, to the first two trimesters of human gestation. Here, we focused on effects of nicotine on the brain cholinergic system during the third trimester equivalent of human gestation. From the 2nd to the 19th day of lactation, dams were exposed either to nicotine (6 mg/kg/day) or to saline via sc osmotic minipumps. Offspring were sacrificed during exposure (PN15, PN, postnatal) or at 2 days (PN21), 11 days (PN30), or 10 weeks (PN90) of withdrawal. In the cerebral cortex, midbrain, and hippocampus, we assessed nicotinic acetylcholine receptor (nAChR) binding, [(3)H]hemicholinium-3 (HC-3) binding to the high-affinity choline transporter, choline acetyltransferase (ChAT), and acetylcholinesterase (AChE) activities. Nicotine-exposed offspring presented nAChR upregulation during exposure in all brain regions, reduced HC-3 binding during and 11 days postexposure, and increased HC-3 binding on PN90. Effects on ChAT and AChE were dependent on the brain region and restricted to the withdrawal period: There were increased activities in the midbrain on PN30. In the hippocampus, AChE as reduced on PN30, whereas, for ChAT, the decrease was followed by late-emergent increased activity. These data indicate that maternal nicotine exposure during the third trimester equivalent of human gestation promotes cholinergic system alterations in the offspring's brain. In addition, detrimental effects are observable even long after the exposure has been interrupted.

Exposure to nicotine and ethanol in adolescent mice: effects on depressive-like behavior during exposure and withdrawal.

Depression and use of addictive substances are two of the most frequent public health problems of adolescents. However, little is known about the association between depression and drug use. Considering that ethanol and nicotine are the most widely used and abused drugs by adolescents, here, we evaluated the depressive-like behavior of C57BL/6 male and female mice exposed to nicotine (NIC) and/or ethanol (ETOH) from the 30th to the 45th (PN30-45) postnatal day. Four groups were analyzed: 1) concomitant NIC (50µg/ml in 2% saccharin to drink) and ETOH (25%, 2g/kg i.p. injected every other day) exposure; 2) NIC exposure; 3) ETOH exposure; 4) vehicle. Immobile behavior, an animal model of depressive behavior, was assessed in the forced swimming test (FST) while the anhedonic state was assessed in the sucrose preference test (SPT) by the end of exposure (PN45-47) as well as during short- (PN50-52) and long-term (PN75-77) withdrawal. In the FST, ETOH female mice showed a reduction in immobility time by the end of exposure while, during long-term withdrawal, immobility time was increased. Short-term withdrawal elicited an increase in immobility time only in female NIC mice. In the SPT, males from both NIC and NIC+ETOH groups showed increased sucrose consumption, suggesting a reward-craving effect during short-term withdrawal. During long-term withdrawal, NIC male mice showed an anhedonic effect. Adolescent nicotine, ethanol and nicotine+ethanol combined exposures during adolescence thus elicit gender-selective effects both during exposure and withdrawal that may contribute to the increased prevalence of depression among drug users.

Neonatal nicotine exposure causes insulin and leptin resistance and inhibits hypothalamic leptin signaling in adult rat offspring.

Maternal nicotine (NIC) exposure during lactation leads to overweight, hyperleptinemia, and hypothyroidism in adult rat offspring. In this model, we analyzed adipocyte morphology, glucose homeostasis (serum insulin and adiponectin; liver and muscle glycogen), serum lipid, and the leptin signaling pathway. After birth, osmotic minipumps were implanted in lactating rats, which were divided into the groups NIC (6 mg/kg per day s.c. for 14 days) and control (C, saline). NIC and C offspring were killed at the age of 180 days. Adult NIC rats showed higher total body fat (+10%, P<0.05), visceral fat mass (+12%, P<0.05), and cross-sectional area of adipocytes (epididymal: +12% and inguinal: +43%, P<0.05). Serum lipid profile showed no alteration except for apolipoprotein AI, which was lower. We detected a lower adiponectin:fat mass ratio (-24%, P<0.05) and higher insulinemia (+56%, P<0.05), insulin resistance index (+43%, P<0.05), leptinemia (+113%, P<0.05), and leptin:adiponectin ratio (+98%, P<0.05) in the adult NIC group. These rats presented lower hypothalamic contents of the proteins of the leptin signaling pathway (leptin receptor (OB-R): -61%, janus tyrosine kinase 2: -41%, and p-signal transducer and activator of transcription 3: -56%, P<0.05), but higher suppressor of cytokine signaling 3 (+81%, P<0.05). Therefore, NIC exposure only during lactation programs rats for adipocyte hypertrophy in adult life, as well as for leptin and insulin resistance. Through the effects of NIC, perinatal maternal cigarette smoking may be responsible for the future development of some components of the metabolic syndrome in the offspring.

Bromeliaceae da Ilha Grande, RJ: revisão da lista de espécies / Bromeliaceae of Ilha Grande: species checklist review

A Ilha Grande, localizada no sul do Estado do Rio de Janeiro, vem se destacando como importante área para fins conservacionistas, especialmente por ser um fragmento representativo de Floresta Atlântica e por apresentar um elevado número de estudos sobre a flora e a fauna local. Este estudo visa analisar o atual status do conhecimento sobre a família Bromeliaceae nesta localidade e analisar o incremento da lista de espécies desta família ao longo do tempo de estudo e do esforço amostral. Foram registradas 58 espécies de Bromeliaceae para a Ilha Grande, das quais 47 foram amostradas apenas com a metodologia empregada neste estudo e constituem registros novos para a Ilha Grande.

Ilha Grande, located at the Southern coast of Rio de Janeiro State, is constantly punctuated as an important area for conservational purposes, specially because it is a representative fragment of Atlantic forest and presents a high number of studies about the local fauna and flora. The aim of this study is to analyze the current knowledge of Bromeliaceae family at this island, and understand how the increase of the family's species list occurred through out the amount of time and sampling effort of this study. A total of 58 species of Bromeliaceae were listed for Ilha Grande, and 47 of them were sampled using only the methodology adopted at this study and, therefore, constitute new records for Ilha Grande.