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Barn owls (Tyto alba) suffered their worst year on record in 2013. Results from barn owl monitoring schemes around the UK revealed the number of sites where nesting took place last year was significantly down in every area compared to previous years, and some surveys found no nests with eggs in at all. Overall the number of occupied nests was down 71% on the average across all previous years, according to the Barn Owl Trust, which collated the information from 21 independent groups stretching from Jersey in the Channel Islands to south-west Scotland. A survey in Berkshire which normally finds 14 nests in use and a surveyor in Yorkshire who normally finds 25-30 occupied nests both found none at all, while surveys in Buckinghamshire and Sussex were both down more than 90% on normal levels. Conservationists described the situation as the "worst year ever recorded" for the flagship farmland species. Almost four times as many dead barn owls were reported to the British Trust for Ornithologyin March 2013 than normal and by mid-April it was possible that there were fewer barn owls alive in the UK than at any time since records began, the report said.

Integrated pest management programs (IPM) promote the use of multiple cultural, biological, and chemical tactics to reduce the abundance of pest insects, while conserving pollinators and beneficial insects. Much research has focused on the impact of systemic neonicotinyl insecticides on the colony health and foraging behavior of bees, but few papers considered these impacts on pollen and nectar-feeding beneficial insects, such as parasitoids, lacewings, lady beetles, and butterflies. Contact insecticides only contaminate pollen and nectar of flowers that are open at the time of spraying. In contrast, soil-applied neonicotinyl insecticides are translocated to pollen and nectar of flowers for a longer duration, often months. Neonicotinyl seed-treated crops (imidacloprid, 0.11 mg/canola seed and 0.625 mg/corn seed) translocate less than 10 ppb to nectar and pollen. However, higher rates of soil-applied imidacloprid are used in urban landscapes and nurseries (270-300 mg/3gallon pot, 67g imidacloprid applied to soil surface for 24 diam. tree), which should result in residues higher than the 10 ppb in nectar and pollen compared to seed-treated crops. This study shows that the translocation of imidacloprid from soil (300 mg) to flowers of Asclepias curassavica resulted in imidacloprid residue in nectar of 6,000 ppb for 1X and 10,000 ppb for 2X treatments. A second imidacloprid soil application 7 months after the first resulted in residues of 21,000 ppb in 1X and 45,000 ppb in 2X treatments. Consequently, landscape use of imidacloprid applied to flowering plants can result in 697 to 1,162 times more imidacloprid in milkweed nectar compared to a seed treatment, where most research has focused. These higher residue levels caused significant mortality in both 1Xand 2X treatments at day 12 in three lady beetle species, Coleomegilla maculata, Harmonia axyridis, and Hippodamia convergens, but not a fourth species, Coccinella septempunctata. Survival and fecundity of two nymphalid butterfly species, monarch, Danaus plexippus and painted lady, Vanessa cardui, were not reduced when free-ranging butterflies foraged on 1X and 2X treated milkweed plants or when butterflies were force-fed lower amounts of imidacloprid (0 ppb, 15 ppb, or 30 ppb imidacloprid). However, larval survival was significantly reduced on plants treated with soil-applied imidacloprid at1X and 2X treatments. Consequently, the use of systemic, neonicotinyl insecticides, such as imidacloprid, increased the insecticide’s duration in pollen and nectar, and increased the insecticide’s exposure to beneficial insects, thereby increasing the risk of mortality.

Exposure even to low levels of imidacloprid, a widely used pesticide, can harm the central nervous system of bees and may be a reason behind the global bee colony collapse, a National Taiwan University research team said yesterday in Taipei. Reports from around the world in recent years have shown that the population of wild bees has rapidly declined in many parts of the world. As bees contribute to the pollination of many crop species, ensuring production of seeds in many flowering plants and playing an important role in the ecosystem, many scientists are concerned about the rapid decline in bee colonies.

Cholinergic modulation of prefrontal cortex is essential for attention. In essence, it focuses the mind on relevant, transient stimuli in support of goal-directed behavior. The excitation of prefrontal layer VI neurons through nicotinic acetylcholine receptors optimizes local and top-down control of attention. Layer VI of prefrontal cortex is the origin of a dense feedback projection to the thalamus and is one of only a handful of brain regions that express the α5 nicotinic receptor subunit, encoded by the gene chrna5. This accessory nicotinic receptor subunit alters the properties of high-affinity nicotinic receptors in layer VI pyramidal neurons in both development and adulthood. Studies investigating the consequences of genetic deletion of α5, as well as other disruptions to nicotinic receptors, find attention deficits together with altered cholinergic excitation of layer VI neurons and aberrant neuronal morphology. Nicotinic receptors in prefrontal layer VI neurons play an essential role in focusing attention under challenging circumstances. In this regard, they do not act in isolation, but rather in concert with cholinergic receptors in other parts of prefrontal circuitry. This review urges an intensification of focus on the cellular mechanisms and plasticity of prefrontal attention circuitry. Disruptions in attention are one of the greatest contributing factors to disease burden in psychiatric and neurological disorders, and enhancing attention may require different approaches in the normal and disordered prefrontal cortex.

Maternal smoking during pregnancy can impair performance of the exposed offspring in tasks that require auditory stimulus processing and perception; however, the tobacco component(s) responsible for these effects and the underlying neurobiological mechanisms remain uncertain. In this study, we show that administration of nicotine during mouse perinatal development can impair performance in an auditory discrimination paradigm when the exposed animals are mature. This suggests that nicotine disrupts auditory pathways via nicotinic acetylcholine receptors (nAChRs) that are expressed at an early stage of development. We have also determined that mice which lack nAChRs containing the β2 subunit (β2* nAChRs) exhibit similarly compromised performance in this task, suggesting that β2* nAChRs are necessary for normal auditory discrimination or that β2* nAChRs play a critical role in development of the circuitry required for task performance. In contrast, no effect of perinatal nicotine exposure or β2 subunit knockout was found on the acquisition and performance of a differential reinforcement of low rate task. This suggests that the auditory discrimination impairments are not a consequence of a general deficit in learning and memory, but may be the result of compromised auditory stimulus processing in the nicotine-exposed and knockout animals

This suggests that some constituent of smoke, such as the primary addictive component, nicotine, alters neurodevelopment. Although many effects of developmental nicotine exposure have been identified in humans and animal models, very few mechanistic studies have identified the molecular and anatomical basis for a defined behavioral consequence of developmental exposure. We show in this study that a mouse model of developmental nicotine exposure results in hypersensitive passive avoidance in adulthood. We have used transgenic mice in which β2 subunit containing nicotinic acetylcholine receptors (β2* nAChRs) are expressed exclusively on corticothalamic neurons (β2 tr(CT) mice) to identify the receptor subtypes involved and also to define the circuit level site of action responsible for this persistent, nicotine-induced behavioral phenotype. Further characterization of the native nAChRs expressed in this circuit indicates that both (α4)2(β2)3 and (α4)2(β2)2α5 nAChR subtypes are present in corticothalamic projections. Consistent with a role for (α4)2(β2)2α5 nAChRs in mediating the effect of developmental nicotine exposure on adult passive avoidance behavior, constitutive deletion of the α5 nAChR subunit also alters this behavior. A critical period for this developmental consequence of nicotine exposure was defined by limiting exposure to the early post-natal period. Taken together, these studies identify a novel consequence of developmental nicotine exposure in the mouse, define the nAChR subtypes and neural circuit involved in this behavioral change and delimit the neurodevelopmental period critical for vulnerability to a behavioral alteration that persists into adulthood.

The very same pesticides accused of causing massive declines in honeybee populations are just as culpable in the loss of songbirds, finds a new report published by the American Bird Conservancy. The pesticides in question, neonicotinoids, are based on nicotine, a natural insecticide, which causes paralysis and, eventually, death in both insects and non-target animals, such as honeybees and songbirds. Introduced in the early 1990s, neonicotinoids are now the most widely used insecticides in the world. And that popularity carries a heavy burden, the report found. After analyzing more than 200 studies conducted by both independent and industry-funded scientists, the authors called for the Environmental Protection Agency (EPA) to ban these pesticides' use until a more thorough investigation into their safety is conducted. "A single corn kernel coated with a neonicotinoid can kill a songbird," said Cynthia Palmer, coauthor of the report and pesticides-program manager for the conservancy, in a statement accompanying the report. "Even a tiny grain of wheat or canola treated with the oldest neonicotinoid—called imidacloprid—can fatally poison a bird. And as little as 1/10th of a neonicotinoid-coated corn seed per day during egg-laying season is all that is needed to affect reproduction."

Cholinergic neurons and nicotinic acetylcholine receptors (nAChRs) in the brain participate in diverse functions: reward, learning and memory, mood, sensory processing, pain, and neuroprotection. Nicotinic systems also have well-known roles in drug abuse. Here, we review recent insights into nicotinic function, linking exogenous and endogenous manipulations of nAChRs to alterations in synapses, circuits, and behavior. We also discuss how these contemporary advances can motivate attempts to exploit nicotinic systems therapeutically in Parkinson’s disease, cognitive decline, epilepsy, and schizophrenia.

Eriopis connexa is a native coccinelid predator in the Neotropical Region. In Argentina it is commonly found associated to sucking pests in several crops and among them aphids and whiteflies. These pests are usually controlled with newly developed systemic insecticides, such as the neonicotinoids. However, the compatibility between selective pesticides and natural enemies is required before incorporating them in integrated pest management (IPM) packages. Within this frame, the objective of this study was to evaluate the side effect of various concentrations/doses of one commonly used neonicotinoid in vegetal crops, acetamiprid, on immature stages of E. connexa by dipping or topical exposure for eggs and larvae, respectively. Acetamiprid reduced egg hatching from 34 to 100 %. Moreover, the embryogenesis was disrupted by insecticide at early embryo
stage at all tested concentrations. Second larval instar was more susceptible to acetamiprid than the fourth one and this susceptibility was positively related with the tested concentrations. On the other hand, the survival reduction at larval stage reached 100 % from 20 mg a.i./L (10 % of maximum field concentration). Besides, the reproduction of the females developed from topical bioassays on fourth instar larvae was strongly affected, with reduction in fecundity and fertility from 22 to 44 % and from 37 to 45 %, respectively. Overall the results showed a high toxicity of acetamiprid on immature stages of E. connexa, demonstrating that this broadly used insecticide could reduce biocontrol services provided by this predator and could also likely disturb IPM programs.