The Center for Biological Diversity filed a formal notice of intent to sue the U.S. Fish and Wildlife Service today for failing to determine whether five increasingly rare northeastern amphibians and reptiles warrant consideration for Endangered Species Act protection. The Center first petitioned for these species — the wood turtle, spotted turtle, green salamander, Peaks of Otter salamander and white-spotted salamander — in July 2012 because habitat loss and other factors are threatening their survival. “These turtles and salamanders are irreplaceable parts of the wild where they live, whether it’s a remote mountain stream or a suburban wetland,” said Collette Adkins Giese, a Center biologist and lawyer focused on protecting amphibians and reptiles. “Losing them will impoverish those places and our own connection with the natural world.”
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.
A year and a half ago, with symposia and reverential speeches, the United States and much of the world marked the 50th anniversary of Rachel Carson's book "Silent Spring" and her courageous warnings about environmental threats. Monday -- the 50th anniversary of Carson's death -- is an opportune time to admire her equally courageous silence about matters that could have blunted the book's impact. Most people are surprised to learn that Carson lived only about 18 months after the publication of "Silent Spring." On April 14, 1964, a month shy of her 57th birthday, Carson died in the Maryland suburb of Silver Spring of complications of metastasizing breast cancer. Sadly, she had become a polarizing figure in an increasingly vituperative political atmosphere. Carson did not live to see the positive impact of her message -- prohibition of the agrichemicals aldrin, dieldrin and heptachlor; passage of the National Environmental Policy Act; establishment of the U.S. Environmental Protection Agency; the banning of DDT in the United States in 1972 and the end of its use by much of the world's agriculture within the half-century.
The unforgettable sight of dancing adders is an overlooked spring spectacular. Liam Creedon reveals why the UK’s only poisonous snake is the most misunderstood treasure of the countryside. Going in search of the UK’s only venomous snake might, on the face of it, not seem like the sharpest of ideas. But an encounter with dancing adders, as males fight each other for breeding rites, is one of spring’s most thrilling and overlooked spectacles. Despite being small, timid and uncommon, the burden of being our only remotely dangerous reptile means an aura of fear and fascination has attached itself to the adder.