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At least 19 recordsLinked to original sources
USGS2007

Ammonia causes decreased brain monoamines in fathead minnows (Pimephales promelas)

Hyperammonemia, arising from variety of disorders, leads to severe neurological dysfunction. The mechanisms of ammonia toxicity in brain are not completely understood. This study investigated the effects of ammonia on monoaminergic systems in brains of fathead minnows (Pimephales promelas). Fish serve as a good model system to investigate hyperammonemic effects on brain function since no liver manipulations are necessary to increase endogenous ammonia concentrations. Using high performance liquid chromatography with electrochemical detection, monoamines and some associated metabolites were measured from whole brain homogenate. Adult males were exposed for 48 h to six different concentrations of ammonia (0.01–2.36 mg/l unionized) which bracketed the 96-h LC50 for this species. Ammonia concentration-dependent decreases were found for the catecholamines (norepinephrine and dopamine) and the indoleamine serotonin (5-HT). After an initial increase in the 5-HT precursor 5-hydroxytryptophan it too decreased with increasing ammonia concentrations. There were also significant increases in the 5-HIAA/5-HT and DOPAC/DA ratios, often used as measures of turnover. There were no changes in epinephrine (Epi) or monoamine catabolites (DOPAC, 5-HIAA) at any ammonia concentrations tested. Results suggest that ammonia causes decreased synthesis while also causing increased release and degradation. Increased release may underlie behavioral reactions to ammonia exposure in fish. This study adds weight to a growing body of evidence demonstrating that ammonia leads to dysfunctional monoaminergic systems in brain which may underlie neurological symptoms associated with human disorders such as hepatic encephalopathy.

Brain Research↗
USGS2018

Female hatchling American kestrels have a larger hippocampus than males: A link with sexual size dimorphism?

The brain and underlying cognition may vary adaptively according to an organism’s ecology. As with all raptor species, adult American kestrels ( Falco sparverius ) are sexually dimorphic with females being larger than males. Related to this sexual dimorphism, kestrels display sex differences in hunting and migration, with females ranging more widely than males, suggesting possible sex differences in spatial cognition. However, hippocampus volume, the brain region responsible for spatial cognition, has not been investigated in raptors. Here, we measured hippocampus and telencephalon volumes in American kestrel hatchlings. Female hatchlings had a significantly larger hippocampus relative to the telencephalon and brain weight than males (∼12% larger), although telencephalon volume relative to brain weight and body size was similar between the sexes. The magnitude of this hippocampal sex difference is similar to that reported between male and female polygynous Microtus voles and migratory and non-migratory subspecies of Zonotrichia sparrows. Future research should determine if this sex difference in relative hippocampus volume of hatchling kestrels persists into adulthood and if similar patterns exist in other raptor species, thus potentially linking sex differences in the brain to sex differences of space use of adults in the wild.

Behavioural Brain Research↗
USGS2007

Otolith research for Puget Sound

Otoliths are hard structures located in the brain cavity of fish. These structures are formed by a buildup of calcium carbonate within a gelatinous matrix that produces light and dark bands similar to the growth rings in trees. The width of the bands corresponds to environmental factors such as temperature and food availability. As juvenile salmon encounter different environments in their migration to sea, they produce growth increments of varying widths and visible 'checks' corresponding to times of stress or change. The resulting pattern of band variations and check marks leave a record of fish growth and residence time in each habitat type. This information helps Puget Sound restoration by determining the importance of different habitats for the optimal health and management of different salmon populations. The USGS Western Fisheries Research Center (WFRC) provides otolith research findings directly to resource managers who put this information to work.

Washington↗
USGS1977

Effects of DDE on experimentally poisoned free-tailed bats (Tadarida brasiliensis): Lethal brain concentrations

Adult female free-tailed bats (Tadarida brasiliensis) were collected at Bracken Cave, Texas, and shipped to the Patuxent Wildlife Research Center. Treated mealworms (Tenebrio molitor) containing 107 ppm DDE were fed to 17 bats; five other bats were fed untreated mealworms. After 40 days on dosage, during which one dosed bat was killed accidentally, four dosed bats were frozen and the remaining 17 were starved to death. The objective was to elevate brain levels of DDE to lethality and measure these concentrations. After the feeding period, dosed bats weighed less than controls. After starvation, the body condition of dosed bats was poorer than that of controls even though there was no difference in the amounts of carcass fat. During starvation, dosed bats lost weight faster than controls. Also, four dosed bats exhibited the prolonged tremoring that characterizes DDE poisoning. DDE increased in brains of starving bats as fat was metabolized. The estimated mean brain concentration of DDE diagnostic of death was 519 ppm with a range of 458-564 ppm. These values resemble diagnostic levels known for two species of passerine birds, but they exceed published levels for two free-tailed bats from Carlsbad Caverns, New Mexico.

Journal of Toxicology and Environmental Health↗
USGS2011

Status and management of moose in the northeastern United States

Moose (Alces alces) populations have recolonized much of their historic range in the northeastern United States in the past 30 years, with their southern range edge extending to southern New England and northern New York. This southerly expansion occurred when certain other populations in the United States were in decline along the southern range edge, with climate change often cited as a probable cause. The areas that moose have recently occupied in the northeastern United States are some of the most densely human populated in moose range, which has raised concern about human safety and moose-vehicle collisions (MVC). We conducted a literature search about moose in the northeastern United States, and distributed a questionnaire and conducted phone interviews with regional biologists responsible for moose management to determine the status of moose, management activity, and research deficiencies and needs. Moose numbers appear stable throughout much of the region, with slow population growth in northern New York. Management activity ranges from regulated harvest of moose in Maine, New Hampshire, and Vermont, to no active management in southern New England and New York. The combined annual harvest in Maine, New Hampshire, and Vermont is >3,000. MVCs are a widespread regional concern with >1,000 occurring annually involving several human fatalities. Research should address impacts of parasitism by winter tick (Dermacentor albipictus) and brain-worm (Parelaphostrongylus tenuis) on productivity and mortality of moose, influence of climate change on population dynamics and range, and conflicts in areas with high human population density.

Alces↗
USGS1979

Delta-aminolevulinic acid dehydratase enzyme activity in blood, brain, and liver of lead-dosed ducks

Mallard ducks were dosed with a single shotgun pellet (ca. 200 mg lead). After 1 month there was about 1 ppm lead in blood, 2.5 in liver, and 0.5 in brain. Lead-induced inhibition of delta-aminolevulinic acid dehydratase enzyme in blood and cerebellum was much greater than in cerebral hemisphere or liver and was strongly correlated with the lead concentration in these tissues. The cerebellar portion of the brain was more sensitive to delta-aminolevulinic acid dehydratase enzyme inhibition by lead than were the other tissues examined. There was also a greater increase in the glial cell marker enzyme, butyrylcholinesterase, in cerebellum than in cerebral hemisphere, suggesting that nonregenerating neuronal cells were destroyed by lead and replaced by glial cells in that portion of the brain. Even partial loss of cerebellar tissue is severely debilitating in waterfowl, because functions critical to survival such as visual, auditory, motor, and reflex responses are integrated at this brain center.

Environmental Research↗
USGS2005

Enhanced zinc consumption causes memory deficits and increased brain levels of zinc

Zinc deficiency has been shown to impair cognitive functioning, but little work has been done on the effects of elevated zinc. This research examined the effect on memory of raising Sprague–Dawley rats on enhanced levels of zinc (10 ppm ZnCO 3 ; 0.153 mM) in the drinking water for periods of 3 or 9 months, both pre- and postnatally. Controls were raised on lab water. Memory was tested in a series of Morris Water Maze (MWM) experiments, and zinc-treated rats were found to have impairments in both reference and working memory. They were significantly slower to find a stationary platform and showed greater thigmotaxicity, a measure of anxiety. On a working memory task, where the platform was moved each day, zinc-treated animals had longer latencies over both trials and days, swam further from the platform, and showed greater thigmotaxicity. On trials using an Atlantis platform, which remained in one place but was lowered on probe trials, the zinc-treated animals had significantly fewer platform crossings, spent less time in the target quadrant, and did not swim as close to the platform position. They had significantly greater latency on nonprobe trials. Microprobe synchrotron X-ray fluorescence (μSXRF) confirmed that brain zinc levels were increased by adding ZnCO 3 to the drinking water. These data show that long-term dietary administration of zinc can lead to impairments in cognitive function.

Physiology & Behavior↗
USGS1987

Case histories of bald eagles and other raptors killed by organophosphorus insecticides topically applied to livestock

Since 1982 when secondary poisoning of a red-tailed hawk ( Buteo jamaicensis ) was documented following the recommended use of famphur applied topically to cattle, the Patuxent Wildlife Research Center has tested dead birds of prey for poisoning by famphur and other pouron organophosphorus (OP) insecticides. Brain cholinesterase (ChE) activity was first determined, then if ChE was depressed ≥50%, stomach and/or crop contents were evaluated for anti-ChE compounds. This report presents the circumstances surrounding the OP-caused deaths of eight bald eagles ( Haliaeetus leucocephalus ), two red-tailed hawks, and one great horned owl ( Bubo virginianus ) between March 1984 and March 1985. OP poisoning of raptors by pour-on insecticides in the United States is widespread, but its magnitude is unknown.

Journal of Wildlife Diseases↗
USGS2024

Transcriptomic profiles of brains in juvenile Atlantic cod (Gadus morhua) exposed to pharmaceuticals and personal care products from a wastewater treatment plant discharge

Pharmaceuticals and personal care products (PPCPs) are frequently detected in marine environments, posing a threat to aquatic organisms. Our previous research demonstrated the occurrence of neuroactive compounds in effluent and sediments from a wastewater treatment plant (WWTP) in a fjord North of Stavanger, the fourth-largest city in Norway. To better understand the influence of PPCP mixtures on fish, Atlantic cod ( Gadus morhua ) were caged for one month in 3 locations: site 1 (reference), site 2 (WWTP discharge), and site 3 (6.7 km west of discharge). Transcriptomic profiling was conducted in the brains of exposed fish and detection of PPCPs in WWTP effluent and muscle fillets were determined. Caffeine (47.8 ng/L), benzotriazole (10.9 ng/L), N,N -diethyl-meta-toluamide (DEET) (5.6 ng/L), methyl-1 H -benzotriazole (5.5 ng/L), trimethoprim (3.4 ng/L), carbamazepine (2.1 ng/L), and nortriptyline (0.4 ng/L) were detected in the WWTP effluent. Octocrylene concentrations were observed in muscle tissue at all sites and ranged from 53 to 193 ng/g. Nervous system function and endocrine system disorders were the top enriched disease and function pathways predicted in male and female fish at site 2, with the top shared canonical pathways involved with estrogen receptor and Sirtuin signaling. At the discharge site, predicted disease and functional responses in female brains were involved in cellular assembly, organization, and function, tissue development, and nervous system development, whereas male brains were involved in connective tissue development, function, and disorders, nervous system development and function, and neurological disease. The top shared canonical pathways in females and males were involved in fatty acid activation and tight junction signaling. This study suggests that pseudopersistent, chronic exposure of native juvenile Atlantic cod from this ecosystem to PPCPs may alter neuroendocrine and neuron development.

Stavanger↗
USGS2009

Developmental toxicity in white leghorn chickens following in ovo exposure to perfluorooctane sulfonate (PFOS)

Studies show that perfluorinated compounds cause various toxicological effects; nevertheless, effects on immune function and developmental endpoints have not been addressed at length. This study examined the effects of perfluorooctane sulfonate (PFOS) in white leghorn hatchlings on various developmental, immunological, and clinical health parameters. In addition, serum PFOS concentrations were determined by LC/MS/MS. Embryonic day (ED) 0 eggs were injected with either safflower oil/10% DMSO (control, 0 mg/kg egg wt) or PFOS in safflower oil/10% DMSO at 1, 2.5, or 5 mg/kg egg wt, and the chicks were grown to post-hatch day (PHD) 14. Treatment with PFOS did not affect hatch rate. Following in ovo exposure chicks exhibited increases in spleen mass at all treatment levels, in liver mass at 2.5 and 5 mg/kg egg wt, and in body length (crown-rump length) at the 5 mg/kg treatment. Right wings were shorter in all treatments compared to control. Increases in the frequency of brain asymmetry were evident in all treatment groups. SRBC-specific immunoglobulin (IgM and IgY combined) titers were decreased significantly at all treatment levels, while plasma lysozyme activity was increased at all treatment levels. The PHA skin test response decreased in relation to increasing PFOS dose. Serum concentrations where significant immunological, morphological, and neurological effects were observed at the lowest dose (1 mg/kg egg wt) averaged 154 ng PFOS/g serum. These concentrations fall within environmental ranges reported in blood samples from wild caught avian species; thereby, verifying that the environmental egg concentrations used for the injections do indeed relate to serum levels in hatchlings that are also environmentally relevant. These data indicate that immune alterations and brain asymmetry can occur in birds following in ovo exposure to environmentally relevant concentrations of PFOS and demonstrates the need for further research on the developmental effects of perfluorinated compounds in various species. ?? 2009 Elsevier Inc.

Reproductive Toxicology↗
USGS1982

DDT poisoning in a Cooper's hawk collected in 1980

In April 1980, a Cooper's hawk ( Accipiter cooperii ) was found on the ground in Lakewood, Colorado, unable to fly and in convulsion. The bird died shortly thereafter. The hawk was packed in dry ice and shipped air express to the Fish and Wildlife Service, U. S. Department of the Interior, National Wildlife Health Laboratory, Madison, Wisconsin, for necropsy. Following necropsy, the brain, gastrointestinal tract, and remaining carcass except skin, feet, wings, liver, and kidney were packed in dry ice and shipped air express to the Patuxent Wildlife Research Center, Laurel, Maryland, for chemical residue analysis. Because the bird's behavior before death suggested some form of poisoning, the kidney was assayed for thallium, the liver for lead, and the gastrointestinal tract for strychnine, sodium fluoroacetate, and arsenic. When these assays proved negative, the bird was analyzed for organochlorine pesticides. Necropsy findings and pesticide residue analyses are reported here.

Colorado↗
USGS2021

Thyroid disruption and oxidative stress in American kestrels following embryonic exposure to the alternative flame retardants, EHTBB and TBPH

Brominated flame retardant chemicals, such as 2-ethylhexyl-2,3,4,5-tetrabromobenzoate (EHTBB) (CAS #: 183658–27-7) and bis(2-ethylhexyl)-2,3,4,5-tetrabromophthalate (TBPH) (CAS #: 26040–51-7), have been detected in avian tissues and eggs from remote regions. Exposure to EHTBB and TBPH has been shown to cause oxidative stress and altered thyroid function in rodents and fish, yet no controlled studies have examined potential adverse effects of exposure in birds. Because flame retardants have been detected in wild raptors, we used American kestrels ( Falco sparverius ) as a model raptor to determine whether in ovo exposure to EHTBB or TBPH affected growth, hatching success, oxidative stress, or thyroid function. We exposed kestrel embryos to nominal concentrations (10, 50, or 100 ng g −1 egg weight) of EHTBB and TBPH via egg-injection on embryonic day 5. Embryonic exposure (~23 d) to EHTBB increased thyroid gland mass, reduced glandular colloid and total thyroxine (T4) in hatchling males and females, whereas deiodinase enzyme activity increased in males but decreased in females. Hatchlings exposed to TBPH in ovo exhibited reduced colloid and increased oxidative stress. Although exposure to EHTBB and TBPH caused several physiological effects (e.g., heart and brain mass), only exposure to 50 ng g −1 EHTBB appeared to reduce hatching success. Our results suggest these flame retardants may be hazardous for predatory birds. Future research should evaluate long-term survival and fitness consequences in birds exposed to these chemicals.

Environment International↗
USGS1984

Sensitivity of nestling and adult starlings to dicrotophos, an organophosphate pesticide

The 24-hr median lethal dose (LD50) of dicrotophos (3-hydroxy-N,N-dimethyl-cis-crotonamide dimethyl phosphate) for free-living 5-day-old nestling European starlings (Sturnus vulgaris, LDso = 4.92 mg/kg body wt) was about one-half that obtained for free-living 15day-old nestlings (9.59 mg/kg) and captive adult males (8.37 mg/kg) and females (8.47 mg/ kg). Nestlings and adults with low pretreatment body weights appeared to be more vulnerable to organophosphate (OP) exposure. Brain cholinesterase (ChE) activity was severely depressed in all birds that died (74-94%); the degree of inhibition did not vary with age or sex. Inhibition of brain ChE in 5-day-old nestlings alive 24 hr post dose (X = 28-43%) was lower than that of 15-day-old (X = 55-68%) and adult (X = 55-77%) survivors. Body weights of OP-dosed birds that died were depressed an average of 20 to 46% in 5-day-olds, 7 to 20% in 15-day-olds, and 0 to 10% in adults; weight losses varied inversely with age and dosage, and directly with time to death. Average weight losses in 5- and 15-day-old survivors (X < 31 and 26%, respectively) varied directly with dose and exceeded comparable values for adults (X = 3-15%). Results suggest that (1) young nestling songbirds may be nearly twice as sensitive as adults to OPs, (2) growth of nestlings may be severely depressed following OP exposure, and (3) recovery of brain ChE activity following exposure to ChE inhibitors may be more rapid in nestlings than adults.

Environmental Research↗
USGS1994

Anticholinesterase exposure of white-winged doves breeding in lower Rio Grande valley, Texas

We studied exposure of breeding white-winged doves (Zenaida asiatica) to anticholinesterase compounds (organophosphorus and carbamate pesticides) in the Lower Rio Grande Valley (LRGV), Texas. Widespread use of organophosphorus pesticides and dove population declines prompted the study. We collected breeding adult doves in May and July 1991 (n = 28) and July 1992 (n = 33) at 6 locations. We used depression of whole-brain cholinesterase (ChE) activity (2 SD below control mean) to detect exposure; values from 4 hand-reared doves fed commercial pigeon chow served as the control. Mean brain ChE activity was lower (P lt 0.027) than the control sample at all 6 locations in 1991; 79% of the birds were diagnostic of exposure ( gt 16.1% ChE depression). Pooled 1992 field samples also were lower (P lt 0.036) than were control samples; doves from 4 of the 6 locations had brain ChE activity below (P lt 0.088) controls. Overall, 39% of 1992 doves were diagnostic of exposure to anticholinesterase compounds. Higher exposure rates in 1991 were probably due to increased use of organophosphorus pesticides. Research is needed documenting effects of sublethal exposure on white-winged dove productivity.

Texas↗
USGS2007

Overview of developmental, reproductive, and behavioral/ neurological effects of mercury exposures in wildlife

We review wildlife/mercury literature and our own research findings that demonstrate the relevance of wildlife toxicity data in protecting human health. Methylmercury affects wildlife through reduced adult survival and reproduction, aberrant behavior, immune system effects, and teratogenic effects. Methylmercury can readily cross the blood-brain barrier, is excreted into eggs in birds, and is transferred to young mammals across the placenta and in milk. Its principal effect on wildlife is on neurological functions. Wild mink (Mustela vison) and otter (Lutra canadensis) have died from methylmercury poisoning, with signs of poisoning including anorexia, loss of weight, incoordination, tremors, and convulsions, which are symptoms similar to those experienced by mercury-poisoned humans. Mammals also may experience tonic and clonic convulsions and an increase in fetal anomalies, again paralleling toxic problems in people. Antibody-producing cells can be suppressed by methylmercury. Microscopically, the most notable lesions are in the cerebrum. Extensive vacuolation of hepatocytes in the liver and necrosis and other changes in the appearance of the proximal convoluted tubules of the kidneys are often noted. When harp seals (Pagophilus groenlandicus) were dosed with methylmercury chloride the number of circulating erythrocytes decreased and white blood cell counts greatly increased. The poisoned seals also suffered from uremia, hyperproteinemia, hypercholesterolemia, hyperbilirubinemia, and elevations in lactic dehydrogenase and alkaline phosphatase. In birds, signs of methylmercury poisoning included emaciation and weakness in the extremities, which progressed until the birds died. Mercury poisoning in birds and mammals can be diagnosed from a combination of the signs of poisoning if the animal is still alive, the pathological effects seen in a gross necropsy, the histopathological effects seen with a microscope, and the concentrations of mercury in various tissues. Our studies with mallards (Anas platyrhynchos) suggest that the dietary concentrations of mercury that cause toxicity are lower than those set in fish consumption advisories to protect humans. Because wild mammals and birds are so sensitive to methylmercury poisoning and cannot escape dietary exposure the way humans can, guidelines set to protect wild birds and mammals may very well provide a margin of safety for human health.

Book chapter↗
USGS1979

Environmental contaminant studies by the Patuxent Wildlife Research Center

Evaluation of the effects of environmental contaminants on wildlife is geared to interpreting events in the field, especially population effects, and both field and laboratory studies are planned for this purpose; procedures are adapted to specific problems and therefore do not include strict protocols or routine testing. Field evaluations include measurements of cholinesterase inhibition in brain or blood, search for dead or disabled animals, study of nesting success of birds, and general ecological observations. Residue analyses are used in evaluating organochlorine chemicals; samples may include whole bodies for determining level of exposure, brains for mortality diagnosis, whole blood for certain special studies, and eggs to help in evaluation of possible reproductive effects. Bird counts, singing-male census counts, small mammal trapping, and cage-in-field tests have proven to be ineffective or misleading and are not considered suitable for field evaluations under most circumstances. Usefulness of simulated field trials is limited to very special situations. Experimental studies that help predict and interpret field effects include determinations of lethal diagnostic levels, comparative lethal dietary toxicity tests, tests of secondary poisoning, measurement of residue loss rates, measurement of blood enzymes, tests of behavioral effects, and studies of reproductive effects.

Maryland↗
USGS1982

Anticholinesterase poisoning of birds: Field monitoring and diagnosis of acute poisoning

Organophosphorus and carbamate pesticides are cholinesterase (ChE) inhibiting chemicals that have been responsible for avian die-offs. Identification of chemicals implicated in these die-offs is difficult and sometimes conclusions are solely circumstantial. However, when marked depression (inhibition) of brain ChE activity accompanies organophosphorus or carbamate residues in body tissues or ingesta, cause-effect diagnosis is enhanced. To achieve this end, normal brain ChE activity is estimated for controls of the affected species and then die-off specimens are individually evaluated for evidence of ChE inhibition. This approach to evaluation of antiChE poisoning may also be used to monitor exposure of vertebrates to field application of organophosphorus or carbamate pesticides. Problems associated with this kind of evaluation, and the main topic of this report, include variability of brain ChE activity among species, postmortem influences of ambient conditions (storage or field) on ChE activity, and differential patterns of ChE activity when inhibited by organophosphorus or carbamate compounds. Other topics discussed are the ChE assay procedure, example case reports and interpretation, and research needed for improving the diagnostic utility of ChE activity in a field situation.

Environmental Toxicology and Chemistry↗
USGS1986

Mortality of captive whooping cranes caused by eastern equine encephalitis virus

Of 39 captive whooping cranes (Grus americana), 7 died during a 7-week period (Sept 17 through Nov 4, 1984) at the Patuxent Wildlife Research Center, Laurel, Md. Before their deaths, 4 cranes did not develop clinical signs, whereas the other 3 cranes were lethargic and ataxic, with high aspartate transaminase, gamma-glutamyl transferase, and lactic acid dehydrogenase activities, and high uric acid concentrations. Necropsies indicated that the birds had ascites, intestinal mucosal discoloration, fat depletion, hepatomegaly, splenomegaly, and visceral gout. Microscopically, extensive necrosis and inflammation were seen in many visceral organs; the CNS was not affected. Eastern equine encephalitis (EEE) virus was isolated from specimens of the livers, kidneys, lungs, brains, and intestines of 4 of the 7 birds that died, and EEE virus-neutralizing antibody was detected in 14 (44%) of the 32 surviving birds. Other infectious or toxic agents were not found. Morbidity or mortality was not detected in 240 sandhill cranes (Grus canadensis) interspersed among the whooping cranes; however, 13 of the 32 sandhill cranes evaluated had EEE virus-neutralizing antibody. Of the 41 wild birds evaluated in the area, 3 (4%) had EEE virus-neutralizing antibody. Immature Culiseta melanura (the most probable mosquito vector) were found in scattered foci 5 km from the research center.

Maryland↗