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  4. Sublethal effects of heavy metal and metalloid exposure in honey bees: behavioral modifications and potential mechanisms
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Sublethal effects of heavy metal and metalloid exposure in honey bees: behavioral modifications and potential mechanisms

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Description

Neurotoxicology has historically focused on substances that directly damage nervous tissue. Behavioral assays that test sensory, cognitive, or motor function are used to identify neurotoxins. But, the outcomes of behavioral assays may also be influenced by the physiological status of non-neural organs. Therefore, toxin induced damage to non- neural organs may contribute to behavioral modifications. Heavy metals and metalloids are persistent environmental pollutants and induce neurological deficits in multiple organisms. However, in the honey bee, an important insect pollinator, little is known about the sublethal effects of heavy metal and metalloid toxicity though they are exposed to these toxins chronically in some environments. In this thesis I investigate the sublethal effects of copper, cadmium, lead, and selenium on honey bee behavior and identify potential mechanisms mediating the behavioral modifications. I explore the honey bees’ ability to detect these toxins, their sensory perception of sucrose following toxin exposure, and the effects of toxin ingestion on performance during learning and memory tasks. The effects depend on the specific metal. Honey bees detect and reject copper containing solutions, but readily consume those contaminated with cadmium and lead. And, exposure to lead may alter the sensory perception of sucrose. I also demonstrate that acute selenium exposure impairs learning and long-term memory formation or recall. Localizing selenium accumulation following chronic exposure reveals that damage to non-neural organs and peripheral sensory structures is more likely than direct neurotoxicity. Probable mechanisms include gut microbiome alterations, gut lining

damage, immune system activation, impaired protein function, or aberrant DNA methylation. In the case of DNA methylation, I demonstrate that inhibiting DNA methylation dynamics can impair long-term memory formation, while the nurse-to- forager transition is not altered. These experiments could serve as the bases for and reference groups of studies testing the effects of metal or metalloid toxicity on DNA methylation. Each potential mechanism provides an avenue for investigating how neural function is influenced by the physiological status of non-neural organs. And from an ecological perspective, my results highlight the need for environmental policy to consider sublethal effects in determining safe environmental toxin loads for honey bees and other insect pollinators.

Date Created
2016
Contributors
  • Burden, Christina Marie (Author)
  • Amdam, Gro (Thesis advisor)
  • Smith, Brian H. (Thesis advisor)
  • Gallitano-Mendel, Amelia (Committee member)
  • Harrison, Jon (Committee member)
  • Vu, Eric (Committee member)
  • Arizona State University (Publisher)
Topical Subject
  • Neurosciences
  • Toxicology
  • DNA Methylation
  • Heavy Metals
  • Honey Bees
  • Learning and Memory
  • sensory sensitivity
  • x-ray fluorescence microscopy
  • Honeybee--Effect of heavy metals on.
  • honeybee
  • Honeybee--Behavior.
Resource Type
Text
Genre
Doctoral Dissertation
Academic theses
Extent
viii, 158 pages : illustrations
Language
eng
Copyright Statement
In Copyright
Reuse Permissions
All Rights Reserved
Primary Member of
ASU Electronic Theses and Dissertations
Peer-reviewed
No
Open Access
No
Handle
https://hdl.handle.net/2286/R.I.40693
Statement of Responsibility
by Christina Marie Burden
Description Source
Retrieved on Feb. 13, 2017
Level of coding
full
Note
Partial requirement for: Ph.D., Arizona State University, 2016
Note type
thesis
Includes bibliographical references (pages 129-157)
Note type
bibliography
Field of study: Neuroscience
System Created
  • 2016-12-01 07:00:16
System Modified
  • 2021-08-30 01:20:59
  •     
  • 1 year 6 months ago
Additional Formats
  • OAI Dublin Core
  • MODS XML

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