Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Long-term Depression01:03

Long-term Depression

3.0K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...
3.0K
Long-term Depression01:05

Long-term Depression

33.0K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
33.0K
Anticholinesterase Agents: Poisoning and Treatment01:26

Anticholinesterase Agents: Poisoning and Treatment

1.5K
Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is...
1.5K
Desensitization and Tachyphylaxis01:20

Desensitization and Tachyphylaxis

3.0K
Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
3.0K
Toxic Reactions: Overview01:26

Toxic Reactions: Overview

1.8K
When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
1.8K
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

2.1K
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
2.1K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

RETRACTED: Maiti et al. Ameliorative Properties of Boronic Compounds in In Vitro and In Vivo Models of Alzheimer's Disease. <i>Int. J. Mol. Sci.</i> 2020, <i>21</i>, 6664.

International journal of molecular sciences·2025
Same author

Semiconductor-metal transition in Bi<sub>2</sub>Se<sub>3</sub> caused by impurity doping.

Scientific reports·2023
Same author

A new protocol for the preparation of superconducting KBi<sub>2</sub>.

RSC advances·2022
Same author

Superconducting properties of BaBi<sub>3</sub> at ambient and high pressures.

Physical chemistry chemical physics : PCCP·2021
Same author

Maine's Bumble Bees (Hymenoptera: Apidae)-Part 2: Comparisons of a Common (Bombus ternarius) and a Rare (Bombus terricola) Species.

Environmental entomology·2021
Same author

Maine's Bumble Bee (Hymenoptera: Apidae) Assemblage-Part 1: Composition, Seasonal and Regional Distribution, and Resource Use.

Environmental entomology·2021

Related Experiment Video

Updated: Jan 10, 2026

Examining the Effect of Pesticides on Caenorhabditis elegans Neurons
05:08

Examining the Effect of Pesticides on Caenorhabditis elegans Neurons

Published on: May 27, 2022

2.7K

Sub-lethal imidacloprid exposure leads to presynaptic and postsynaptic alterations.

Katya Tjahaja1, Emma Stoner1, Akari Miura1

  • 1Eckerd College.

Research Square
|November 24, 2025
PubMed
Summary

Field-relevant pesticide imidacloprid exposure reduced neural structures in both honey bees and nematodes. This neonicotinoid pesticide impacts the nervous systems of crucial off-target organisms.

More Related Videos

Assessing Agrochemical Risk to Mated Honey Bee Queens
08:49

Assessing Agrochemical Risk to Mated Honey Bee Queens

Published on: March 3, 2021

3.2K
Paradigms for Pharmacological Characterization of C. elegans Synaptic Transmission Mutants
18:01

Paradigms for Pharmacological Characterization of C. elegans Synaptic Transmission Mutants

Published on: August 18, 2008

14.6K

Related Experiment Videos

Last Updated: Jan 10, 2026

Examining the Effect of Pesticides on Caenorhabditis elegans Neurons
05:08

Examining the Effect of Pesticides on Caenorhabditis elegans Neurons

Published on: May 27, 2022

2.7K
Assessing Agrochemical Risk to Mated Honey Bee Queens
08:49

Assessing Agrochemical Risk to Mated Honey Bee Queens

Published on: March 3, 2021

3.2K
Paradigms for Pharmacological Characterization of C. elegans Synaptic Transmission Mutants
18:01

Paradigms for Pharmacological Characterization of C. elegans Synaptic Transmission Mutants

Published on: August 18, 2008

14.6K

Area of Science:

  • Neuroscience
  • Environmental Science
  • Toxicology

Background:

  • Pesticides, particularly neonicotinoids like imidacloprid, are widely used in agriculture.
  • Imidacloprid is known to affect the nervous systems of various organisms, including beneficial insects and other invertebrates.
  • Sub-lethal doses of pesticides can have significant impacts on non-target species.

Purpose of the Study:

  • To investigate the neurotoxic effects of field-relevant, sub-lethal doses of imidacloprid on honey bees and nematodes.
  • To compare the impact of imidacloprid on cholinergic signaling in two distinct off-target organisms.

Main Methods:

  • Comparative neuroscience approach exposing honey bees and nematodes to imidacloprid.
  • Honey bee brains were analyzed for microglomeruli density using synapsin immunostaining.
  • Transgenic nematodes were used to assess changes in presynaptic and postsynaptic cholinergic structures.

Main Results:

  • Exposure to imidacloprid led to a decreased density of microglomeruli in the honey bee brain after one week.
  • In nematodes, imidacloprid exposure for 48 hours resulted in decreased expression in both presynaptic and postsynaptic cholinergic structures.
  • Both species showed alterations in neural structures following exposure to common field concentrations of imidacloprid.

Conclusions:

  • Field-relevant concentrations of imidacloprid alter the nervous systems of off-target organisms, including honey bees and nematodes.
  • The study highlights the neurotoxic potential of neonicotinoids on non-target species.
  • Comparative neuroscience provides valuable insights into the ecological risks of pesticide exposure.