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Alan Yanahan CPSC 270, 2009. Imidacloprid. A Neonicotinoid. History. Late 1970s: chemists at Shell Chemical Company laid the groundwork for the future synthesis of imidacloprid through their investigations of potential insecticides 1984: chemists as Nikon Bayer Agrochem create imidacloprid
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Alan Yanahan CPSC 270, 2009 Imidacloprid A Neonicotinoid
History • Late 1970s: chemists at Shell Chemical Company laid the groundwork for the future synthesis of imidacloprid through their investigations of potential insecticides • 1984: chemists as Nikon Bayer Agrochem create imidacloprid • First neonicotinoid insecticide registered for use
Imidacloprid • Compared to nicotine • Less human toxicity and greater effectiveness against insects • Systemic insecticide • Used on a wide variety of fruit and vegetable crops • Used in termite control and in flea control on pets
How Does Imidacloprid Work? Have to understand the nervous system first
The Nervous System • Nerve cells transmit messages from one another by means of electrical impulses (action potentials) • The axon carries the message away from one nerve cell to the dendrites of another nerve cell
The Nervous System • Between the axon and dendrite is a gap referred to as the synapse • In order for the electrical message to cross the synapse, it must be converted into a chemical message
The Nervous System • When an electrical impulse reaches the end of an axon, it leads to the release of chemicals called neurotransmitters • These neurotransmitters bind with receptors on the dendrites of neighboring nerve cells to cause the generation of another electrical impulse • Enzymes break down neurotransmitters to prevent nerve cells from repeatedly firing
Vesicle releases acetylcholine (neurotransmitter) into nerve synapse Acetylcholine binds with the enzyme acetylcholinesterase Axon of pre-synaptic cell receives action potential and voltage gated Ca2+ channel opens Voltage gated Ca2+ channel closes Acetylcholine Vesicle Na+ Na+ Choline is released Ca2+ Acetylcholine is released from nicotinic acetylcholine receptor Calcium ions (Ca2+) enter axon Nicotinic acetylcholine receptor opens Na+ Ca2+ Ca2+ Acetate is released Nicotinic acetylcholine receptor closes Sodium ions (Na+) enter the dendrite and cause an action potential in post-synaptic cell Acetylcholine binds with receptor (nicotinic acetylcholine receptor)
When Imidacloprid is Present in the Synapse • Imidacloprid mimics the molecular shape of the neurotransmitter acetylcholine • Acts on various nicotinic acetylcholine receptors to cause nerves to fire • Is not recognized by the enzyme acetylcholinesterase • Leads to tremors, convulsion, and death in insects
Acetylcholine binds with the enzyme acetylcholinesterase Ca2+ Ca2+ Ca2+ Choline is released Na+ Acetylcholine is released from nicotinic acetylcholine receptor Na+ Acetylcholine Nicotinic acetylcholine receptor opens Na+ Acetate is released Imidacloprid binds with the nicotinic acetylcholine receptor Sodium ions (Na+) enter the dendrite to produce another action potential Nicotinic acetylcholine receptor closes Na+ Na+ Na+
Sources • Kreiger, Robert I. Handbook of Pesticide Toxicology 2nd Edition: Agents. Sheets, Larry P. Chapter 54—Imidacloprid: A Neonicotinoid Insecticide. San Diego: Academic Press, 2001 • Silverthorn, Dee Unglaub. Human Physiology An Integrated Approach 4th Edition. San Francisco: Pearson Education Inc., 2007.