In recent years many of the conventional methods of insect control by broad spectrum synthetic chemicals have come under scrutiny because of their unde sirable effects on human health and the environment. In addition, some classes of pesticide chemistry, which generated resistance problems and severely affected the environment, are no longer used. It is against this background that the authors of this book present up-to-date findings-relating to biochemical sites that can serve as targets for developing insecticides with selective prop erties, and as the basis for the elucidation of resistance…mehr
In recent years many of the conventional methods of insect control by broad spectrum synthetic chemicals have come under scrutiny because of their unde sirable effects on human health and the environment. In addition, some classes of pesticide chemistry, which generated resistance problems and severely affected the environment, are no longer used. It is against this background that the authors of this book present up-to-date findings-relating to biochemical sites that can serve as targets for developing insecticides with selective prop erties, and as the basis for the elucidation of resistance mechanisms and countermeasures. The book consists of eight chapters relating to biochemical targets for insec ticide action and seven chapters relating to biochemical modes of resistance and countermeasures. The authors of the chapters are world leaders in pesti cide chemistry, biochemical modes of action and mechanisms of resistance. Biochemical sites such as chitin formation, juvenile hormone and ecdysone receptors, acetylcholine and GABA receptors, ion channels, and neuropeptides are potential targets for insecticide action. The progress made in recent years in molecular biology (presented in depth in this volume) has led to the iden tification of genes that confer mechanisms of resistance, such as increased detoxification, decreased penetration and insensitive target sites. A combina tion of factors can lead to potentiation of the resistance level. Classifications of these mechanisms are termed gene amplification, changes in structural genes, and modification of gene expression.
Biochemical Processes Related to Insecticide Action: an Overview.- 1 Introduction.- 2 Chitin Synthesis Inhibition.- 3 Ecdysone and Juvenile Hormone Receptors.- 4 Acetylcholine Receptors.- 5 GABA and Glutamate Receptors and Ion Channels.- 6 Other Biochemical Sites.- 7 Conclusions.- References.- GABA and Glutamate Receptors as Biochemical Sites for Insecticide Action.- 1 Introduction.- 2 GABA Receptors in Mammals and Insects.- 2.1 Classification of GABA Receptors.- 2.2 Structure and Physiological Role of Insect GABA Receptors.- 2.3 Pharmacology of GABA Receptors.- 3 Summary of Effects of Convulsants and Avermectins on the GABA Receptor.- 3.1 Polychlorocycloalkanes and Related Norbornanes.- 3.2 Picrodendrin and Silphinene Natural Products.- 3.3 Fipronil and Fipronil Analogs.- 3.4 Trioxabicyclooctanes and Related Compounds.- 3.5 New Avermectins and the Mammalian GABA Receptor.- 3.6 Altered GABA Receptors in Resistance.- 3.7 Resistance to New and Experimental Insecticides.- 4 Glutamate-Gated Chloride Channels.- 4.1 Physiology, Pharmacology, and Molecular Structure.- 4.2 Effects of the Avermectins.- 4.3 New Avermectins and Their Uses.- 4.4 Target Site Resistance to the Avermectins.- 5 Conclusions.- References.- Insecticides Affecting Voltage-Gated Ion Channels.- 1 Insecticides and Ion Channels.- 1.1 Scope and Aim.- 1.2 Voltage-Gated Ion Channels.- 2 Industrial Insecticides Targeting Ion Channels.- 2.1 Insecticides of the Voltage-Gated Sodium Channels.- 2.2 Insecticides of the Potassium and Calcium Channels.- 3 The Functional Diversity of Insecticides.- 3.1 Multiplicity of Effects.- 3.2 Distinction Between Mammals and Insects.- 4 Neurotoxic Polypeptides.- 4.1 Animal Group Specificity.- 4.2 Insect-Selective Neurotoxins Affecting the Voltage-Gated Sodium Channels.- 4.2.1 Scorpion Venom Toxins.- 4.2.2 Spider Venom Toxins.- 4.3 Insect-Selective Neurotoxins Affecting the Voltage-Gated Calcium Channel.- 5 Recombinant Baculovirus Bioinsecticides.- 6 Allosteric Coupling and Allosteric Antagonism.- References.- Acetylcholine Receptors as Sites for Developing Neonicotinoid Insecticides.- 1 Introduction.- 2 Insect Nicotinic Acetylcholine Receptors.- 2.1 Structure.- 2.2 Diversity.- 3 Compounds Acting on the Nicotinic Acetylcholine Receptor.- 3.1 Radioligand Binding Studies.- 3.2 Neonicotinoids.- 3.2.1 Imidacloprid and Related Structures.- 3.2.2 Mannich Adducts as Experimental Pro-Neonicotinoids.- 4 Electrophysiological Considerations.- 4.1 Whole Cell Voltage Clamp of Native Neuron Preparations.- 4.1.1 Correlation Between Electrophysiology and Radioligand Binding Studies.- 4.2 Agonists vs. Antagonists.- 4.3 Receptor Subtypes in Locusta migratoria.- References.- Ecdysteroid and Juvenile Hormone Receptors: Properties and Importance in Developing Novel Insecticides.- 1 Introduction.- 2 Ecdysteroids.- 2.1 Biology, Endocrinology and Molecular Biology.- 2.2 Receptors and Other Target Sites.- 2.3 Non-Steroidal Ecdysone Analogs and Their Mode of Action.- 2.4 Receptor-Based Screening Assays.- 2.5 Future Directions.- 3 Juvenile Hormone.- 3.1 Biology, Endocrinology and Molecular Biology.- 3.2 Receptors and Other Target Sites.- 3.3 JH Analogs and Their Modes of Action.- 3.4 Receptor-Based Screening Assays.- 3.5 Future Directions.- References.- Imaginal Discs and Tissue Cultures as Targets for Insecticide Action.- 1 Introduction.- 2 Imaginal Discs as Targets of Insect Hormones in Vivo and in Vitro.- 3 Insecticide Action in Vitro: Juvenile Hormone Mimics.- 4 Insecticide Action in Vitro: Chitin Synthesis Inhibitors.- 4.1 Organ Cultures.- 4.2 Cell Lines.- 5 Insecticide Action in Vitro: Ecdysteroid Agonists.- 5.1 Organ Cultures.- 5.2 Cell Lines.- References.- Insect Neuropeptide Antagonists: a Novel Approach for Insect Control.- 1 Introduction.- 2 Backbone Cyclic Neuropeptide-Based Antagonist (BBC-NBA) Approach.- 2.1 Determination of the Active Sequence in the Neuropeptide.- 2.2 Development of a Competitive Lead Antagonist.- 2.3 Improvement of the Antagonisti
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