By Ernest D. Olfert (auth.), Alan A. Boulton, Glen B. Baker, Roger F. Butterworth (eds.)
to the Animal versions Volumes This and several volumes within the Neuromethods sequence will describe a couple of animal versions of neu- psychiatric problems. as a result of expanding public problem over the moral therapy of animals in examine, we felt it incumbent upon us to incorporate this normal preface to those volumes to be able to point out why we expect additional examine utilizing animals is critical and why animal types of psychi- ric and neurologic issues, specifically, are so vital. We realize that animals may still basically be used while appropriate choices are usually not on hand. we expect it self-e- dent, even if, that people can in basic terms be experimented upon in seriously proscribed conditions and substitute professional- dures utilizing cellphone or tissue tradition are insufficient in any types requiring checks of behavioral swap or of complicated in vivo methods. even if, whilst the misery, soreness, or discomfort to the animals outweighs the expected profits for human welfare, then the examine isn't moral and shouldn't be carried out.
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Extra info for Animal Models of Neurological Disease, I: Neurodegenerative Diseases
Choiceof Animal Species The choice of animal species is determined by a number of factors, including: the cost to purchase and house the species; the general level of knowledge on the neuroanatomy (particu- 38 larly of the basal forebrain cholinergic system) and neurochemistry, and the behavioral capabilities that can be reliably investigated and manipulated in a particular species; and the availability of the species. The last factor is particularly important when using nonhuman primates. Rats are well-suited for these studies because they are relatively inexpensive and are easy to train and test in a variety of behavioral tasks.
Cytotoxicity is probably determined by the specific subtype of glutamate receptor that the neuron expresses (Cotman and Iversen, 1987). For example, KA is a potent agonist at the kainate subtype of glutamate receptors and is far less potent at sites that are sensitive to IBO or QA. QA and QN are effective neurotoxins in the basal forebrain and destroy many cholinergic and noncholinergic neurons throughout the ventral pallidum/substantia innominata. However, neither acid effectively destroys neurons in the medial septal area (Perkins and Stone, 1983; Schwartz and Kohler, 1983).
These neurofibrillary aggregates are composed of normal neurofilament triplet proteins in contrast to the paired helical filaments associated with AD (Bertholf, 1987). , 1982). , 1982). Similar neurofibrillary changes can be produced by intracerebroventricular (ICV) or subcutaneous injections of aluminum salts into rabbits, cats, and rats. Neurofibrillary tangles usually develop in frontal and occipital cortex; the concentration of aluminum directly correlates with the number of neurofibrillary tangles in each affected region.
Animal Models of Neurological Disease, I: Neurodegenerative Diseases by Ernest D. Olfert (auth.), Alan A. Boulton, Glen B. Baker, Roger F. Butterworth (eds.)