Selected Publication:
Maggi, CA; Astolfi, M; Donnerer, J; Amann, R.
Which mechanisms account for the sensory neuron blocking action of capsaicin on primary afferents in the rat urinary bladder?
Neurosci Lett. 1990; 110(3):267-272
Doi: 10.1016/0304-3940(90)90858-7
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- Co-authors Med Uni Graz
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Donnerer Josef
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- Abstract:
- In the rat isolated bladder, capsaicin produced a concentration-dependent contraction, shown previously to depend upon transmitter release from peripheral endings of primary afferents. When using low concentrations (30-300 nM) of capsaicin, exposure to a second and third dose of capsaicin produced smaller responses than the first application, although a subsequent challenge with 10 microM capsaicin still elicited a contraction which was not reduced as compared to the response produced by the first exposure to a low dose of capsaicin. Capsaicin also evoked a prompt outflow of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI), taken as a marker for sensory nerve activation. A second or third application of a submaximal concentration of the drug was ineffective, although a subsequent challenge with 1 microM capsaicin was effective. These findings indicate that neuropeptide depletion does not necessarily account for the early stage of capsaicin 'desensitization' of primary afferents.
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Animals -
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Calcitonin Gene-Related Peptide - metabolism
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Capsaicin - pharmacology
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Dose-Response Relationship, Drug - pharmacology
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Immunohistochemistry - pharmacology
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Male - pharmacology
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Muscle Contraction - drug effects
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Neurons, Afferent - drug effects
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Rats - drug effects
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Rats, Inbred Strains - drug effects
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Urinary Bladder - drug effects