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Monroe, P J; Smith, D J
Journal of neurochemistry, December 1985, Letnik: 45, Številka: 6Journal Article
A superfusion system employed to measure the K+-stimulated release of 3H5-hydroxytryptamine (3H5-HT, 3Hserotonin) from a synaptosomal-rich spinal cord tissue preparation was carefully characterized, then used to examine the regulation of spinal 5-HT release. Spinal 5-HT release is apparently modulated by an autoreceptor. Exogenous 5-HT depressed, in a concentration-dependent manner, the K+-stimulated release of 3H5-HT. Similarly, lysergic acid diethylamide (LSD) produced a concentration-dependent decrease in 3H5-HT release. Methiothepin and quipazine blocked the inhibition of release induced by exogenous 5-HT. The 5-HT2 receptor antagonists spiperone and ketanserin failed to alter the action of 5-HT at the spinal 5-HT autoreceptor. Spiperone and ketanserin were shown, however, to alter the storage of 3H5-HT. When used in concentrations greater than 10 nM, the drugs evoked increases in basal 3H5-HT and 3H5-hydroxyindoleacetic acid ( 3H5-HIAA) effluxes which were independent of the presence of calcium ions. A good agreement existed between the potencies of drugs for modifying autoreceptor function and their abilities to compete for high-affinity 3H5-HT binding in the spinal cord (designated 5-HT1). Furthermore quipazine, in concentrations that preferentially interact with the 5-HT1B subtype, antagonized the actions of exogenous 5-HT on K+-stimulated release. Spiperone, in a concentration that approximated the affinity constant of 5-HT1A sites for the drug, was ineffective in altering the ability of exogenous 5-HT to modulate K+-stimulated 3H5-HT release. These results suggest that 5-HT1B sites are associated with serotonergic autoreceptor function in the spinal cord.
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