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Department of Biology, Georgia State University, P.O. Box 4010, Atlanta, Georgia 30302-4010
* Present Address: Santa Monica College, Life Sciences, 1900 Pico Boulevard, Santa Monica, California 90405. E-mail: fickbohm_david{at}smc.edu
To whom correspondence should be addressed. E-mail: pkatz{at}gsu.edu
Serotonin-related disorders can be treated by manipulating serotonin synthesis with the serotonin precursor 5-hydroxytryptophan (5-HTP) or other pharmacological agents. The mollusc Tritonia diomedea is a model for investigating the effects of altering serotonin content on the functions of identified neurons. We used high-performance liquid chromatography and immunohistochemistry to examine the amount and localization of 5-HTP, serotonin, and the serotonin breakdown product 5-hydroxyindolacetic acid (5-HIAA) in the Tritonia brain after various pharmacological treatments. Exposure to 5-HTP (2 mM for 30 min1 h) caused an immediate and massive increase in total 5-HTP content, which lasted more than 20 h, and the widespread appearance of 5-HTP immunoreactivity in neurons. Serotonin levels rose gradually, but only a restricted number of additional neurons displayed serotonin immunoreactivity. 5-HTP treatment also caused an increase in the total amount of 5-HIAA and the appearance of 5-HIAA immunoreactivity throughout the brain. Treatment with the synthesis cofactor tetrahydrobiopterin, the initial precursor tryptophan, or serotonin itself had no persistent effect on total serotonin content. The amino acid decarboxylase inhibitor hydroxybenzylhydrazine (NSD-1015) also had no effect on the total serotonin content, although it caused an accumulation of 5-HTP. Thus, serotonin levels in the brain of T. diomedea appear to be maintained by a homeostatic mechanism that can be disrupted by 5-HTP.
Abbreviations: AADC, aromatic amino acid decarboxylase BH4, tetrahydrobiopterin DSI, dorsal swim interneuron 5- HTP, 5-hydroxytryptophan 5-HIAA, 5-hydroxyindolacetic acid NSD-1015, hydroxybenzylhydrazine
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