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Release of [ 3 H]5‐hydroxytryptamine from the intermediate area of rat thoracic spinal cord is modulated by presynaptic autoreceptors
Author(s) -
Yang Ling,
Jacocks Henry M.,
Helke Cinda J.
Publication year - 1994
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890180305
Subject(s) - autoreceptor , agonist , spinal cord , serotonin , chemistry , postsynaptic potential , 5 ht receptor , medicine , endocrinology , biophysics , receptor , neuroscience , biology , biochemistry
Serotonin (5‐HT) nerve terminals innervate sympathetic preganglionic neurons of the intermediolateral cell column (IML); however, neither the depolarization‐induced release of 5‐HT nor the presence of presynaptic modulatory autoreceptors have been directly studied in this system. We used in vitro superfusion of the microdissected intermediate area (including the intermediolateral cell column, intercalated nucleus, and central autonomic nucleus) of the rat thoracic spinal cord to measure basal and stimulated release of preloaded [ 3 H]5‐HT. Elevated K + evoked a concentration‐ and Ca 2+ dependent release of [ 3 H]5‐HT. Exogenous 5‐HT and the 5‐HT 1B agonist, CGS‐12066B, both decreased the K + ‐stimulated release of [ 3 H]5‐HT. A 5‐HT 1B antagonist (methiothepin) blocked the 5‐HT‐ and the CGS‐12066B‐induced inhibition of K + ‐evoked release of [ 3 H]5‐HT. A 5‐HT 1A antagonist (NAN‐190) did not alter the inhibitory actions of exogenous 5‐HT. Moreover, a 5‐HT 1A agonist (8‐OH‐DPAT), a 5‐HT 2A/2C agonist [(+/‐)‐DOI hydrochloride], and a 5‐HT 3 agonist (2‐methyl‐5‐HT) did not alter the K + evoked release of [ 3 H]5‐HT. These data demonstrate that 5‐HT is released from the intermediate area of the rat thoracic spinal cord. The 5‐HT receptor subtype involved in the inhibition of the evoked release of [ 3 H]5‐HT is of the 5‐HT 1B subtype. These findings may help clarify the complex role of 5‐HT in spinal regulation of the sympathetic nervous system. © 1994 Wiley‐Liss, Inc This article is US Government work and, as such, is in the public domain in the United States of America.