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5‐Hydoxytryptamine evokes depolarizations and membrane potential oscillations in rat sympathetic preganglionic neurones.
Author(s) -
Pickering A E,
Spanswick D,
Logan S D
Publication year - 1994
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1994.sp020345
Subject(s) - hyperpolarization (physics) , inhibitory postsynaptic potential , depolarization , membrane potential , chemistry , agonist , excitatory postsynaptic potential , ketanserin , reversal potential , medicine , ritanserin , endocrinology , electrophysiology , biophysics , neuroscience , 5 ht receptor , receptor , patch clamp , biology , serotonin , organic chemistry , nuclear magnetic resonance spectroscopy
1. Whole‐cell recordings were made from seventy‐seven identified rat sympathetic preganglionic neurones (SPN) in spinal cord slices. Perfusion of 5‐HT (0.5‐30 microM) strongly depolarized 90% of neurones. The response was slow in onset, could last over 10 min and was associated with an increase in input resistance. 5‐HT could also evoke rhythmical membrane potential oscillations in a population of previously quiescent neurones. 2. The 5‐HT response persisted in TTX and also in low‐Ca(2+)‐high‐Mg2+ artificial cerebrospinal fluid (ACSF), suggesting that the receptors are on SPN. The 5‐HT uptake inhibitor 6‐nitroquipazine potentiated the 5‐HT‐induced depolarization. 3. The 5‐HT‐induced depolarization was reduced and then abolished by membrane hyperpolarization to potentials of about ‐100 mV, but was not reversed in sign by further hyperpolarization. In voltage clamp, 5‐HT evoked inward currents associated with the reduction of an outwardly rectifying potassium conductance. 4. The 5‐HT2 receptor agonist alpha‐methyl‐5‐HT mimicked the 5‐HT response on all neurones, as did the 5‐HT1 receptor agonist 5‐carboxamidotryptamine (5‐CT) on 71% of SPN. The responses to 5‐HT, alpha‐methyl‐5‐HT and 5‐CT were inhibited by the 5‐HT2 antagonists ketanserin and ritanserin. 5. Pressure ejection of 5‐HT over the central canal region could evoke a biphasic inhibitory‐excitatory response. This response persisted in TTX, suggesting that an inhibitory 5‐HT receptor may be located on the medial dendrites. 6. SPN are powerfully depolarized by 5‐HT acting at 5‐HT2 receptors, via the closure of an outwardly rectifying potassium conductance. The long duration of the response and the ability of 5‐HT to induce rhythmical oscillations suggest that 5‐HT may have an important role in regulating SPN excitability.