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5‐Hydroxytryptamine acts at 5‐HT2 receptors to decrease potassium conductance in rat nucleus accumbens neurones.
Author(s) -
North R A,
Uchimura N
Publication year - 1989
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.1989.sp017786
Subject(s) - nucleus accumbens , chemistry , neuroscience , receptor , potassium , potassium channel , conductance , serotonin , biophysics , biology , biochemistry , physics , organic chemistry , condensed matter physics
1. Intracellular recordings were made from neurones in the nucleus accumbens in slices from the rat brain maintained in vitro. 2. 5‐Hydroxytryptamine (5‐HT.1‐100 microM) depolarized 170 of 203 (84%) neurones and caused them to discharge action potentials. The depolarization was associated with an increase in the input resistance, and was reversed in polarity by conditioning hyperpolarization; this reversal potential was linearly related to the logarithm of the extracellular potassium concentration. 3. Application of 5‐HT to neurones voltage‐clamped near their resting potential (typically about ‐80 mV) caused an inward current and a decrease in the slope conductance. The current caused by 5‐HT reversed polarity at the potassium equilibrium potential. Analysis with an equivalent circuit model of the neurone at steady state indicated that 5‐HT selectively reduced the inward rectifier potassium conductance. 4. The depolarization caused by 5‐HT persisted in tetrodotoxin (1 microM). It was reduced but not abolished by a solution that contained lower levels of calcium (0.24 instead of 2.4 mM), higher levels of magnesium (5 instead of 1.2 mM), and cobalt (2 mM). 5. The depolarization caused by 5‐HT was competitively antagonized by the 5‐HT2 antagonists ketanserin and mianserin with dissociation equilibrium constants of 3 and 45 nM respectively: spiperone (300 nM) also blocked the action of 5‐HT. The depolarization was not mimicked or blocked by a number of other agonists and antagonists selective for the 5‐HT1 and 5‐HT3 receptor types.