Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

5‐Hydroxytryptamine acts at 5‐HT2 receptors to decrease potassium conductance in rat nucleus accumbens neurones.

5‐Hydroxytryptamine acts at 5‐HT2 receptors to decrease potassium conductance in rat nucleus... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Physiology Wiley

5‐Hydroxytryptamine acts at 5‐HT2 receptors to decrease potassium conductance in rat nucleus accumbens neurones.

The Journal of Physiology , Volume 417 (1) – Oct 1, 1989

Loading next page...
 
/lp/wiley/5-hydroxytryptamine-acts-at-5-ht2-receptors-to-decrease-potassium-JJzgRmmdvO

References (44)

Publisher
Wiley
Copyright
© 2014 The Physiological Society
ISSN
0022-3751
eISSN
1469-7793
DOI
10.1113/jphysiol.1989.sp017786
Publisher site
See Article on Publisher Site

Abstract

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.

Journal

The Journal of PhysiologyWiley

Published: Oct 1, 1989

There are no references for this article.