Presynaptic 5‐HT 3 receptor‐mediated modulation of synaptic GABA release in the mechanically dissociated rat amygdala neurons

Presynaptic 5‐HT 3 receptor‐mediated modulation of synaptic GABA release in the mechanically... 1 Nystatin‐perforated patch recordings were made from mechanically dissociated basolateral amygdala neurons with preserved intact native presynaptic nerve terminals to study the mechanism of 5‐HT3 receptor‐mediated serotonergic modulation of GABAergic inhibition. 2 The specific 5‐HT3 agonist mCPBG (1 μM) rapidly facilitated the frequency of GABAergic miniature inhibitory postsynaptic currents (mIPSCs) and this facilitation desensitized within 1 min. Tropisetron (30 nM), a specific 5‐HT3 antagonist, blocked the mCPBG effect. 3 mCPBG augmented mIPSC amplitude. However, no direct postsynaptic serotonergic currents were evoked by mCPBG. Neither GABA‐evoked current amplitude nor the kinetics of individual GABAergic mIPSCs were affected by mCPBG. Therefore, the augmentation is unlikely to be due to postsynaptic effects evoked by mCPBG. At higher concentrations mCPBG produced shorter‐duration facilitation of miniature events. 4 While mCPBG increased the mIPSC frequency in calcium‐containing solution with Cd2+, this increase was absent in Ca2+‐free external solution. It appears that the Ca2+ influx through voltage‐dependent calcium channels was not as crucial as that through 5‐HT3 receptors for synaptic GABA release. 5 When two pulses of mCPBG (each 1 μM, 1 min) were given, the response to the second pulse elicited full recovery when the interval between pulses was at least 9 min. Protein kinase A (PKA) activation by 8‐Br‐cAMP (300 μM) shortened and PKA inhibition by Rp‐cAMP (100 μM) prolonged the recovery time. PKA activity did not affect the time course of fast desensitization. 6 Our results suggest that a 5‐HT3‐specific agonist acts on presynaptic nerve terminals facilitating synaptic GABA release without postsynaptic effects. The facilitation requires calcium influx through presynaptic 5‐HT3 receptors. PKA modulates the recovery process from desensitization of presynaptic 5‐HT3 receptor‐mediated regulation of synaptic GABA release. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Physiology Wiley

Presynaptic 5‐HT 3 receptor‐mediated modulation of synaptic GABA release in the mechanically dissociated rat amygdala neurons

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Publisher
Wiley
Copyright
Copyright © 2000 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0022-3751
eISSN
1469-7793
DOI
10.1111/j.1469-7793.2000.00373.x
Publisher site
See Article on Publisher Site

Abstract

1 Nystatin‐perforated patch recordings were made from mechanically dissociated basolateral amygdala neurons with preserved intact native presynaptic nerve terminals to study the mechanism of 5‐HT3 receptor‐mediated serotonergic modulation of GABAergic inhibition. 2 The specific 5‐HT3 agonist mCPBG (1 μM) rapidly facilitated the frequency of GABAergic miniature inhibitory postsynaptic currents (mIPSCs) and this facilitation desensitized within 1 min. Tropisetron (30 nM), a specific 5‐HT3 antagonist, blocked the mCPBG effect. 3 mCPBG augmented mIPSC amplitude. However, no direct postsynaptic serotonergic currents were evoked by mCPBG. Neither GABA‐evoked current amplitude nor the kinetics of individual GABAergic mIPSCs were affected by mCPBG. Therefore, the augmentation is unlikely to be due to postsynaptic effects evoked by mCPBG. At higher concentrations mCPBG produced shorter‐duration facilitation of miniature events. 4 While mCPBG increased the mIPSC frequency in calcium‐containing solution with Cd2+, this increase was absent in Ca2+‐free external solution. It appears that the Ca2+ influx through voltage‐dependent calcium channels was not as crucial as that through 5‐HT3 receptors for synaptic GABA release. 5 When two pulses of mCPBG (each 1 μM, 1 min) were given, the response to the second pulse elicited full recovery when the interval between pulses was at least 9 min. Protein kinase A (PKA) activation by 8‐Br‐cAMP (300 μM) shortened and PKA inhibition by Rp‐cAMP (100 μM) prolonged the recovery time. PKA activity did not affect the time course of fast desensitization. 6 Our results suggest that a 5‐HT3‐specific agonist acts on presynaptic nerve terminals facilitating synaptic GABA release without postsynaptic effects. The facilitation requires calcium influx through presynaptic 5‐HT3 receptors. PKA modulates the recovery process from desensitization of presynaptic 5‐HT3 receptor‐mediated regulation of synaptic GABA release.

Journal

The Journal of PhysiologyWiley

Published: Dec 1, 2000

References

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