Serotonin depresses excitatory synaptic transmission and depolarization‐evoked Ca2+ influx in rat basolateral amygdala via 5‐HT1A receptors

Serotonin depresses excitatory synaptic transmission and depolarization‐evoked Ca2+ influx in... The actions of serotonin on rat basolateral amygdala neurons were studied with conventional intracellular recording techniques and fura‐2 fluorimetric recordings. Bath application of 5‐hydroxytryptamine (5‐HT or serotonin) reversibly suppressed the excitatory postsynaptic potential in a concentration‐dependent manner without affecting the resting membrane potential and neuronal input resistance. Extracellular Ba2+ or pertussis toxin pretreatment did not affect the depressing effect of 5‐HT suggesting that it is not mediated through activation of Gi/o protein‐coupled K+ conductance. The sensitivity of postsynaptic neurons to glutamate receptor agonist was unaltered by the 5‐HT pretreatment. In addition, the magnitude of paired‐pulse facilitation was increased in the presence of 5‐HT indicating a presynaptic mode of action. The effect of 5‐HT was mimicked by the selective 5‐HT1A agonist 8‐hydroxy‐dipropylaminotetralin (8‐OH‐DPAT) and was blocked by the selective 5‐HT1A antagonist 1‐(2‐methoxyphenyl)‐4[4‐(2‐phthalimido)butyl]piperazine oxadiazol‐3‐yl]methyl]phenyl]methanesulphonamide. In contrast, the selective 5‐HT2 receptor antagonist ketanserin failed to affect the action of 5‐HT. The effects of 5‐HT and 8‐OH‐DPAT on the high K+‐induced increase in [Ca2+]i were studied in acutely dissociated basolateral amygdala neurons. High K+‐induced increase in [Ca2+]i was blocked by Ca2+‐free solution and Cd2+ suggesting that Ca2+ entry responsible for the depolarizaton‐evoked increase in [Ca2+]i occurred through voltage‐dependent Ca2+ channels. Application of 5‐HT and 8‐OH‐DPAT reduced the K+‐induced Ca2+ influx in a concentration‐dependent manner. The effect of 5‐HT was completely abolished in slices pretreated with Rp‐cyclic adenosine 3′,5′‐monophosphothioate (Rp‐cAMP), a regulatory site antagonist of protein kinase A, suggesting that 5‐HT may act through a cAMP‐dependent mechanism. Taken together, these results suggest that functional 5‐HT1A receptors are present in the excitatory terminals and mediate the 5‐HT inhibition of synaptic transmission in the amygdala. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Neuroscience Wiley

Serotonin depresses excitatory synaptic transmission and depolarization‐evoked Ca2+ influx in rat basolateral amygdala via 5‐HT1A receptors

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Publisher
Wiley
Copyright
Copyright © 1998 Wiley Subscription Services
ISSN
0953-816X
eISSN
1460-9568
DOI
10.1046/j.1460-9568.1998.00229.x
Publisher site
See Article on Publisher Site

Abstract

The actions of serotonin on rat basolateral amygdala neurons were studied with conventional intracellular recording techniques and fura‐2 fluorimetric recordings. Bath application of 5‐hydroxytryptamine (5‐HT or serotonin) reversibly suppressed the excitatory postsynaptic potential in a concentration‐dependent manner without affecting the resting membrane potential and neuronal input resistance. Extracellular Ba2+ or pertussis toxin pretreatment did not affect the depressing effect of 5‐HT suggesting that it is not mediated through activation of Gi/o protein‐coupled K+ conductance. The sensitivity of postsynaptic neurons to glutamate receptor agonist was unaltered by the 5‐HT pretreatment. In addition, the magnitude of paired‐pulse facilitation was increased in the presence of 5‐HT indicating a presynaptic mode of action. The effect of 5‐HT was mimicked by the selective 5‐HT1A agonist 8‐hydroxy‐dipropylaminotetralin (8‐OH‐DPAT) and was blocked by the selective 5‐HT1A antagonist 1‐(2‐methoxyphenyl)‐4[4‐(2‐phthalimido)butyl]piperazine oxadiazol‐3‐yl]methyl]phenyl]methanesulphonamide. In contrast, the selective 5‐HT2 receptor antagonist ketanserin failed to affect the action of 5‐HT. The effects of 5‐HT and 8‐OH‐DPAT on the high K+‐induced increase in [Ca2+]i were studied in acutely dissociated basolateral amygdala neurons. High K+‐induced increase in [Ca2+]i was blocked by Ca2+‐free solution and Cd2+ suggesting that Ca2+ entry responsible for the depolarizaton‐evoked increase in [Ca2+]i occurred through voltage‐dependent Ca2+ channels. Application of 5‐HT and 8‐OH‐DPAT reduced the K+‐induced Ca2+ influx in a concentration‐dependent manner. The effect of 5‐HT was completely abolished in slices pretreated with Rp‐cyclic adenosine 3′,5′‐monophosphothioate (Rp‐cAMP), a regulatory site antagonist of protein kinase A, suggesting that 5‐HT may act through a cAMP‐dependent mechanism. Taken together, these results suggest that functional 5‐HT1A receptors are present in the excitatory terminals and mediate the 5‐HT inhibition of synaptic transmission in the amygdala.

Journal

European Journal of NeuroscienceWiley

Published: Jan 1, 1998

Keywords: ; ; ;

References

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