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Serotonin depresses excitatory synaptic transmission and depolarization‐evoked Ca 2+ influx in rat basolateral amygdala via 5‐HT 1A receptors
Author(s) -
Cheng LiLing,
Wang SuJane,
Gean PoWu
Publication year - 1998
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1998.00229.x
Subject(s) - ketanserin , basolateral amygdala , chemistry , serotonin , agonist , excitatory postsynaptic potential , neurotransmission , 5 ht receptor , neural facilitation , postsynaptic potential , medicine , biophysics , endocrinology , receptor , biology , biochemistry
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 Ba 2+ or pertussis toxin pretreatment did not affect the depressing effect of 5‐HT suggesting that it is not mediated through activation of G i/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‐HT 1A agonist 8‐hydroxy‐dipropylaminotetralin (8‐OH‐DPAT) and was blocked by the selective 5‐HT 1A antagonist 1‐(2‐methoxyphenyl)‐4[4‐(2‐phthalimido)butyl]piperazine oxadiazol‐3‐yl]methyl]phenyl]methanesulphonamide. In contrast, the selective 5‐HT 2 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 [Ca 2+ ] i were studied in acutely dissociated basolateral amygdala neurons. High K + ‐induced increase in [Ca 2+ ] i was blocked by Ca 2+ ‐free solution and Cd 2+ suggesting that Ca 2+ entry responsible for the depolarizaton‐evoked increase in [Ca 2+ ] i occurred through voltage‐dependent Ca 2+ channels. Application of 5‐HT and 8‐OH‐DPAT reduced the K + ‐induced Ca 2+ 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‐HT 1A receptors are present in the excitatory terminals and mediate the 5‐HT inhibition of synaptic transmission in the amygdala. Introduction