Hesen W, Karten Y J, van de Witte S V, Joëls M
Department of Experimental Zoology, Institute for Neurobiology, University of Amsterdam, The Netherlands.
J Neuroendocrinol. 1998 Jan;10(1):9-19. doi: 10.1046/j.1365-2826.1998.00167.x.
Serotonin (5HT) and the cholinergic analogue carbachol (CCh) act on neurons in the hippocampal CA1 area through pre- and post-synaptic receptors. Previously, it was shown that post-synaptic actions of 5HT and CCh are affected by corticosteroids: predominant activation of high affinity mineralocorticoid receptors resulted in small hyperpolarizing responses to 5HT and small depolarizing responses to CCh; additional activation of low affinity glucocorticoid receptors led to increased 5HT and CCh responses. In the present study, we examined the consequences of steroid modulation of these post-synaptic membrane effects and/or possible pre-synaptic effects by 5HT and CCh for the excitability in the CA1 area, using extracellular field potential or intracellular recordings from individual pyramidal neurons. Steroid treatment by itself did not affect the amplitude or paired pulse properties of synaptic responses. In slices from adrenally intact rats, both 5HT (3-30 microM) and CCh (1-10 microM) induced a dose-dependent suppression of the synaptic field responses evoked in the CA1 area by stimulation of the Schaffer collaterals. No changes in these transmitter effects were observed after adrenalectomy. The 5HT induced suppression of the population spike amplitude was, however, reduced after selective occupation of mineralocorticoid receptors. Intracellularly, no significant steroid dependent modulation of (pre-synaptic) 5HT evoked changes in synaptic responses was observed. These data suggest that the steroids modulate post-synaptic but not pre-synaptic 5HT effects and that this modulation is reflected in the excitability of the CA1 region. The CCh induced suppression of the population spike was not affected by corticosteroid receptor activation, indicating that the previously found steroid modulation of post-synaptic CCh effects has no clear consequences for the CA1 excitability.
血清素（5-羟色胺，5HT）和胆碱能类似物卡巴胆碱（CCh）通过突触前和突触后受体作用于海马CA1区的神经元。此前研究表明，5HT和CCh的突触后作用受皮质类固醇影响：高亲和力盐皮质激素受体的主要激活导致对5HT的微小超极化反应和对CCh的微小去极化反应；低亲和力糖皮质激素受体的额外激活导致5HT和CCh反应增强。在本研究中，我们使用细胞外场电位或单个锥体神经元的细胞内记录，研究了这些突触后膜效应的类固醇调节以及/或者5HT和CCh可能的突触前效应对CA1区兴奋性的影响。单独的类固醇处理并不影响突触反应的幅度或双脉冲特性。在肾上腺完整大鼠的脑片中，5HT（3 - 30微摩尔）和CCh（1 - 10微摩尔）均诱导了刺激海马体传入侧支纤维在CA1区诱发的突触场反应的剂量依赖性抑制。肾上腺切除术后，这些递质效应未观察到变化。然而，在选择性占据盐皮质激素受体后，5HT诱导的群体峰电位幅度抑制作用减弱。在细胞内，未观察到（突触前）5HT诱发的突触反应变化有明显的类固醇依赖性调节。这些数据表明，类固醇调节突触后而非突触前的5HT效应，且这种调节反映在CA1区的兴奋性上。CCh诱导的群体峰电位抑制不受皮质类固醇受体激活的影响，表明先前发现的突触后CCh效应的类固醇调节对CA1区兴奋性没有明确影响。
