Smriga M, Nishiyama N, Saito H
Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Japan.
J Neurosci Res. 1998 Mar 1;51(5):593-601. doi: 10.1002/(SICI)1097-4547(19980301)51:5<593::AID-JNR6>3.0.CO;2-A.
The dentate gyrus neurons in the hippocampus contain a high density of both mineralocorticoid and adrenergic receptors. By in vivo extracellular recording from adrenalectomized rats we investigated the possible relationships between the two systems with regard to neuronal excitability and activity-dependent synaptic plasticity. Pretreatment with aldosterone significantly enhanced both basal neuronal excitability and tetanically evoked synaptic plasticity in adrenalectomized, but not sham-operated rats. The enhancement was blocked by spironolactone, indicating a mineralocorticoid receptor-dependent effect. The adrenomedullary hormone epinephrine also significantly enhanced synaptic plasticity via activation of beta-adrenergic receptors. Beta-adrenergic antagonist propranolol, infused directly into the dentate gyrus granule cell layer, significantly reduced the effect of aldosterone on neuronal excitability and partly canceled the aldosterone-enhanced synaptic plasticity. No effect of propranolol was found after its amygdaloid infusion. The mineralocorticoid receptor antagonist spironolactone did not affect the epinephrine-induced effects. These results indicate that the pretreated adrenal steroids interact with the catecholaminergic system in the dentate gyrus of adrenalectomized rats and that the functional beta-adrenergic pathway is involved in the mechanism of mineralocorticoid-induced cellular effects in vivo.
海马体中的齿状回神经元含有高密度的盐皮质激素受体和肾上腺素能受体。通过对肾上腺切除大鼠进行体内细胞外记录，我们研究了这两个系统在神经元兴奋性和活动依赖性突触可塑性方面可能存在的关系。在肾上腺切除但未进行假手术的大鼠中，用醛固酮预处理可显著增强基础神经元兴奋性和强直诱发的突触可塑性。这种增强被螺内酯阻断，表明这是一种依赖盐皮质激素受体的效应。肾上腺髓质激素肾上腺素也通过激活β-肾上腺素能受体显著增强突触可塑性。直接注入齿状回颗粒细胞层的β-肾上腺素能拮抗剂普萘洛尔，显著降低了醛固酮对神经元兴奋性的影响，并部分抵消了醛固酮增强的突触可塑性。将普萘洛尔注入杏仁核后未发现其有作用。盐皮质激素受体拮抗剂螺内酯不影响肾上腺素诱导的效应。这些结果表明，预处理的肾上腺类固醇与肾上腺切除大鼠齿状回中的儿茶酚胺能系统相互作用，并且功能性β-肾上腺素能通路参与了体内盐皮质激素诱导的细胞效应机制。
