Navarro C E, Cabrera R J, Donoso A O
Laboratorio de Investigaciones Cerebrales, LINCE-CONICET, Facultad de Ciencias Médicas, Mendoza, Argentina.
Brain Res Bull. 1995;37(2):119-22. doi: 10.1016/0361-9230(94)00261-x.
Glutamate has been shown to stimulate noradrenaline (NA) release from hypothalamic nerve terminals. In the present study, we evaluated the possible interaction between the excitatory amino acid glutamate and gamma-aminobutyric acid (GABA), an inhibitory transmitter, on noradrenaline (NA) release from mediobasal hypothalamus (MBH) of adult male rats. Hypothalamic slices loaded in vitro with 3H-NA were superfused and exposed to glutamate, N-methyl-D-aspartic acid (NMDA), or kainate (KA). We found that 3H-NA release evoked by the excitatory amino acids glutamate and NMDA was dramatically decreased by GABA. The facilitatory effects of NMDA and KA were prevented concentration-dependently by the GABAB receptor antagonist 2-hydroxy saclofen which restored the NMDA effect. In addition, baclofen blocked K(+)-induced 3H-NA release. Activation of GABAA receptors by muscimol and THIP was ineffective. In conclusion, glutamate and GABA, through GABAB receptors, may interact to modulate NA release from the rat mediobasal hypothalamus.
谷氨酸已被证明可刺激下丘脑神经末梢释放去甲肾上腺素(NA)。在本研究中,我们评估了兴奋性氨基酸谷氨酸与抑制性递质γ-氨基丁酸(GABA)之间可能存在的相互作用,这种相互作用对成年雄性大鼠中基底部下丘脑(MBH)释放去甲肾上腺素(NA)的影响。将体外加载有3H-NA的下丘脑切片进行灌流,并使其暴露于谷氨酸、N-甲基-D-天冬氨酸(NMDA)或海人藻酸(KA)中。我们发现,兴奋性氨基酸谷氨酸和NMDA诱发的3H-NA释放被GABA显著降低。GABAB受体拮抗剂2-羟基-舒洛芬可浓度依赖性地阻止NMDA和KA的促进作用,该拮抗剂可恢复NMDA的作用。此外,巴氯芬可阻断K⁺诱导的3H-NA释放。蝇蕈醇和四氢异喹啉对GABAA受体的激活无效。总之,谷氨酸和GABA可能通过GABAB受体相互作用,调节大鼠中基底部下丘脑释放NA。