Keller A, Yagodin S, Aroniadou-Anderjaska V, Zimmer L A, Ennis M, Sheppard N F, Shipley M T
Department of Anatomy and Neurobiology and the Program in Neuroscience, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
J Neurosci. 1998 Apr 1;18(7):2602-12. doi: 10.1523/JNEUROSCI.18-07-02602.1998.
The functional organization and synaptic physiology of olfactory bulb glomeruli were studied in rat in vitro slice preparations stained with the voltage-sensitive dye RH-155. Optical signals were recorded with a 100-element photodiode array at high temporal resolution. Pharmacological and ionic manipulations were used to investigate synaptic responses to stimulation of the olfactory nerve layer (ONL). ONL stimulation evoked a sodium-mediated compound action potential that propagated across the ONL and invaded individual glomeruli. This presynaptic volley evoked calcium-dependent synaptic responses the amplitudes of which were largest within the glomerular layer (GL); smaller amplitude responses were recorded in deeper layers of the olfactory bulb. Synaptic responses in the GL were attenuated by the non-NMDA ionotropic glutamate receptor antagonist CNQX; the residual component was suppressed by the NMDA glutamate receptor antagonist AP-5. The GABAA receptor antagonist bicuculline methiodide had little effect, whereas the GABAB receptor agonist baclofen dramatically attenuated ONL-evoked synaptic responses. The effects of baclofen were reversed by the GABAB receptor antagonist CGP35348. Paired-pulse depression of ONL-evoked synaptic responses in the GL was partially reversed by CGP35348. These findings suggest that olfactory nerve axons release glutamate to activate both NMDA and non-NMDA receptors on GL neurons, that GABAA receptor-mediated inhibition has little effect on these responses, and that GABAB receptor-mediated inhibition may act presynaptically on olfactory nerve axons to modulate their inputs to olfactory bulb neurons.
利用电压敏感染料RH - 155对大鼠体外脑片进行染色,研究了嗅球小球的功能组织和突触生理学。采用100元光电二极管阵列以高时间分辨率记录光信号。运用药理学和离子操作方法,研究对嗅神经层(ONL)刺激的突触反应。ONL刺激诱发了一种钠介导的复合动作电位,该电位在ONL上传播并侵入单个小球。这种突触前冲动诱发了钙依赖性突触反应,其幅度在小球层(GL)内最大;在嗅球深层记录到的反应幅度较小。GL中的突触反应被非NMDA离子型谷氨酸受体拮抗剂CNQX减弱;残余成分被NMDA谷氨酸受体拮抗剂AP - 5抑制。GABAA受体拮抗剂甲基荷包牡丹碱作用不大,而GABAB受体激动剂巴氯芬显著减弱了ONL诱发的突触反应。GABAB受体拮抗剂CGP35348可逆转巴氯芬的作用。CGP35348部分逆转了GL中ONL诱发突触反应的成对脉冲抑制。这些发现表明,嗅神经轴突释放谷氨酸以激活GL神经元上的NMDA和非NMDA受体,GABAA受体介导的抑制对这些反应影响不大,且GABAB受体介导的抑制可能在突触前作用于嗅神经轴突,以调节其对嗅球神经元的输入。