CHOLINERGIC SUPPRESSION SPECIFIC TO INTRINSIC NOT AFFERENT FIBER SYNAPSES IN RAT PIRIFORM (OLFACTORY) CORTEX
CHOLINERGIC SUPPRESSION SPECIFIC TO INTRINSIC NOT AFFERENT FIBER SYNAPSES IN RAT PIRIFORM (OLFACTORY) CORTEX
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DOI：
10.1152/jn.1992.67.5.1222
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发表时间：
1992-05-01
影响因子：
2.5
通讯作者：
BOWER, JM
中科院分区：
文献类型：
--
作者：
HASSELMO, ME;BOWER, JM
1.在大鼠梨状皮质的传入和内在纤维突触传递的胆碱能抑制的差异进行了研究。细胞外和细胞内记录技术应用于体外横切片制备。传入和内在纤维系统分别用放置在Ia层或Ib层的电极进行差分刺激。在胆碱能激动剂和拮抗剂的存在下监测突触反应.传入和内在的纤维突触电位的细胞外测量显示大的差异敏感性微摩尔浓度的胆碱能激动剂卡巴胆碱或（+/-）-毒蕈碱，或乙酰胆碱与新斯的明相结合。在胆碱能激动剂的存在下，LB层中的内在纤维突触反应强烈减少，而在LA层中的传入纤维突触反应在很大程度上不受影响。在100 μ M的浓度下，所有三种激动剂引起内在纤维突触电位高度降低> 60%，但传入纤维突触电位降低< 15%。细胞内记录证实，胆碱能激动剂卡巴胆碱选择性抑制内源性纤维突触电位，但不抑制来自同一锥体细胞的传入纤维突触电位.剂量反应曲线卡巴胆碱获得两个纤维系统使用细胞外记录诱发场电位。卡巴胆碱抑制内在纤维突触电位，解离系数（K（DA））估计为2.9 μ M，50%响应的抑制浓度估计为6.6 μ M。卡巴胆碱产生的第一个脉冲比第二个脉冲的脉冲对更大的抑制成比例。这种易化水平的增加伴随着抑制，提示了一种突触前机制。卡巴胆碱不改变细胞内记录的突触电位的时间过程，表明这种抑制不是由于突触后抑制。胆碱能拮抗剂阿托品、东莨菪碱和哌仑西平对突触电位无直接影响。然而.在灌注这些拮抗剂后，随后灌注卡巴胆碱引起的对内在纤维突触电位的抑制要小得多，这表明这种抑制是由于M1亚型的毒蕈碱胆碱能受体。随着灌注高浓度的卡巴胆碱或乙酰胆碱，群体尖峰出现在Ia层突触电位，这表明更大的兴奋性的锥体细胞传入纤维刺激。群体尖峰没有出现与内在的纤维刺激。细胞内记录显示在卡巴胆碱存在下对电流注入的尖峰响应增加。在学习过程中选择性抑制内源性纤维突触传递可能会增强皮层联想记忆的表现。如配套文件所示。
1. Differences in the cholinergic suppression of afferent and intrinsic fiber synaptic transmission were studied in the rat piriform cortex. Extracellular and intracellular recording techniques were applied in an in vitro transverse slice preparation. Afferent and intrinsic fiber systems were differentially stimulated with electrodes placed in layer Ia or layer Ib, respectively. Synaptic responses were monitored in the presence of cholinergic agonists and antagonists.2. Afferent and intrinsic fiber synaptic potentials measured extracellularly showed large differences in sensitivity to micromolar concentrations of the cholinergic agonists carbachol or (+/-)-muscarine, or to acetylcholine combined with neostigmine. Intrinsic fiber synaptic responses in layer lb were strongly reduced in the presence of cholinergic agonists, whereas afferent fiber synaptic responses in layer la were largely unaffected. At a concentration of 100-mu-M, all three agonists caused a > 60% decrease in the height of the intrinsic fiber synaptic potential but < 15% reduction in the afferent fiber synaptic potential.3. Intracellular recordings confirmed that the cholinergic agonist carbachol selectively suppresses intrinsic fiber synaptic potentials but not afferent fiber synaptic potentials recorded from the same pyramidal cell.4. Dose-response curves to carbachol were obtained for both fiber systems using extracellular recording of evoked field potentials. Carbachol suppressed intrinsic fiber synaptic potentials with a coefficient of dissociation (K(DA)) estimated at 2.9-mu-M and an inhibitory concentration for 50% response estimated at 6.6-mu-M.5. Carbachol produced a proportionately greater suppression of the first pulse than the second pulse of a pulse pair. This increase in the level of facilitation accompanying suppression suggests a presynaptic mechanism. Carbachol did not change the time course of intracellularly recorded synaptic potentials, suggesting that the suppression is not due to postsynaptic inhibition.6. The cholinergic antagonists atropine, scopolamine, and pirenzepine had no direct effect on the synaptic potentials. However. after perfusion with these antagonists, subsequent perfusion with carbachol caused much less suppression of the intrinsic fiber synaptic potential, suggesting the suppression is due to a muscarinic cholinergic receptor of the M 1 subtype.7. With perfusion of high concentrations of carbachol or acetylcholine, a population spike appeared in the layer Ia synaptic potential, suggesting greater excitability of pyramidal cells to afferent fiber stimulation. Population spikes did not appear with intrinsic fiber stimulation. Intracellular recording showed increased spiking response to current injection in the presence of carbachol.8. The selective suppression of intrinsic fiber synaptic transmission during learning may enhance cortical associative memory performance. as shown in the companion paper.