CELLULAR AND SYNAPTIC PROPERTIES OF AMYGDALA-KINDLED PYRIFORM CORTEX INVITRO
CELLULAR AND SYNAPTIC PROPERTIES OF AMYGDALA-KINDLED PYRIFORM CORTEX INVITRO
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DOI：
10.1152/jn.1986.55.6.1295
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发表时间：
1986-06-01
影响因子：
2.5
通讯作者：
WONG, RKS
中科院分区：
文献类型：
--
作者：
MCINTYRE, DC;WONG, RKS
使用含有杏仁核-梨状区的冠状切片制备，检查了对照和点燃大鼠梨状皮质神经元的诱发和自发活动。杏仁核的电刺激引起同步爆发反应梨状细胞的切片从控制和点燃的动物。点燃制备的细胞的爆发的平均持续时间大大延长。当Mg 2+增加以抑制但不阻断突触传递时，可以检查点燃动物和对照动物中的猝发反应的去极化突触事件。电刺激诱发短潜伏期分级突触去极化，随后是长潜伏期全或无去极化事件，这似乎是参与产生的爆发性反应。去甲肾上腺素（NE），在4 μ M的浓度，可逆地阻断了控制准备的爆发反应。点燃制剂引起的爆发反应也被NE抑制。对于后一种情况，需要更高浓度的NE才能产生这种效果。α-2-激动剂可乐定模拟NE对诱发事件的抑制作用。相反，β-激动剂异丙肾上腺素促进了自发同步爆发和延长诱发的爆发性放电的发生在控制和点燃的准备。NE和可乐定通过抑制潜在的突触事件来阻断爆发反应。异丙肾上腺素对自发反应和诱发反应的易化作用表明NE也可能发挥兴奋作用。
The evoked and spontaneous activity of neurons in the pyriform cortex of control and kindled rats was examined using a coronal slice preparation containing the amygdala-pyriform region. Electrical stimulation of the amygdala nuclei elicited synchronized burst responses in pyriform cells of slices from both control and kindled animals. The mean duration of the burst was greatly prolonged in cells from kindled preparations. The depolarizing synaptic events underlying the burst response in the kindled and control animals could be examined when Mg2+ was increased to suppress but not block synaptic transmission. Electrical stimulation evoked a short-latency graded synaptic depolarization, followed by a long-latency all-or-none depolarizing event, which appeared to be involved in generating the burst response. Norepinephrine (NE), in a 4-microM concentration, reversibly blocked the burst responses in the control preparation. Burst responses elicited from kindled preparations were also suppressed by NE. For the latter cases, higher concentrations of NE were required to produce this effect. The alpha-2-agonist clonidine mimicked the suppressive action of NE on the evoked events. In contrast the beta-agonist isoproterenol facilitated the occurrence of spontaneous synchronous bursts and prolonged evoked burst discharges in both the control and kindled preparations. NE and clonidine block the burst response by suppressing the underlying synaptic events. The facilitatory action of isoproterenol on spontaneous and evoked responses suggests that NE may also exert an excitatory effect.