Bidirectional synaptic plasticity at nociceptive afferents in the rat central amygdala
Bidirectional synaptic plasticity at nociceptive afferents in the rat central amygdala
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DOI：
10.1113/jphysiol.2007.101822
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发表时间：
2007-06-15
影响因子：
5.5
通讯作者：
Sah, Pankaj
中科院分区：
文献类型：
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作者：
Lopez de Armentia, Mikel;Sah, Pankaj
在离体条件下研究了臂旁核对中央杏仁核外侧区神经元的谷氨酸能输入。强直刺激这些输入导致LTP，不需要激活NMDA受体或突触后钙的上升。LTP伴随着成对脉冲比的减少，表明LTP的结果从发射机释放概率的增加。用毛喉素激活腺苷酸环化酶可增强这些输入，并类似地减少配对脉冲易化和阻断LTP诱导。LTP被蛋白激酶A阻断剂H89抑制。低频刺激导致LTD，需要激活突触后NMDA受体和突触后钙离子的升高。LTD对双脉冲易化作用无明显变化，LTD可被蛋白磷酸酶阻断剂calyculin和冈田酸阻断。我们的结论是，parabrachial输入到中央杏仁核的横向部门显示突触前LTP，需要激活的突触前蛋白激酶A通过钙依赖性腺苷酸环化酶，而LTD在相同的突触是突触后的，需要在突触后钙和激活的蛋白磷酸酶的上升。
Glutamatergic inputs arising from the parabrachial nucleus to neurons in the lateral sector of the central amygdala were studied in vitro. Tetanic stimulation of these inputs led to LTP that did not require activation of NMDA receptors or a rise of postsynaptic calcium. LTP was accompanied by a reduction in the paired-pulse ratio, indicating that LTP results from an increase in transmitter release probability. Activation of adenylyl cyclase with forskolin potentiated these inputs with a similar reduction in paired-pulse facilitation and occluded LTP induction. LTP was inhibited by the protein kinase A blocker H89. Low-frequency stimulation led to LTD that required activation of postsynaptic NMDA receptors and a rise in postsynaptic calcium. There was no change in paired-pulse facilitation with LTD. LTD was blocked by protein phosphatase blockers calyculin and okadaic acid. We conclude that parabrachial inputs to the lateral sector of the central amygdala show presynaptic LTP that requires activation of a presynaptic protein kinase A via a calcium-dependent adenylyl cyclase while LTD at the same synapses is postsynaptic and requires a rise in postsynaptic calcium and activation of protein phosphatase.