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首页> 外文期刊>The European Journal of Neuroscience >Somatostatin receptors differentially affect spontaneous epileptiform activity in mouse hippocampal slices.
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Somatostatin receptors differentially affect spontaneous epileptiform activity in mouse hippocampal slices.

机译：生长抑素受体差异影响小鼠海马切片中的自发性癫痫样活动。

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Abstract Somatostatin-14 [somatotropin release-inhibiting factor (SRIF)] reduces hippocampal epileptiform activity but the contribution of its specific receptors (sst(1-5)) is poorly understood. We have focused on the role of sst(1) and sst(2) in mediating SRIF modulation of epilepsy using hippocampal slices of wild-type (WT) and sst(1) or sst(2) knockout (KO) mice. Recordings of epileptiform discharge induced by Mg(2+)-free medium with 4-aminopyridine were performed from the CA3 region before and after the application of SRIF compounds. In WT mice, SRIF and the sst(1) agonist CH-275 reduce epilepsy whereas sst(1) blockade with its antagonist SRA-880 increases the bursting discharge. Activation of sst(2) does not affect the bursting frequency unless its agonist octreotide is applied with SRA-880, indicating that sst(1) masks sst(2)-mediated modulation of epilepsy. In sst(1) KO mice: (i) the bursting frequency is lower than in WT; (ii) SRIF, CH-275 and SRA-880 are ineffective on epilepsy and (iii) octreotide is also devoid of effects, whereas blockade of sst(2) with the antagonist d-Tyr(8) Cyn 154806 increases the bursting frequency. In sst(2) KO mice, the SRIF ligand effects are similar to those in WT. In the whole hippocampus of sst(1) KO mice, sst(2) mRNA, protein and binding are higher than in WT and reverse transcription-polymerase chain reaction of the CA3 subarea confirms an increase of the sst(2) messenger. We conclude that sst(1) mediates inhibitory actions of SRIF and that interactions between sst(1) and sst(2) may prevent sst(2) modulation of epilepsy. We suggest that, in sst(1) KO mice, activation of over-expressed sst(2) reduces the bursting frequency, indicating that sst(2) density represents the rate-limiting factor for sst(2)-mediated modulation of epilepsy.
机译：摘要生长抑素14 [生长激素释放抑制因子（SRIF）]降低海马癫痫样活动，但其特定受体（sst（1-5））的作用尚不清楚。我们已经集中研究了sst（1）和sst（2）在使用野生型（WT）和sst（1）或sst（2）敲除（KO）小鼠的海马切片介导癫痫的SRIF调节中的作用。 SRIF化合物的应用之前和之后，从CA3地区进行记录的无Mg（2+）介质与4-氨基吡啶诱导的癫痫样放电。在野生型小鼠中，SRIF和sst（1）激动剂CH-275减少癫痫病，而用其拮抗剂SRA-880阻断sst（1）则增加爆发放电。除非将其激动剂奥曲肽与SRA-880一起使用，否则sst（2）的激活不会影响猝发频率，这表明sst（1）掩盖了sst（2）介导的癫痫调节。在sst（1）KO小鼠中：（i）爆发频率低于野生型; （ii）SRIF，CH-275和SRA-880对癫痫病无效，（iii）奥曲肽也没有作用，而用拮抗剂d-Tyr（8）Cyn 154806阻断sst（2）则增加了猝发频率。在sst（2）KO小鼠中，SRIF配体的作用与野生型相似。在sst（1）KO小鼠的整个海马中，sst（2）mRNA，蛋白质和结合均高于WT，CA3子区域的逆转录聚合酶链反应证实了sst（2）信使的增加。我们得出的结论是，sst（1）介导SRIF的抑制作用，并且sst（1）和sst（2）之间的相互作用可能会阻止sst（2）调节癫痫。我们建议，在sst（1）KO小鼠中，过度表达的sst（2）的激活降低了猝发频率，表明sst（2）密度代表sst（2）介导的癫痫调节的速率限制因素。

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