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Effect of L‐thyroxine administration on long‐term potentiation and accompanying mitogen‐activated protein kinases in rats
International Journal of Developmental Neuroscience ( IF 1.8 ) Pub Date : 2021-02-12 , DOI: 10.1002/jdn.10097
Burak Tan 1 , Ercan Babur 2 , Meral Aşçıoğlu 1 , Cem Süer 1
Affiliation  

The present study investigated the differences in the activation of c‐Jun NH2‐terminal kinases (JNK), p38 mitogen‐activated protein kinases (p38MAPK), and extracellular signal‐regulated kinases 1/2 (Erk1/2) 1 hr after the induction of long‐term potentiation (LTP) between rats with hyperthyroidism that was produced at two different stages of development. Hyperthyroidism was produced in rats by daily injections of L‐thyroxine (T4, ip., 0.2 mg/kg) to their dams for lactation period or to the rats itself during the young adult period. LTP was induced by application of high‐frequency stimulation protocol. Five‐min averages of the excitatory postsynaptic potential (EPSP) slopes and population spike (PS) amplitudes at the end of recording were averaged to measure the magnitude of LTP. Total and phosphorylated levels of Erk1/2, JNK, and P38‐MAPK were assessed via western blotting in these hippocampi. LTP was found to be impaired in both groups of hyperthyroidisms, but this impairment observed together with increased expression and phosphorylation of ERK1/2, and increased phosphorylation of JNK in rats treated maternally with T4 compared to those treated adultly. These results suggest that excessiveness of thyroid hormone has longstanding effects on hippocampal function and may account for failed LTP in both early and relatively late stage of development depending on various molecular pathways, such as ERK1/2 and JNK.

中文翻译:

L-甲状腺素给药对大鼠长时程增强和伴随的丝裂原活化蛋白激酶的影响

本研究调查了 c-Jun NH2 末端激酶 (JNK)、p38 丝裂原活化蛋白激酶 (p38 MAPK ) 和细胞外信号调节激酶 1/2 (Erk1/2)激活后 1 小时的差异。在两个不同发育阶段产生的甲亢大鼠之间诱导长时程增强(LTP)。大鼠在哺乳期每天注射 L-甲状腺素(T4, ip., 0.2 mg/kg)会产生甲状腺功能亢进症,或在年轻成年期向大鼠本身注射 L-甲状腺素。LTP 是通过应用高频刺激方案诱导的。记录结束时兴奋性突触后电位 (EPSP) 斜率和种群峰值 (PS) 幅度的五分钟平均值被平均以测量 LTP 的大小。通过蛋白质印迹在这些海马中评估 Erk1/2、JNK 和 P38-MAPK 的总水平和磷酸化水平。发现两组甲状腺功能亢进症的 LTP 均受损,但观察到这种受损与 ERK1/2 的表达和磷酸化增加,以及与成人治疗的大鼠相比,用 T4 母体治疗的大鼠中 JNK 的磷酸化增加。这些结果表明,甲状腺激素过多对海马功能有长期影响,并且可能是由于各种分子途径(如 ERK1/2 和 JNK)在发育的早期和相对晚期阶段 LTP 失败的原因。
更新日期:2021-02-12
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