Aging represents the largest risk factor for developing Parkinson's disease (PD); another salient feature of this disorder is a decreased brain levels of somatostatin. Recently, in aged Wistar rats, we simulated the central somatostatinergic deficiency by intracerebroventricular injections of a somatostatin antagonist, cyclosomatostatin (cSST). The treated animals displayed catalepsy, a state that resembles the extrapyramidal signs of Parkinson's disease; young animals were insensitive to cSST. The neuroanatomical substrates responsible for the increased cataleptogenic activity of cSST in aged animals, are currently unknown. To study this issue, we assessed the cSST effect on brain c-Fos-protein expression in aged and young rats; thirty three brain regions were examined. cSST was employed at the dose cataleptogenic for aged animals and non-cataleptogenic for young ones. c-Fos expression patterns in the 'cataleptic' and 'non-cataleptic' animals were very similar, with the only distinction being a decrease in the c-Fos expression in the aged lateral entorhinal cortex (LEntCx). This decrease was not observed when the cSST-induced cataleptic response was inhibited by administration of diphenhydramine and nicotine. Thus, the development of catalepsy in the aged Wistar rats appeared to be associated with a hypoactivation of the LEntCx; possibly, there exists a mechanistic link between the LEntCx hypoactivation and increased susceptibility of aged rats to catalepsy. Apparently, these findings may provide novel insight into the link between mechanisms of parkinsonian motor disorders and aging.

中文翻译：

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环生长抑素诱导的老年大鼠僵住症：外侧内嗅皮层中脑 c-Fos 蛋白表达的特定变化。

衰老是发展成帕金森病 (PD) 的最大风险因素；这种疾病的另一个显着特征是大脑中生长抑素水平下降。最近，在老年 Wistar 大鼠中，我们通过脑室内注射生长抑素拮抗剂环生长抑素 (cSST) 来模拟中枢生长抑素能缺乏。接受治疗的动物表现出僵住症，这种状态类似于帕金森病的锥体外系症状；年轻的动物对 cSST 不敏感。导致老年动物 cSST 致麻痹活性增加的神经解剖学底物目前尚不清楚。为了研究这个问题，我们评估了 cSST 对老年和年轻大鼠大脑 c-Fos-蛋白表达的影响；检查了三十三个大脑区域。cSST 用于老年动物的致盲性剂量和非致盲性动物的年轻动物。“僵硬”和“非僵直”动物中的 c-Fos 表达模式非常相似，唯一的区别是老年外侧内嗅皮层 (LEntCx) 中 c-Fos 表达的降低。当使用苯海拉明和尼古丁抑制 cSST 诱导的僵直反应时，没有观察到这种降低。因此，老年 Wistar 大鼠僵住症的发展似乎与 LEntCx 的低活化有关。可能，在 LEntCx 低激活与老年大鼠对僵住症的易感性增加之间存在机制联系。显然，这些发现可能为帕金森运动障碍与衰老机制之间的联系提供新的见解。