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首页> 外文期刊>Life sciences >Acute and persistent nociceptive paw sensitisation in mice: the involvement of distinct signalling pathways.
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Acute and persistent nociceptive paw sensitisation in mice: the involvement of distinct signalling pathways.

机译：小鼠急性和持续伤害感受性足敏化：涉及不同的信号通路。

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AIMS: Many fundamental pharmacological studies in pain and inflammation have been performed on rats. However, the pharmacological findings were generally not extended to other species in order to increase their predictive therapeutic value. We studied acute and chronic inflammatory nociceptive sensitisation of mouse hind paws by prostaglandin E(2) (PGE(2)) or dopamine (DA), as previously described in rats. We also investigated the participation of the signalling pathways in acute and persistent sensitisation. MAIN METHODS: Mechanical sensitisation (hypernociception) induced by intraplantar administrations of PGE(2) or DA was evaluated with an electronic pressure meter. The signalling pathways were pharmacologically investigated with the pre-administration of adenylyl cyclase (AC), cAMP-dependent protein kinase (PKA), protein kinase Cepsilon (PKCepsilon), and the extracellular signal-related kinase (ERK) inhibitors. KEY FINDINGS: Single or 14days of successive intraplantar injections of PGE(2) or DA-induced acute and persistent hypernociception (lasting for more than 30days), respectively. The involvement of AC, PKA or PKCepsilon was observed in the acute hypernociception induced by PGE(2), while PKA or PKCepsilon were continuously activated during the period of persistent hypernociception. The acute hypernociception induced by DA involves activation of ERK, PKCepsilon, AC or PKA, while persistent hypernociception implicated ERK activation, but not PKA, PKCepsilon or AC. SIGNIFICANCE: In mice, acute and persistent paw sensitisation involves the different activation of kinases, as previously described for rats. This study opens the possibility of comparing pharmacological approaches in both species to further understand acute and chronic inflammatory sensitisation, and possibly associated genetic manipulations.
机译：目的：已经在大鼠上进行了许多关于疼痛和炎症的基本药理研究。但是，药理学发现通常并未扩展到其他物种，以增加其预测治疗价值。如先前在大鼠中所述，我们研究了前列腺素E（2）（PGE（2））或多巴胺（DA）对小鼠后爪的急性和慢性炎症伤害性敏化作用。我们还调查了急性和持续性致敏中信号通路的参与。主要方法：用电子压力计评估足底内施用PGE（2）或DA引起的机械过敏（痛觉过敏）。使用腺苷酸环化酶（AC），cAMP依赖性蛋白激酶（PKA），蛋白激酶Cepsilon（PKCepsilon）和细胞外信号相关激酶（ERK）抑制剂预给药进行药理学研究。主要发现：分别足底注射PGE（2）或DA引起的急性和持续性高伤害感的持续时间为单天或14天（持续超过30天）。在PGE（2）诱发的急性痛觉超敏中观察到AC，PKA或PKCepsilon的参与，而在持续痛觉超敏期间，PKA或PKCepsilon持续被激活。由DA引起的急性痛觉超敏反应涉及ERK，PKCepsilon，AC或PKA的激活，而持续性痛觉超敏反应涉及ERK的激活，但不涉及PKA，PKCepsilon或AC。意义：在小鼠中，急性和持续性爪子致敏涉及激酶的不同激活，如先前在大鼠中所述。这项研究为比较两个物种的药理方法开辟了可能性，以进一步了解急性和慢性炎症致敏性，以及可能的相关基因操作。

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