Excitatory and inhibitory roles of central ganglia in initiation of the insect ecdysis behavioural sequence.
Excitatory and inhibitory roles of central ganglia in initiation of the insect ecdysis behavioural sequence.
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发表时间：
2000-04
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通讯作者：
D. Z̆itn̆an;M. Adams
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作者：
D. Z̆itn̆an;M. Adams
昆虫通过蜕皮行为序列来脱落它们的旧角质层。为了激活Manduca sexta中这组程序化行为的每个亚基，特定的中央神经节被Inka细胞分泌的蜕皮前触发（PETH）和蜕皮触发（ETH）激素靶向。PETH和ETH作用于每个腹部神经节，在几分钟内分别启动蜕皮前期I和II。此后不久，ETH靶向中脑和食管下神经节，通过升高环GMP（cGMP）水平激活腹神经节中的蜕皮神经网络。然而，蜕皮行为的发生被来自头神经节和胸神经节的抑制因子延迟。从蜕皮前到蜕皮的转换是由每个腹神经节中的独立时钟控制的，并且在去除头部和胸部后大大加速。蜕皮激素（EH）似乎是引起cGMP水平升高和蜕皮的中枢信号之一，但这些作用是相当可变的，通常仅限于前神经节。去鞘神经节的EH治疗也在完整神经节中激发cGMP的强烈产生，表明这种诱导通过释放额外的下游因子而发生。我们的数据表明，蜕皮前的启动和蜕皮的过渡是由中枢神经系统内释放的刺激和抑制因子的PETH和ETH的初始行动后调节。
Insects shed their old cuticle by performing the ecdysis behavioural sequence. To activate each subunit of this set of programmed behaviours in Manduca sexta, specific central ganglia are targeted by pre-ecdysis-triggering (PETH) and ecdysis-triggering (ETH) hormones secreted from Inka cells. PETH and ETH act on each abdominal ganglion to initiate, within a few minutes, pre-ecdysis I and II, respectively. Shortly thereafter, ETH targets the tritocerebrum and suboesophageal ganglion to activate the ecdysis neural network in abdominal ganglia through the elevation of cyclic GMP (cGMP) levels. However, the onset of ecdysis behaviour is delayed by inhibitory factor(s) from the cephalic and thoracic ganglia. The switch from pre-ecdysis to ecdysis is controlled by an independent clock in each abdominal ganglion and is considerably accelerated after removal of the head and thorax. Eclosion hormone (EH) appears to be one of the central signals inducing elevation of cGMP levels and ecdysis, but these actions are quite variable and usually restricted to anterior ganglia. EH treatment of desheathed ganglia also elicits strong production of cGMP in intact ganglia, suggesting that this induction occurs via the release of additional downstream factors. Our data suggest that the initiation of pre-ecdysis and the transition to ecdysis are regulated by stimulatory and inhibitory factors released within the central nervous system after the initial actions of PETH and ETH.