A peritracheal neuropeptide system in insects: release of myomodulin-like peptides at ecdysis.

1998 ◽  
Vol 201 (2) ◽  
pp. 193-209 ◽  
Author(s):  
M A O'Brien ◽  
P H Taghert

We identified of a set of neuropeptide-expressing cells sited along the respiratory system of Drosophila melanogaster using an antibody to the molluscan neuropeptide myomodulin. The number and positions of these 'peritracheal' myomodulin (PM) cells were reminiscent of the epitracheal Inka cells in the moth Manduca sexta. These Inka cells release the peptide ecdysis-triggering hormone, which helps elicit ecdysial behavior at the molt, and we show that they are also recognized by the myomodulin (MM) antibody. In both D. melanogaster and M. sexta, the PM and Inka cells are the only MM-positive cells outside the central nervous system. In both insects, MM immunoreactivity disappears at the end of the molt. In D. melanogaster, we have monitored the PM cells throughout development using two enhancer trap lines; the PM cells persist throughout development, but at larval, pupal and adult ecdyses, they display a loss of MM immunoreactivity. This transient loss occurs at a predictable time, just prior to ecdysis. In contrast, MM-positive neurons in the central nervous system do not show these changes. The PM cells also reveal a concomitant loss of immunostaining for an enzyme contained in secretory granules. The results are consistent with the hypothesis that the PM cells release MM-like peptides just prior to each ecdysis. In addition, we demonstrate that peritracheal cells of five widely divergent insect orders show a myomodulin phenotype. The peritracheal cell size, morphology, numbers and distribution vary in these different orders. These data suggest that peritracheal cells release MM-like peptides as part of a conserved feature of the endocrine regulation of insect ecdysis.

2001 ◽  
Vol 204 (20) ◽  
pp. 3483-3495 ◽  
Author(s):  
Inka Žitňanová ◽  
Michael E. Adams ◽  
Dušan Žitňan

SUMMARY Initiation of the ecdysis behavioural sequence in insects requires activation of the central nervous system (CNS) by pre-ecdysis-triggering hormone (PETH) and ecdysis-triggering hormone (ETH), which are released from the Inka cells of the epitracheal glands. Here, we show that the developmental events preceding larval and pupal ecdysis of Manduca sexta involve a dual action of ecdysteroids on the epitracheal glands and CNS. The low steroid levels in freshly ecdysed and feeding larvae are associated with small-sized epitracheal glands, reduced peptide production in Inka cells and insensitivity of the CNS to ETH. The elevated ecdysteroid levels before each ecdysis lead to a dramatic enlargement of Inka cells and increased production of peptide hormones and their precursors. As blood ecdysteroids reach peak levels, the CNS becomes responsive to Inka cell peptides. These effects of natural ecdysteroid pulses can be experimentally induced by injection of 20-hydroxyecdysone or the ecdysteroid agonist tebufenozide (RH-5992) into ecdysed larvae, thus stimulating peptide production in Inka cells and inducing CNS sensitivity to ETH. A direct steroid action on the CNS is demonstrated by subsequent treatment of isolated nerve cords from ecdysed larvae with 20-hydroxyecdysone and ETH, which results in pre-ecdysis or ecdysis bursts. Our data show that ecdysteroid-induced transcriptional activity in both the epitracheal glands and the CNS are necessary events for the initiation of the ecdysis behavioural sequence.


2000 ◽  
Vol 203 (8) ◽  
pp. 1329-1340 ◽  
Author(s):  
D. Zitnan ◽  
M.E. Adams

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.


1989 ◽  
Vol 147 (1) ◽  
pp. 457-470 ◽  
Author(s):  
JAMES W. TRUMAN ◽  
PHILIP F. COPENHAVER

Larval and pupal ecdyses of the moth Manduca sexta are triggered by eclosion hormone (EH) released from the ventral nervous system. The major store of EH activity in the latter resides in the proctodeal nerves that extend along the larval hindgut. At pupal ecdysis, the proctodeal nerves show a 90% depletion of stored activity, suggesting that they are the major release site for the circulating EH that causes ecdysis. Surgical experiments involving the transection of the nerve cord or removal of parts of the brain showed that the proctodeal nerve activity originates from the brain. Retrograde and anterograde cobalt fills and immunocytochemistry using antibodies against EH revealed two pairs of neurons that reside in the ventromedial region of the brain and whose axons travel ipsilaterally along the length of the central nervous system (CNS) and project into the proctodeal nerve, where they show varicose release sites. These neurons constitute a novel neuroendocrine pathway in insects which appears to be dedicated solely to the release of EH.


1995 ◽  
Vol 198 (6) ◽  
pp. 1307-1311
Author(s):  
J J Milde ◽  
R Ziegler ◽  
M Wallstein

A simple preparation designed to screen and compare the central action of putative neuroactive agents in the moth Manduca sexta is described. This approach combines microinjections into the central nervous system with myograms recorded from a pair of spontaneously active mesothoracic muscles. Pressure injection of either octopamine or Manduca adipokinetic hormone (M-AKH) into the mesothoracic neuropile increases the monitored motor activity. Under the conditions used, the excitatory effects of M-AKH exceed those of the potent neuromodulator octopamine. This suggests that M-AKH plays a role in the central nervous system in addition to its known metabolic functions and supports recent evidence that neuropeptides in insects can be multifunctional.


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