Excitatory and inhibitory roles of central ganglia in initiation of the insect ecdysis behavioural sequence

2000 ◽  
Vol 203 (8) ◽  
pp. 1329-1340 ◽  
Author(s):  
D. Zitnan ◽  
M.E. Adams
Keyword(s):  
Neural Network ◽  
Central Nervous System ◽  
Nervous System ◽  
Manduca Sexta ◽  
Abdominal Ganglion ◽  
Suboesophageal Ganglion ◽  
Eclosion Hormone ◽  
The Central Nervous System ◽  
Inka Cells ◽  
Behavioural Sequence

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.

Dual ecdysteroid action on the epitracheal glands and central nervous system preceding ecdysis of Manduca sexta

2001 ◽  
Vol 204 (20) ◽  
pp. 3483-3495 ◽  
Author(s):  
Inka Žitňanová ◽  
Michael E. Adams ◽  
Dušan Žitňan
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Manduca Sexta ◽  
Transcriptional Activity ◽  
Subsequent Treatment ◽  
Dual Action ◽  
The Central Nervous System ◽  
Inka Cells ◽  
Ecdysis Triggering Hormone ◽  
Behavioural Sequence

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.

The Larval Eclosion Hormone Neurones in Manduca Sexta: Identification of the Brain-Proctodeal Neurosecretory System

1989 ◽  
Vol 147 (1) ◽  
pp. 457-470 ◽  
Author(s):  
JAMES W. TRUMAN ◽  
PHILIP F. COPENHAVER
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Manduca Sexta ◽  
Nerve Cord ◽  
Release Site ◽  
Neurosecretory System ◽  
Nerve Activity ◽  
Eclosion Hormone ◽  
The Central Nervous System ◽  
The Brain

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.

scholarly journals The initiation of pre-ecdysis and ecdysis behaviors in larval Manduca sexta: the roles of the brain, terminal ganglion and eclosion hormone.

1996 ◽  
Vol 199 (8) ◽  
pp. 1757-1769 ◽  
Author(s):  
A Novicki ◽  
J C Weeks
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Manduca Sexta ◽  
Brain Neurons ◽  
Eclosion Hormone ◽  
Terminal Ganglion ◽  
The Central Nervous System ◽  
Time Required ◽  
The Brain ◽  
Larval Molt

Each larval molt of Manduca sexta culminates in the sequential performance of pre-ecdysis (cuticle loosening) and ecdysis (cuticle shedding) behaviors. Both behaviors are thought to be triggered by the release of a peptide, eclosion hormone (EH), from brain neurons whose axons extend the length of the nervous system. EH bioactivity appears in the hemolymph at the onset of pre-ecdysis behavior, and EH injection can trigger pre-ecdysis and ecdysis behaviors prematurely. The present study examined the effects of removing or disconnecting portions of the central nervous system prior to the time of EH release on the initiation of pre-ecdysis and ecdysis behaviors at the final larval molt. We found that the initiation of pre-ecdysis abdominal compressions at the appropriate time required the terminal abdominal ganglion (AT) but not the brain; the initiation of pre-ecdysis proleg retractions at the appropriate time required neither the AT nor the brain; the initiation of ecdysis at the appropriate time usually required the brain but did not require the AT; and premature pre-ecdysis (but not ecdysis) could be elicited in isolated abdomens by injection of EH. Finally, pre-ecdysis behavior performed by brainless larvae was not associated with the normal elevation of EH bioactivity in the hemolymph or the normal loss of EH immunoreactivity from peripheral neurohemal release sites.

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
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Manduca Sexta ◽  
Secretory Granules ◽  
Endocrine Regulation ◽  
Transient Loss ◽  
The Central Nervous System ◽  
Inka Cells ◽  
Enhancer Trap Lines ◽  
Ecdysis Triggering Hormone

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.

The development of central nervous system control of the gill withdrawal reflex evoked by siphon stimulation in Aplysia

1979 ◽  
Vol 57 (9) ◽  
pp. 987-997 ◽  
Author(s):  
Ken Lukowiak
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Abdominal Ganglion ◽  
System Control ◽  
Reflex Amplitude ◽  
Withdrawal Reflex ◽  
Reflex Latency ◽  
Neural Processes ◽  
The Central Nervous System ◽  
Cns Control

In older Aplysia, the central nervous system (CNS) (abdominal ganglion) exerts suppressive and facilitatory control over the peripheral nervous system (PNS) which initially mediates the gill withdrawal reflex and its subsequent habituation evoked by tactile stimulation of the siphon. In young animals, both the suppressive and facilitatory CNS control were found to be absent. In older animals, removal of branchial nerve (Br) input to the gill resulted in a significantly reduced reflex latency and, with ctenidial (Ct) and siphon (Sn) nerves intact, a significantly increased reflex amplitude and an inability of the reflex to habituate with repeated siphon stimulation. In young animals, removal of Br had no effect on reflex latency and with Ct and Sn intact, the reflex amplitude latency was not increased and the reflex habituated. Older animals can easily discriminate between different intensity stimuli applied to the siphon as evidenced by differences in reflex amplitude, rates of habituation, and evoked neural activity. On the other hand, young animals cannot discriminate well between different stimulus intensities. The lack of CNS control in young animals was found to be due to incompletely developed neural processes within the abdominal ganglion and not the PNS. The lack of CNS control in young Aplysia results in gill reflex behaviours being less adaptive in light of changing stimulus conditions, but may be of positive survival value in that the young will not habituate as easily. The fact that CNS control is present in older animals strengthens the idea that in any analysis of the underlying neural mechanisms of habituation the entire integrated CNS–PNS must be taken into account.

Adipokinetic hormone stimulates neurones in the insect central nervous system.

1995 ◽  
Vol 198 (6) ◽  
pp. 1307-1311
Author(s):  
J J Milde ◽  
R Ziegler ◽  
M Wallstein
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Manduca Sexta ◽  
Central Action ◽  
Adipokinetic Hormone ◽  
Metabolic Functions ◽  
Simple Preparation ◽  
Pressure Injection ◽  
The Central Nervous System ◽  
Insect Central Nervous System

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.

scholarly journals Drosophila Zic family member odd-paired is needed for adult post-ecdysis maturation

Open Biology ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 190245
Author(s):  
Eléanor Simon ◽  
Sergio Fernández de la Puebla ◽  
Isabel Guerrero
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Transcription Factor ◽  
Drosophila Melanogaster ◽  
Family Member ◽  
Ectopic Expression ◽  
Functional Conservation ◽  
The Central Nervous System ◽  
Behavioural Sequence

Specific neuropeptides regulate in arthropods the shedding of the old cuticle (ecdysis) followed by maturation of the new cuticle. In Drosophila melanogaster , the last ecdysis occurs at eclosion from the pupal case, with a post-eclosion behavioural sequence that leads to wing extension, cuticle stretching and tanning. These events are highly stereotyped and are controlled by a subset of crustacean cardioactive peptide (CCAP) neurons through the expression of the neuropeptide Bursicon (Burs). We have studied the role of the transcription factor Odd-paired (Opa) during the post-eclosion period. We report that opa is expressed in the CCAP neurons of the central nervous system during various steps of the ecdysis process and in peripheral CCAP neurons innerving the larval muscles involved in adult ecdysis. We show that its downregulation alters Burs expression in the CCAP neurons. Ectopic expression of Opa, or the vertebrate homologue Zic2 , in the CCAP neurons also affects Burs expression, indicating an evolutionary functional conservation. Finally, our results show that, independently of its role in Burs regulation, Opa prevents death of CCAP neurons during larval development.

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