scholarly journals Inactivation of the Corpora Allata in the Final Instar of the Tobacco Hornworm,Manduca sexta, Requires Integrity of Certain Neural Pathways from the Brain

1989 ◽  
Vol 177 (3) ◽  
pp. 396-400 ◽  
Author(s):  
LOUIS SAFRANEK ◽  
CARROLL M. WILLIAMS

1974 ◽  
Vol 61 (2) ◽  
pp. 493-501 ◽  
Author(s):  
H. FREDERIK NIJHOUT ◽  
CARROLL M. WILLIAMS

During the final larval instar of the tobacco hornworm the presence of juvenile hormone (JH) inhibits the secretion of the brain's prothoracicotropic hormone (PTTH). The corpora allata cease to secrete JH when the larvae attain a weight of approximately 5 g. The JH is cleared from the haemolymph in about 24 h. This process in itself renders the brain competent to release PTTH. The actual release of PTTH occurs at the very first photo-periodic gate after the JH has disappeared from the haemolymph. A functional failure of this normal mechanism is apparently responsible for the developmental standstill of Lepidoptera which diapause as mature larvae.







1987 ◽  
Vol 128 (1) ◽  
pp. 175-192
Author(s):  
W. E. Bollenbacher ◽  
N. A. Granger ◽  
E. J. Katahira ◽  
M. A. O'Brien

A larval moult in the tobacco hornworm, Manduca sexta, involves an endocrine cascade that begins with the release of a cerebral peptide hormone, the prothoracicotropic hormone (PTTH). The release of PTTH is gated, occurs during the scotophase and appears to be developmentally cued. In fourth instar Manduca larvae, PTTH release into the haemolymph occurs as a single burst over a few hours during the head critical period, i.e. the time during which the head (brain) is needed for the initiation of the moult to the fifth (last) instar. Released PTTH activates the prothoracic glands (PGs), and within a few hours the cumulative effect of this event results in a dramatic increase in the haemolymph ecdysteroid titre, which then elicits the moult. An assessment of the capacity of the corpora allata (CA) to synthesize juvenile hormone (JH) in vitro indicates that the above sequence of endocrine events begins only when JH synthesis has reached a nadir for the instar. Since CA activity is an indirect measure of the haemolymph titre of the hormone, it is conceivable that the developmentally cued release of PTTH is permissively controlled by a decreasing haemolymph titre of JH. With the increase in the ecdysteroid titre which marks the end of this endocrine cascade, the CA again become active, presumably to cause the increase in the JH haemolymph titre which directs the larval moult. This investigation has thus established the temporal and quantitative dynamics of the PTTH-PG axis that drive larval moulting and provides insight into the interendocrine regulatory relationships that may exist between the ecdysteroids and JHs. These possible relationships and the role of the brain in their regulation are discussed.



1977 ◽  
Vol 70 (1) ◽  
pp. 27-39
Author(s):  
STUART E. REYNOLDS

The wings of pharate adult tobacco hornworm moths, Manduca sexta, are relatively inextensible until 3 or 4 h before emergence from the pupal case. At this time the wing cuticle becomes plasticized, so that by the time of eclosion, the wings are readily extensible. This change in the mechanical properties of the wing cuticle is shown to be under the control of a factor from the head. This factor is present in the corpora cardiaca/corpora allata complex, and in the protocerebrum of the brain, being released into the blood prior to eclosion. It is able to act directly on isolated wings. The active principle was found to be indistinguishable in a number of ways from the hormone which triggers emergence from the pupal case, the eclosion hormone. Partial purification of the eclosion hormone failed to separate activity causing eclosion from activity causing wing cuticle plasticization. It is concluded that the same hormone is probably responsible for both effects. The cuticle plasticizing activity of the eclosion hormone forms the basis for a new, highly sensitive bioassay. Another factor, distinct from the eclosion hormone, is able to cause wing cuticle plasticization. This factor is found in the abdominal nerve cord, and is only released into the blood after eclosion has occurred. It is probably identical with the tanning hormone, bursicon, which is released at this time. The factor in the nerve cord which causes cuticle plasticization is indistinguishable from bursicon in a number of ways, including partial purification by gel filtration. Bursicon evidently causes a further increase in wing cuticle extensibility after eclosion, at the time of wing inflation.



1985 ◽  
Vol 15 (5) ◽  
pp. 579-588 ◽  
Author(s):  
Wendell L. Combest ◽  
David Sheridan ◽  
Lawrence I. Gilbert




1983 ◽  
Vol 24 (12) ◽  
pp. 1586-1594
Author(s):  
F C Baker ◽  
B Mauchamp ◽  
L W Tsai ◽  
D A Schooley


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