Involvement of cyclic GMP in the release of stereotyped behaviour patterns in moths by a peptide hormone

1980 ◽  
Vol 84 (1) ◽  
pp. 201-212
Author(s):  
J. W. Truman ◽  
S. M. Mumby ◽  
S. K. Welch
Keyword(s):  
Nervous System ◽  
Cyclic Nucleotides ◽  
Phosphodiesterase Inhibitor ◽  
Peptide Hormone ◽  
Behavioural Responses ◽  
Eclosion Hormone ◽  
Behavioural Effects ◽  
Hormone Injection ◽  
Behavioural Patterns ◽  
Characteristic Motor

A peptide hormone, the eclosion hormone, triggers two behavioural patterns--the pre-eclosion and eclosion patterns--when injected into pharate silkmoths. Injection of cyclic nucleotides caused the same behavioural responses with cGMP being 10 to 100 times more potent than cAMP. Exogenous cGMP also acted directly on the isolated nervous system to evoke the characteristic motor programmes. Protection of endogenous cyclic nucleotides by pretreatment of moths with a phosphodiesterase inhibitor, theophylline, markedly enhanced the sensitivity of the moths to the hormone. Injection of partially purified hormone preparations was followed by an increase in nervous system cGMP but not cAMP. The increase preceded the behavioural effectiveness of each dose was correlated with its ability to cause a cGMP increase. It was concluded that the behavioural effects of the eclosion hormone are mediated through an increase in cGMP in the nervous system.

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.

Coupling of Environmental and Endogenous Factors in the Control of Rhythmic Behaviour in Decapod Crustaceans

1997 ◽  
Vol 77 (1) ◽  
pp. 17-29 ◽  
Author(s):  
Hugo Aréchiga ◽  
Leonardo Rodríguez-Sosa
Keyword(s):  
Higher Order ◽  
Circadian Rhythmicity ◽  
Decapod Crustaceans ◽  
Endogenous Factors ◽  
Environmental Signals ◽  
Motor Responses ◽  
Behavioural Responses ◽  
Retinal Photoreceptors ◽  
Behavioural Patterns ◽  
Chemical Stimuli

Behavioural patterns of crustaceans are known to vary within the 24 hour cycle and in relation to environmental signals. Light and chemical stimuli induce specific behavioural responses. Retinal and extra-retinal photoreceptors use different motor responses to illumination selectively. Light responsiveness is modulated at various levels, from the light admittance to the retina, up to the integration in higher order interneurones and motorneurones. An endogenous circadian rhythmicity contributes to the various elements of the system.

scholarly journals The Heat Shock Protein 26 Gene is Required for Ethanol Tolerance in Drosophila

2011 ◽  
Vol 5 ◽  
pp. JEN.S6280 ◽  
Author(s):  
Awoyemi A. Awofala ◽  
Susan Jones ◽  
Jane A. Davies
Keyword(s):  
Nervous System ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Ethanol Tolerance ◽  
Stress Proteins ◽  
Ethanol Exposure ◽  
P Element ◽  
Behavioural Responses ◽  
Percentage Difference

Stress plays an important role in drug- and addiction-related behaviours. However, the mechanisms underlying these behavioural responses are still poorly understood. In the light of recent reports that show consistent regulation of many genes encoding stress proteins including heat shock proteins following ethanol exposure in Drosophila, it was hypothesised that transition to alcohol dependence may involve the dysregulation of the circuits that mediate behavioural responses to stressors. Thus, behavioural genetic methodologies were used to investigate the role of the Drosophila hsp26 gene, a small heat shock protein coding gene which is induced in response to various stresses, in the development of rapid tolerance to ethanol sedation. Rapid tolerance was quantified as the percentage difference in the mean sedation times between the second and first ethanol exposure. Two independently isolated P-element mutations near the hsp26 gene eliminated the capacity for tolerance. In addition, RNAi-mediated functional knockdown of hsp26 expression in the glial cells and the whole nervous system also caused a defect in tolerance development. The rapid tolerance phenotype of the hsp26 mutants was rescued by the expression of the wild-type hsp26 gene in the nervous system. None of these manipulations of the hsp26 gene caused changes in the rate of ethanol absorption. Hsp26 genes are evolutionary conserved, thus the role of hsp26 in ethanol tolerance may present a new direction for research into alcohol dependency.

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