THE ROLE OF CYCLIC-AMP IN THE OCTOPAMINERGIC MODULATION OF FLIGHT-MUSCLE IN THE LOCUST

被引:0
作者
WHIM, MD [1 ]
EVANS, PD [1 ]
机构
[1] UNIV CAMBRIDGE,AFRC,DEPT ZOOL,MOLEC SIGNALLING LAB,CAMBRIDGE CB2 3EJ,ENGLAND
关键词
OCTOPAMINE; CYCLIC AMP; FLIGHT MUSCLE; LOCUST; INSECT; SCHISTOCERCA-GREGARIA;
D O I
暂无
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The role of cyclic AMP in the octopaminergic modulation of the dorsal longitudinal flight muscles of the locust Schistocerca gregaria has been investigated. Several techniques have been used to elevate cyclic AMP levels in this tissue by mechanisms that bypass the receptor activation stage. These include the use of phosphodiesterase inhibitors to block the metabolism of cyclic nucleotides, the use of forskolin, the diterpene activator of adenylate cyclase, and the direct application of permeable and phosphodiesterase-resistant analogues of cyclic AMP. All these approaches can be shown to mimic the modulatory effects of octopamine on the flight muscle. Surprisingly, the phosphodiesterase inhibitors used were not able to potentiate the actions of octopamine on this preparation. Octopamine increases cyclic AMP levels in a similar fashion in all five motor units of this muscle, an effect that is selectively blocked by phentolamine, an alpha-adrenergic blocking agent that blocks octopamine receptors in other preparations. In addition, stimulation of the dorsal unpaired median neurone to the dorsal longitudinal flight muscles (DUMDL) results in a frequency-dependent increase in cyclic AMP levels in the muscle that is also blocked by phentolamine. The data presented suggest that the octopamine-mediated modulation of neurally evoked tension in this muscle is brought about by a mechanism that involves an increase in cyclic AMP levels in the tissue.
引用
收藏
页码:423 / 438
页数:16
相关论文
共 36 条
[1]  
ARAKAWA S, 1990, NEURON, V2, P343
[2]   REDUCTION OF VOLTAGE-ACTIVATED K+-CURRENTS BY FORSKOLIN IS NOT MEDIATED VIA CAMP IN PLEURAL SENSORY NEURONS OF APLYSIA [J].
BAXTER, DA ;
BYRNE, JH .
JOURNAL OF NEUROPHYSIOLOGY, 1990, 64 (05) :1474-1483
[3]  
Beam K G, 1976, Cold Spring Harb Symp Quant Biol, V40, P157
[4]  
BROWN BL, 1972, ADV CYCL NUCL RES<D>, V2, P25
[5]  
BUCHAN PB, 1980, J EXP BIOL, V85, P349
[6]  
DALY JW, 1984, ADV CYCLIC NUCL PROT, V17, P81
[7]  
EVANS PD, 1984, J EXP BIOL, V110, P231
[8]  
EVANS PD, 1987, J EXP BIOL, V129, P239
[9]  
EVANS PD, 1981, J PHYSIOL-LONDON, V318, P99
[10]  
EVANS PD, 1986, J EXP BIOL, V124, P143