MYOMODULIN APPLICATION INCREASES CAMP AND ACTIVATES CAMP-DEPENDENT PROTEIN-KINASE IN THE ACCESSORY RADUAL CLOSER MUSCLE OF APLYSIA

被引：16

作者：

HOOPER, SL

PROBST, WC

CROPPER, EC

KUPFERMANN, I

WEISS, KR

机构：

[1] CUNY MT SINAI SCH MED,DEPT PHYSIOL & BIOPHYS,NEW YORK,NY 10022

[2] COLUMBIA UNIV,COLL PHYS & SURG,CTR NEUROBIOL & BEHAV,NEW YORK,NY 10032

[3] NEW YORK STATE PSYCHIAT INST & HOSP,NEW YORK,NY 10032

来源：

NEUROSCIENCE LETTERS | 1994年 / 179卷 / 1-2期

关键词：

NEUROMODULATION; PEPTIDE; 2ND-MESSENGER; INVERTEBRATE; CAMP; BUCCALIN; BUCCAL; CAPK; PKA; MOLLUSK;

D O I：

10.1016/0304-3940(94)90960-1

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Myomodulin A (MM(A)) application or stimulation of neuron B16, which releases MM(A), increases cAMP levels in the accessory radula closer (ARC) muscle of Aplysia. MM(A) application also increases cAMP-dependent protein kinase (cAPK) activity in one subcellular compartment of the muscle. These results suggest that at least part of MM(A)'s effects in this system are mediated via the cAPK signal transduction pathway. Since the effects of the small cardioactive peptides (SCPs) on ARC muscle contraction are similar to those of MM(A), our results suggest that the convergent physiological effects of MM(A) and SCPB in this system may be due, in part, to the two peptide neuromodulators utilizing the same signal transduction pathway.

引用

页码：167 / 170

页数：4