Modulation of radula opener muscles in Aplysia.
We observed fibers immunoreactive (IR) to serotonin (5-HT), the myomodulins (MMs), and FMRFamide on the I7-I10 complex in the marine mollusk Aplysia californica. The I7-I10 muscle complex, which produces radula opening, is innervated primarily by one motor neuron, B48. B48 is MM-IR and synthesizes authentic MM(A). When B48 is stimulated in a physiological manner, cAMP levels are increased in opener muscles. cAMP increases also are seen when the MMs are applied to opener muscles but are not seen with application of the B48 primary neurotransmitter acetylcholine (ACh). Possible physiological sources of 5-HT and FMRFamide are discussed. When modulators are applied to resting opener muscles, changes in membrane potential are observed. Specifically, 5-HT, MM(B), and low concentrations of MM(A) all depolarize muscle fibers. This depolarization is generally not sufficient to elicit myogenic activity in the absence of neural activity under "rest" conditions. However, if opener muscles are stretched beyond rest length, stretch- and modulator-induced depolarizations can summate and elicit contractions. This only occurs, however, if "depolarizing" modulators are applied alone. Thus other modulators (i.e., FMRFamide and high concentrations of MM(A)) hyperpolarize opener muscle fibers and can prevent depolarizing modulators from eliciting myogenic activity. All modulators tested affected parameters of motor neuron-elicited contractions of opener muscles. MM(B) and 5-HT increased contraction size over the range of concentrations tested, whereas MM(A) potentiated contractions when it was applied at lower concentrations but decreased contraction size at higher concentrations. FMRFamide decreased contraction size at all concentrations and did not affect relaxation rate. Additionally, the MMs and 5-HT increased muscle relaxation rate, decreased contraction latency, and decreased the rate at which tension was developed during motor neuron-elicited muscle contractions. Thus these modulators dramatically affect the ability of opener muscles to follow activity in the opener motor neuron B48. The possible physiological significance of these findings is discussed.
Evans
C G
CG
Department of Physiology and Biophysics,Mt. Sinai Medical Center, New York City, New York 10032, USA.
Vilim
F S
FS
Harish
O
O
Kupfermann
I
I
Weiss
K R
KR
Cropper
E C
EC
D000818:Animals; D001048:Aplysia; D000242:Cyclic AMP / Q000378:metabolism; D004594:Electrophysiology; D019835:FMRFamide / Q000378:metabolism / Q000502:physiology; D008564:Membrane Potentials / Q000502:physiology; D009119:Muscle Contraction / Q000502:physiology; D009132:Muscles / Q000294:innervation / Q000378:metabolism / Q000502:physiology*; D009469:Neuromuscular Junction / Q000378:metabolism; D009474:Neurons / Q000502:physiology; D009479:Neuropeptides / Q000378:metabolism / Q000502:physiology; D012701:Serotonin / Q000378:metabolism / Q000502:physiology
D009479:Neuropeptides; C053302:myomodulin; D012701:Serotonin; D019835:FMRFamide; D000242:Cyclic AMP