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Myosuppressin’s effect on the stretch-sensitive dendrite feedback system in the crustacean cardiac
neuromuscular system
Catherine Liu, 2019
The generation of rhythmic movements, like breathing and chewing, is one important function of the
brain. The brain needs to be able to not only generate these specific motor patterns, but also modify the pattern to
adapt to changes in the environment. To further investigate how this mechanism works, I used the crustacean
cardiac neuromuscular system, because this model is well understood and is one of the simplest central pattern
generator (CPG)-effector systems known (Cooke, 2002). Rhythmic movements in this model are controlled by the
cardiac ganglion (CG), which is composed of a network of nine neurons. The contractions of the crustacean heart
depend directly on the cycle frequency of bursting in the motor neurons of the CG. In addition, the CG receives
input from feedback systems and neuromodulators.
Many studies have found evidence for a stretch-mediated feedback pathway from the cardiac muscle cells
to the CG in several species, including the crab Callinectes sapidus, the isopod Idotea pallasii, and the lobster
Homarus americanus. This feedback pathway operates through stretch-sensitive dendrites, which are attached to
the cardiac muscle, and can detect stretching and modify the motor output of the CG accordingly. However, the
manner in which these stretch-sensitive dendrites modify motor output is complex and not well understood. Even
in such a simple system, this stretch-sensitive mechanism can interact with multiple different feedback systems
and neuromodulators.
The crustacean heart is modulated by many peptides and amines known as neuromodulators.
Myosuppressin is one such neuromodulator that has been found to regulate the CG of the lobster. When
myosuppressin is perfused into the CG, it increases the amplitude of contractions of the lobster heart (Stevens et
al., 2009). This increase of contraction amplitude should activate the stretch-sensitive dendrite feedback loop and
lead to an increase of frequency output in the CG, as mentioned earlier. However, frequency of contraction has
been found to decrease when myosuppressin is added, which is the opposite effect of what is predicted (Stevens et
al., 2009). These results suggest that myosuppressin may overcome the mechanism that increases cycle frequency
in the CG, perhaps by de-emphasizing the effect of this stretch feedback pathway. The manner in which
myosuppressin modulation works in conjunction with other feedback systems to modulate the CG had been
previously unstudied. This study aimed to explore the effect of myosuppressin on the stretch-sensitive feedback
loop, in hopes to better understand how these two functions work together in the CG to regulate adaptive motor
outputs.
American lobsters, H. americanus, were used in this experiment. After anesthetizing the lobster, the heart
was removed and the cardiac ganglion with some muscle attached was isolated. With small hooks, a force
transducer was attached to one side of the muscle to measure the amount of stretch, and a motor was attached to
the other side to perform stretch in a controlled, precise manner. An electrode was placed at the end of the neuron
to record the action potential of that motor neuron. This enabled me to measure the frequency, duration, and
amplitude of CG output. I performed stretches in control saline as well as in saline containing myosuppressin to
investigate the effects of myosuppressin on the stretch feedback loop.
After analyzing my data, I found that myosuppressin has a negative effect on the stretch-sensitive dendrite
feedback system. When the cardiac muscle of the lobster heart is stretched in the presence of myosuppressin,
there is a smaller decrease in both cycle period as well as burst duration. Also, myosuppressin causes the stretchfeedback system to react less to an increase in stretch force. When myosuppressin is added, there is a smaller
decrease in both burst duration and cycle period as force increases. These results suggest that myosuppressin does
modulate the stretch-sensitive dendrite feedback system by reducing the reaction to stretch. For future studies, it
would be interesting to look at how myosuppressin works through taking intracellular recordings, or perhaps look
at other modulators, such as nitric oxide, and their effect on the stretch feedback system.
Faculty Mentor: Patsy Dickinson
Funded by the Doherty Coastal Studies Fellowship
References:
Stevens, J.S., Cashman, C.R., Smith, C.M., Beale, K.M., Towle, D.W., Christie, A.E.,
Dickinson, P.S. 2009. The peptide hormone pQDLDHVFLRFamide (crustacean
myosuppressin) modulates the Homarus americanus cardiac neuromuscular
system at multiple sites. The Journal of Experimental Biology. 212: 3961-3976.
Cooke, I.M. 2002. Reliable, responsive, pacemaking and pattern generation with minimal
cell numbers: the crustacean cardiac ganglion. Biology Bulletin. 202: 108-136.