CARDIAC INHIBITION IN DECAPOD CRUSTACEA 177 



(Wiersma and Novitski, 1942; Maynard. 1953). It seems possible that the 

 excitabiHty increases during acceleration do not involve the same mechanisms 

 as the excitability increases during post-inhibitory rebound, for the latter 

 have not been correlated with depolarizing soma membrane potentials. 



Since the time course of facilitation is similar for both inhibitor and 

 accelerator postsynaptic potentials, and since they usually appear to have 

 opposite effects on neuron discharge, one might assume symmetrical and 

 opposite effects on the heart rate. As seen from Fig. 29, however, this is 

 not so. Several seconds are required for maximum acceleratory effects, and 

 adaptation, though presumably present (Wiersma and Novitski, 1942), 

 generally has a longer time course than inhibitory adaptation. Post-accelera- 

 tory inhibition is normally absent (Fig. 29 and Maynard, 1953). When both 

 inhibitor and accelerator are stimulated simultaneously in Homarus, the 

 time course of inhibition is almost indistinguishable from that observed 

 during stimulation of the inhibitor alone. Wiersma and Novitski (1942) 

 find prolonged post-inhibitory excitation when both accelerator and in- 

 hibitor are stimulated together, again indicating the asymmetrical charac- 

 teristics of inhibition and acceleration. 



SUMMARY 



Direct cardiac inhibition in the decapod Crustacea is mediated via a single 

 pair of inhibitor neurons which terminate upon the neurons of the cardiac 

 ganglion. As in many other systems, activity in the inhibitor elements results 

 in postsynaptic membrane changes and inhibitory postsynaptic potentials in 

 individual ganglion neurons. Depending upon the membrane potential of 

 the post unit, such i.p.s.p. may be hyper- or de-polarizing. When hyper- 

 polarizing, the facilitated i.p.s.p. leads to a suppression of spontaneous 

 discharges and a reduction in postsynaptic responses. It has been suggested, 

 however, that some ganglion neurons may be normally set at membrane 

 potentials which lead to depolarizing and consequently exciting (?) i.p.s.p. 

 Both facilitation and post-inhibitory rebound are prominent in the ganglion 

 neurons. 



The correlation between inhibition of the individual ganglion unit and 

 inhibition of the heartbeat which is the result of the integrated output of the 

 nine ganglion neurons is not always simple. Interactions between the ganglion 

 elements are superimposed on the generalized decrease in excitability caused 

 by inhibitor action, and as a result a single parameter such as heartbeat 

 frequency, duration of beat, or amplitude of beat does not necessarily reflect 

 the degree of inhibition of any individual unit. As an example, such pheno- 

 mena as adaptation to inhibition or post-inhibitory rebound present in the 

 individual ganglion neuron may be apparently absent in records of the 

 integrated heartbeat. 



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