are freshly dug rather than held in running seawater or in a refrigerator. 

 Sensitivity varies seasonally, highest in spring and low from late summer to 

 early winter. Atropine is extremely toxic to Venus heart. In low concen- 

 trations it makes beat irregular and frequently stops beat. When non-toxic 

 concentrations of atropine are used with or before ACh there is no consistent 

 antagonism of ACh inhibition. Adrenaline increases frequency of trie heart 

 beat and tonus slightly. In high concentrations it may stop heart in systole. 

 Nicotine acts much like ACh in reduction of amplitude and arrest in systole. 

 Histological preparations show nerve endings but no nerve cells in Venus 

 heart. ACh appears to leave the contracting mechanism intact and to act on 

 the pacemaker and conducting mechanisms of this myogenic heart. Stimulation 

 of visceral ganglion causes inhibition in diastole resembling the effect of 

 ACh. Fluid from a clam heart inhibited by visceral ganglion stimulation 

 often depresses beat of an eserinized test heart. Eserine prolongs 

 inhibition caused by ACh or by nerve stimulation. ACh probably is liberated 

 as the normal cardiac inhibitory agent in Venus. - J.L.M. 



1509 



Prosser, C. Ladd. 1942. 



An analysis of the action of acetylcholine on hearts, particularly in 

 arthropods. Biol. Bull. 83(2): 145-164. 



Hearts of higher arthropods and some annelids and tunicates which are 

 accelerated by acetylcholine (ACh) are neurogenic. Hearts of adult 

 vertebrates, mollusks, and probably Daphnia, which are inhibited by ACh, 

 are myogenic but innervated. Embryonic hearts of vertebrates, Limulus , 

 and hearts of Artemia and Eubranehipus are unaffected by ACh and are 

 probably non-innervated. Meraenaria (Venus) meraenaria is not mentioned. 

 - M.W.S. and J.L.M. 



1510 



Prosser, C. Ladd, and Hazel B. Prosser. 1937. 



The action of acetylcholine and of inhibitory nerves upon the heart of Venus. 

 Anat. Rec. 70(1), suppl. 1: 112. 



The heart of Venus is extremely sensitive to acetylcholine (ACh) . Sensitivity 

 is greater early in summer than later. Threshold concentration in June is 1 in 

 lO 12 ^ in Sept 1 in 10 9 . Action of ACh is mainly negatively intropic but rate 

 of beat also slows slightly. Eserine increases sensitivity to ACh. Ventricles 

 inhibited by ACh contract in response to mechanical stimulation, and conduction 

 is not stopped. There is no localized pacemaker, the beat can start at any 

 point on the surface of the ventricle. Stimulation of visceral ganglion 

 inhibits heart as much as does ACh, but a much more marked fall in tonus is set 

 up by nervous inhibition than by ACh. Reflex inhibition can be caused by 

 stimulation of mantle and other regions. This natural inhibition is not 

 increased nor is its threshold lowered by application of eserine or ACh to 

 heart. But transfer of sea water from heart and pericardium of an inhibited 

 preparation to a normally beating heart inhibits beat of the second heart. 

 It is concluded that normal inhibition of clam heart is mediated by a substance 

 similar to but not identical with ACh. - J.L.M. 



1511 



Prosser, C. L., R. A. Nystrom,and T. Nagai. 1965. 



Electrical and mechanical activity in intestinal muscles of several 

 invertebrate animals. Comp. Biochem. Physiol. 14: 53-70. 



Sections of the hindgut of Meroenaria (Venus) meraenaria showed phasic (fast) 

 contractions (0.25-2 sec contraction time) and tonic (slow) contractions (3-15 

 sec for contraction, 10-45 sec for half-relaxation) . Strength-duration curves 

 of the 2 responses intersect, so that brief pulses elicit phasic contractions, 

 long pulses elicit tonic contractions. Similar experiments with other animals 

 led to the conclusion that conduction in echinoderm intestine may be from 

 muscle fiber to muscle fiber, as in vertebrate visceral smooth muscle, while 

 conduction in molluscan and crustacean intestines appears to be by nerves. 

 Intestinal muscle of bivalve mollusks has multiple innervation. - from authors' 

 summary - J.L.M. 



422 



