102 MARTIN G. LARRABEE AND PAUL HOROWICZ 



tivity? Perhaps a useless consequence of increased intracellular inorganic- 

 phosphate or phosphate acceptors? Or an inadvertent result of increased inter- 

 mingling of the ingredients of the hexokinase reaction, caused by transitory 

 changes in the structure of the cell membrane where this reaction is supposed 

 to take place? 



Such a waste of material, although not categorically refutable, is at least 

 teleologically unsatisfying. Moreover, there is evidence that the need for glu- 

 cose actually does increase during activity, since failure of function in the ab- 

 sence of this material occurred sooner the more rapidly repeated was the nerv- 

 ous action (see below). This acceleration of failure was much greater than can 

 be accounted for by accelerated depletion of endogenous substrate, at least on 

 the basis of the few relevant data presently available. Consequently glucose 

 seems to serve some need during activity, the nature of which is by no means 

 obvious at the present time. 



Effects of Glucose Lack 



Failure of function. It has previously been reported that conduction of im- 

 pulses along sympathetic nerve fibers and transmission through sympathetic 

 ganglia is lost in the absence of glucose (Kahlson and Macintosh, 1939; Larra- 

 bee and Bronk, 1952; Larrabee, Edwards and Ramos, 1951). For example, 

 each time glucose was withdrawn in the experiment illustrated in Fig. 11, 

 the response declined considerably after 10 min. and was almost gone after 20 

 minutes. Each restoration of glucose was followed by recovery, but this was 

 incomplete. Indeed, incomplete recovery, or almost none at all, was charac- 

 teristic of the effects of temporary removal of glucose. 



Rate of failure in the absence of glucose increased with the frequency of 

 stimulation. This is in agreement with the fact that activity causes an increase 

 in the normal rate of glucose uptake. With the ganglion kept at rest, or more 

 precisely with stimulation once every few minutes to test capacity for response, 

 failure was much slower than that illustrated: the postganglioic action poten- 

 tial of a rat ganglion then usually took 1}>2 to 2 hours to fall to half its initial 

 height (Fig. 12, upper graph). 



60 90 \ 100 110 120 T 130 140 150 160 1 170 180 190 T 200 210 



Fig. 11. Effects of glucose lack on the postganglionic response to stimulation of the 

 preganglionic nerve of a superior cervical ganglion from a rat. Records were taken at 

 10 minute intervals during continual supramaximal stimulation at a frequency of 6 

 per second. Glucose was alternately withdrawn and restored at times indicated by the 

 arrows. (Larrabee and Bronk, 1952). 



