186 N. CHALAZONITIS 



If we consider now the depolarization events during asphyxia already 

 described by many authors (Kolmodin and Skoglund, 1959; Lloyd, 1952- 

 1953; Van Harreveld, 1946), the CO2 accumulation on the membrane is 

 highly probable, not only during the second phase,* but even after the re- 

 duction of the DPN, because of the proton accumulation in the cytoplasm 

 owing to the anaerobic glycolysis products. 



4. EXCITATION-INHIBITION BY INJECTION OF CO2 



The CO2 action on such differentiated cells seems to be pertinent to 

 this general problem. There is first the common future: CO2 depolarizes, 

 with a negligible delay, all types of the examined nerve cells. A depolarization 

 of 5 mV is suflricient to elicit the autoactivity of the initially resting cells, or 



Fig. 20. Electron micrograph of glial junctions with the somatic membrane. 

 Independently of the well known "long-range" intimate connections between 

 glial cell and somatic membrane, one often observes a filamentous type of glial 

 terminals on the somatic membrane. These glial terminals — about 50 m/t in 

 diameter — are thus connected with the somatic membrane directly or sometimes 

 through small bulges of about 100 m/i of diameter (see (gl) on the membrane of 

 a small somatic portion (S2)). As the connective tissue of the visceral ganglion 

 normally exhibits contractility, a possible stretch of the non-synaptic portions of 

 the membrane by these glial filaments has to be considered as a probable physio- 

 logical stimulus for the somata. In the portion Si of the upper soma, lipochondria 

 ig) are observable. They are in intimate contact with small mitochondria (/»). 

 Nevertheless the majority of lipochondria are not necessarily in contact with 

 mitochondria. Particularly the smaller lipochondria lying deeply in the cytoplasm 

 near the nucleus are held by filamentous processes to the walls of small vacuoles. 



* As was previously noted, even after tne exhaustion of the oxygen DPN is available 

 for some time. This means that during this phase a further production of CO2 remains 

 possible by the simultaneous dehydrogenation-decarboxylation of the following: 6-phos- 

 phogluconate, pyruvate, a-ketoglutarate, D-isocitrate (see Chalazonitis, 1959). During the 

 same phase the deamination of glutamic acid may give a-ketoglutaric acid, its decarboxyl- 

 ation may give GABA, all those products such as CO2, ammonia, acids, GABA (Curtis 

 et ai, 1960; Florey and Florey, 1958; Florey and McLennan, 1955; Hayashi, 1959) being 

 highly important regulators of membrane excitability. 



