Overton demonstrated in 1902 (13) that sodium ions are necessary to maintain the excitability of the nerve fibers, since (a) the nerve fibers become inexcitable if the concentration of sodium ions in their external medium is decreased below a certain value (about 0.012 ~) and (b) the excitability of the nerve fibers can be restored by increasing the external concentration of sodium ions. In recent years the role of sodium in nerve function has been analyzed by and by Gallego (3) with frog nerve, and by Hodgkin and Katz (5) with invertebrate nerve fibers.Overton also demonstrated that lithium ions can substitute for sodium ions in so far as they can restore the excitability of nerve fibers that have become inexcitable in a sodium-free medium; the restoring action of lithium ions, however, is only temporary since the continued presence of lithium ions in the external medium again renders the nerve fibers inexcitable. The ability of lithium ions to substitute for sodium ions has been confirmed by Hodgkin and Katz who worked with the giant axon of the squid.In this paper an analysis is made of the effect of lithium ions upon frog nerve deprived of sodium. It has been found that lithium ions can restore the excitability of fibers of fast conduction (A fibers in Erlanger and Gasser's classification, cf. Erlanger, 1) as well as the excitability of fibers of slow conduction (C fibers in Erlanger and Gasser's classification). The effect of lithium ions upon sodium-deficient B fibers has not been investigated. On the other hand, it has been found that lithium ions cannot substitute for sodium ions in other aspects of nerve function, as should be expected from the observation made by Overton that prolonged action of lithium ions renders the nerve fibers inexcitable, and from the observation made by Gallego and Lorente de N6 (4) that lithium ions when present in the external medium of the nerve fibers at a high concentration cause a depolarization of the nerve fibers.According to Overton (13) ammonium ions are not able to restore the excitability of nerve deprived of sodium. Reexamination of this question seemed desirable, however, because Overton worked only with fibers of the A group (motor fibers) while Lorente de N6 (8) has shown that a number of quaternary ammonium ions, which are not able to restore the excitability of A fibers, 227
SIX FIGURESThe fact that at the 0.11 M concentration Rbt, NH+,, Cs+ and Lit ions depolarize the nerve fiber is well known (Hober and Strohe, '29 ; Lorente de N6, '47, section 1.5) but no information is available in the literature regarding 2 questions: (1) the effect of those ions at smaller concentrations and ( 2 ) the re-189
According to observations made by Overton (13) frog nerve deprived of sodium does not become inexcitable until after it has been kept in a sodium-free medium for several hours. This observation was confirmed by Lorente de N6 (6) who later presented the results of an analysis of the progressive changes in the properties of the nerve fibers which precede the development of inexcitability as well as of those changes which follow after the onset of total inexcitability (7-11, cf. also 4). In bullfrog sciatic nerve fibers of the A group do not begin to become inexcitable until after the nerve has been kept in the sodinmfree medium for 2 or 3 hours and the number of inexcitable fibers increases progressively with advancing time until after 8 or 10 hours of lack of sodium all the A fibers are inexcitable; at that time, however, there are many fibers of the B and C groups which are still able to conduct impulses; inexcitability of all the C fibers does not develop in less than 14 to 16 hours. The onset of inexcitability is preceded by progressive decreases in the speed of conduction and in the ability of the nerve fibers to conduct rhythmic trains of impulses. This paper describes certain aspects of the temporal courses of (a) the loss of excitability of the A fibers of frog nerve deprived of sodium and (b) the recovery of excitability after sodium ions are made available to the nerve. Observations were made with normal nerves and with nerves in various stages of degeneration after interruption of the continuity of the nerve fibers (Walleman degeneration). I TechniqueDuring the experiments recordings were made of the spike of the action potential of impulses that were initiated in an untreated segment of the nerve and that propagated themselves into a segment treated first with a sodium-free medium and then with Ringer's solution (approximately 0.1 M sodium chloride).Tmmediately after excision the nerves (peroneal with its two main branches dissected up to the level of the ankle) were mounted in humid chambers in a horizontal position, resting upon the electrodes of the stimulating and recording circuits, under slight tension so as to maintain their natural length. The impulses were always initiated near the central end of the nerve; the distance from the stimulating cathode 129
Gastrin secretion is induced by vagal stimuli, local distension, peptides or aminoacid solutions, and Ca2+ concentration both in stomach lumen and blood. However, the cellular and molecular mechanisms of gastrin-release are unknown. We have tested the effects of different pH fixative solutions on gastrin distribution by the immunolabeling of antral gastrin cells (G cells).Samples from different portions of adult dog digestive tract and related glands (salivary glands, liver and pancreas) were embedded in paraffin by conventional methods. Another samples from the antral mucosa of adult dogs and rats were fixed using mixtures of glutaraldehyde and paraformaldehyde at different pH (from 4 to 7,6 pH), and embedded in araldite and Unicryl. For post-embedding immnunocytochemical staining purposes, sections were incubated with pre - diluted policlonal rabbit anti-human gastrin (Zimed Labs.Inc., San Francisco, USA), rinsed in TBS and incubated with a 15 nm gold-conjugated IgG as secondary antibody. These sections were stained with uranil acetate and examined with TEM.
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