j62 



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY 



IT 



CX " B I C 



FIG. 14. Reversals of hyperpolarizing p.s.p.'s. Intracellular 

 recording from biceps-semitendinosus motoneuron of cat; hy- 

 perpolarizing p.s.p.'s evoked by stimulating quadriceps nerve. 

 I. A to G: The resting potential was —74 mv (Z)). Depolari- 

 zation augmented the p.s.p. (.4 to C). Hyperpolarization at 

 first diminished the p.s.p., the equilibrium potential for ionic 

 movements without electrogenesis being at —82 mv (£). Fur- 

 ther hyperpolarization reversed the sign of the p.s.p. (F, G). 

 The Cl~ content of the motoneuron was then increased and 

 K+ decreased (H to Z,). Immediately thereafter (J to Z.) the 

 p.s.p. was 'depolarizing' at all but the least negative values 

 '(//, /) of the membrane potential. M to Q: Recovery toward 

 initial condition not yet complete 3 to 4 min. later. II. Reversal 

 of the sign of the p.s.p. was produced by changing the ionic 

 gradient of Cl~. Initial response 0-1) was altered in B and C by 

 increeising intracellular Cl~ as a result of diffusion out of the 

 tip of the microelectrode. Depolarization of the membrane to 

 — 27 mv by an applied current restored the sign of the p.s.p. 

 (D). The Cl~ gradient was then changed drastically. The re- 

 versals of the p.s.p.'s produced soon thereafter (is to G) oc- 

 curred without significant change of the resting potential and 

 were sufficient to excite spikes, at first with brief latency (£), 

 then progressively later (F and G). Each record is formed by 

 superposition of many traces. In G it is seen that the depolari- 



The initial resting potential may then be altered little 

 or not at all, as is also the case with microinjections of 

 ions into squid giant axons (cf. 91, 105). The changed 

 chemical gradient of the motoneuron then causes a 

 reversal of hyperpolarizing p.s.p.'s into depolarization 

 which develops at, or near, the initial resting poten- 

 tial. The reversed 'inhibitory' p.s.p. now may elicit a 

 spike (fig. 14II). 



In crustacean muscle fibers (68, 73) and stretch 

 receptors (130) the equilibrium potential for the 

 inhibitory p.s.p. is nearly identical with the resting 

 potential. Stimulating the inhibitory axon therefore 

 may elicit no p.s.p., or the latter may be small, and 

 of either sign. Nevertheless, the membrane potential 

 tends to be clamped at or near the resting potential, 

 particularly if the activity of the inhibitory synaptic 

 membrane increases markedly the permittivity of 

 the membrane for the relevant ions (K+, Cl~ or 

 both). Excitatory depolarization, elicited at the 

 same time, by p.s.p.'s in muscle fibers or by mechano- 

 sensory dendrites in stretch receptors, therefore tends 

 to be depressed. When the inhibitory synapses of 

 lobster muscle fibers are maximally activated by 

 7-aminobutyric acid the membrane potential is 

 increased by about 4 mv, but the membrane con- 

 ductance is increased about 8-fold (Grundfest, 

 Reuben & Rickles, in preparation; cf. 99). 



d) LATENCY OF posTSYN.-^PTic POTENTIALS. As men- 

 tioned above, the onset of the explosive response of 

 electrically excitable membrane depends upon the 

 attainment of a critical level of depolarization. A 

 strong electrical stimulus, causing rapid depolariza- 

 tion to that level, therefore evokes a spike with vanish- 

 ingly brief latency (fig. 6), this fact having been 

 established by Bernstein in 1871 (19). In all cases 



zation occasionally fell below the critical firing level and con- 

 tinued to decrease in the later records (// to L). III. The 

 membrane generating hyperpolarizing p.s.p.'s maintains its 

 pharmacological individuality, although the electrical response 

 may be reversed and is then indistinguishable from that of a 

 depolarizing p.s.p. Prior to taking this scries of records the 

 hyperpolarizing p.s.p. evoked in the biceps-semitendinosus 

 motoneuron by stimulating quadriceps afTercnts was reversed 

 (by diflfusing Cl~ from the electrode into the cell). This response 

 is shown at the beginning of each record (/). Following it is a 

 depolarizing p.s.p. (£) evoked by stimulating afferents in the 

 biceps-semitendinosus nerve. Strychnine salicylate (o. i mg per 

 kg) was injected after record A and caused progressive diminu- 

 tion of 7, but no change in £ during the next 4 lo-sec. intervals 

 (fi to £). The reversed hyperpolarizing p.s.p. almost disap- 

 peared after a second injection (f ). [From Eccles (60).] 



