LONDON. Royal Society, Feb. 26. J. C. Eccles and Sir Charles Sherrington: Studies on the flexor reflex. (1) Latent period. A method for measuring the latent period of the flexor reflex is described. The values obtained for the central reflex time range from 2¢7 ¹r to 4¢35Ï and are in general agreement with the values calculated by Jolly and by Forbes and Gregg. The central reflex time is shortened when the stimulus applied to the afferent nerve is strengthened. The temporal dispersion of many reflex discharges is shown to be due, not to the discharge of more than one impulse from motoneurones, but to variations in the latent periods of the single responses of different motoneurones. The latent period of the response to a centripetal volley is greatly shortened if another volley precedes it by certain intervals. This shortening occurs at the expense of the central reflex time. It is concluded that all the time is saved in the reduction of the normal synaptic delay by facilitation. If that is so, the actual conduction time through the spinal cord must be less than O¢5Ï. On the assumption that the normal synaptic delay is due to time taken for a succession of excitatory impulses (owing to their temporal dispersion) to build up a c.e.s. of threshold intensity, all the observations are satisfactorily explained. The experiments support the conclusions that in the flexor reflex, centripetal impulses are not transmitted straight through the spinal cord, but at certain points (synapses) they are transformed into an enduring excitatory condition, c.e.s., which may in turn set up fresh nerve impulses the reflex discharge. (2) The reflex response evoked by two centripetal volleys. When the interval between two centripetal volleys is short, the reflex contraction evoked by the second volley is due largely to the discharge of motoneurones which fail to respond to either volley alone. The response of these motoneurones is due to summation of the subliminal excitatory effects of each volley. In addition to this facilitation at short intervals, a centripetal volley gives rise to a period of unresponsiveness of motoneurones. Three types of unresponsiveness have been met with: (a) Recovery complete in less than 16Ï. (b) Recovery complete in less than 50Ï. (c) Recovery not complete for more than 80Ï. From theoretical considerations, the duration of the relatively refractory period following an antidromic volley (10¢5Ï) is likely to be identical with the duration of the relatively refractory period of the reflex arc. J. C. Eccles: Studies on the flexor reflex. (3) The central effects produced by an antidromic volley. When a single stimulus is applied to an intact motor nerve, a volley of impulses (called an antidromic volley) passes into the spinal cord through the ventral roots. A single centripetal volley gives rise to c.e.s. during a considerable period. Persistence of the c.e.s. set up by such a volley is due partly to the temporal dispersion of the incident excitatory impulses and partly to the c.e.s. produced by any particular impulse itself enduring for some time. In any motoneurone an antidromic impulse removes preformed c.e.s. J. C. Eccles and Sir Charles Sherrington: (4) After - discharge. A period of quiescence follows an antidromic volley set up during the after-discharge of a reflex either by a single centripetal volley or by a repetitive series of centripetal volleys (confirming Denny-Brown). It is concluded that preformed c.e.s. of a motoneurone is removed by a reflex discharge, and has to be built up again by delayed excitatory impulses before another discharge can occur. J. C. Eccles and Sir Charles Sherrington: (5) General conclusions. A brief statement with discussion of various views of the nature of central excitation in reflex activity. A. V. Hill and J. L. Parkinson: Heat and osmotic change in muscular contraction without lactic acid formation. Frogs muscles poisoned with iodo-acetic acid, in which no lactic acid is formed, when stimulated to exhaustion in nitrogen gave total heat 0¢367 cal. per 1 gm. and showed a rise of osmotic pressure. This change of osmotic pressure cannot be explained in full without assuming either (a) that some chemical reaction, hitherto unrecognised, occurs in such poisoned muscles when stimulated, or (b) that phosphagen (and perhaps adenyl-pyrophosphoric acid) exist not as simple molecules in the resting muscle but in some combined form.