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1. Rhesus monkeys were trained to exert steady biting forces of 3--60 N for 1--2 sec. This behaviour was well maintained while sinusoidal or step opening and closing movements were imposed on the jaw. 2. The amplitude of the force modulation during sinusoidal stretching was divided by the amplitude of movement to obtain the magnitude of stiffness. This estimate was made at frequencies from 2 to 50 Hz at amplitudes of 100 and 500 micrometer (half the peak-to-peak movement at the incisors). 3. Peak magnitudes of stiffness were seen with frequencies of 8--15 Hz when the amplitude of movement was small; there was a great deal of variation between individual animals. This variation was most striking with mean forces of 25--35 N. The stiffness was greatest in animals that showed considerable spontaneous tremor, and the highest levels of stiffness were often recorded with frequencies near which tremor amplitude was large. A marked phase lag in the force response was often seen during small amplitude stretching at 8--30 Hz. 4. Estimates of stiffness for larger amplitude (500 micrometer) stretching showed less variation; the magnitude of stiffness showed maximum values below 10 Hz and a minimum at 15--30 Hz. Force always showed a phase lead on position although this lead became small in the frequency range where with smaller movement there had been phase lags. The magnitude of stiffness increased with increasing mean force. 5. Bilateral electrolytic lesions were made in the brain stems of three animals; they reduced by over 95% the expected number of cells in the mesencephalic nucleus of the fifth cranial nerve on either side. These lesions interrupted the afferent pathway for the stretch reflex and so abolished excitatory electromyogram (e.m.g.) responses to step stretches of the jaw closing muscles. 6. Such reflex responses as persisted after the lesions were small and inhibitory. E.m.g. silences followed both step stretch and release; the response to release was a 'load compensation' that could not be attributed to spindle afferents. 7. After the lesions the responses to movements of 100 micrometer showed neither negative values for the phase nor marked peaks in the stiffness magnitude at low frequencies; these features therefore take origin in the action of the stretch reflex. The stiffness that was measured after the lesions may be attributed to the non-reflex components resisting stretch, particularly to the properties of the contracting muscles. Thus, the phase of the force response was markedly advanced at all frequencies and the stiffness seen for 100 micrometer was similar to that for 500 micrometer. Stiffness increased with increasing mean force, as before surgery. 8. Vector subtraction of the stiffness seen at each frequency after interrupting the stretch reflex from that seen before doing so gave a quantitative estimate of the strength of the stretch reflex. The reflex activity calculated in this way showed attenuation and progressive phase lag as the frequency increased above 10 Hz...