The effects of electrical stimulation in the hypothalamus on the monosynaptic jaw closing and the disynaptic jaw opening reflexes were investigated in cats anaesthetized with chloralose. The hypothalamic electrodes were located by observation of behavioural attack responses in the unanaesthetized animal and by means of Horsley-Clarke coordinates. The locations were verified in histological serial sections. Hypothalamic conditioning with trains of 3--10 pulses, 0.5 ms duration, 0.5 mA, 500 Hz, evoked a strong facilitation of the jaw closing reflex and a facilitation followed by an inhibition of the jaw opening reflex. These effects differed from those elicited from the cerebral cortex. The hypothalamic effects had a longer latency (11--13 ms) and required a longer train of conditioning stimuli than was the case with those evoked from the cortex. Bilateral ablation of the sensorimotor cerebral cortex or lesion of the pyramids at the lower pontine level diminished but did not abolish the hypothalamic effects. They did, however, disappear after lesions including the ventral midbrain tegmentum. The stimulus positions eliciting the largest hypothalamic effects on the jaw reflexes were located in a region extending medio-laterally from the perifornical area to the entrance of the ansa lenticularis in the lateral hypothalamus. Rostro-caudally the location was found at the level of the ventromedial hypothalamic nucleus and the anterior hypothalamus just rostral to this nucleus. The region corresponds to those parts of the hypothalamus from which agonistic and feeding responses have been evoked. It is suggested that the observed hypothalamotrigeminal mechanism may exercise a tonic influence on the trigeminal motoneurones, thereby controlling the set point of the biting force. The implications of this hypothesis on the etiology of bruxism and the myofascial pain dysfunction are discussed.