SUMMARY1. Stimulation of Group I muscle afferents in contralateral forelimb nerves evoked a response in nucleus ventralis posterolateralis (VPL) in the thalamus of the cat. This response was located in the rostral twothirds of VPL in a narrow zone near the dorsomedial border of the nucleus.2. Group I afferents in nerves from more than one of the muscles in the contralateral forelimb often excited the same thalamic relay cell. In addition these cells were often discharged by skin afferents from the contralateral forelimb. They were not affected by electrical stimulation of the dorsal column-lemniscal or the spino-cervico-lemniscal paths from the contralateral hind limb.3. In experiments with peripheral conduction paths of similar length, the latency of the thalamic focal potential evoked by stimulation of Group I muscle afferents in the nerve to m. extensor carpi radialis was 3x8 S.E. + 0-1 msec, and that of the focal potential evoked by skin afferents (n. radialis superficialis) in the centromedial part ofVPL was 4x3 + 0.1 msec. 4. The majority of the thalamic neurones discharged by Group I muscle afferents responded with a latency shorter than 1 msec to electrical stimulation of the cerebral cortex in the region of the post-cruciate dimple. A considerable number of the thalamic Group I relay cells were also discharged with a similar short latency from another cortical focus located on either side of the anterior suprasylvian sulcus near the S II hind limb areas. These responses were considered to be antidromic in nature, and the findings were interpreted as indicating two separate cortical projection areas for the Group I path. The second projection area was assumed to be located in the cortical fold formed by the anterior suprasylvian sulcus.5. Cortical stimulation also excited the thalamic Group I relay cells trans-synaptically. Trans-synaptic excitation with short (1-2 msec) and * Present address: University of Michigan, Ann Arbor, U.S.A. CENTRAL PROJECTIONS OF MUSCLE AFFERENTS 577 longer (2-7 msec) latency was observed. The cortical focus near the S II area was particularly potent in evoking trans-synaptic excitation in the thalamic region where the Group I relays were located.
SUMMARY1. Cats anaesthetized with chloralose and paralysed with Flaxedil were used. The projections of muscle, joint and skin afferents to the cortical fold hidden in the anterior suprasylvian sulcus were investigated with micro-electrode recording techniques.2. Electrical stimulation of Group I muscle afferents from the contralateral forelimb evoked a negative focal potential (latency 5 msec) in a locus of 1-2 mm diameter found in the lower bank of the fold. In one experiment a response to Group I muscle afferents from the contralateral hind limb was observed. The Group I potentials disappeared after sectioning of the dorsal columns at C3.3. Groups II and III muscle afferents, low threshold skin afferents and joint afferents also evoked potentials in the Group I locus. It was concluded that the joint afferents originated mainly in the Ruffini endings of the joint capsule.4. Groups II and III muscle afferents, low threshold skin and low threshold joint afferents projected to the upper bank of the suprasylvian fold. A certain somatotopic arrangement was observed.5. The possibility of connexions between the cortex of the anterior suprasylvianfold andthe primary somato-sensory projection areas was discussed, as well as the organization ofthe loci in the fold in terms of cell colonies with different properties.
Corti, in 18 51, 1 described the cells of the stria vascularis and sug gested that they might be the structure for secreting endolymph. Also in 1851 Reissner 2 described the membrane which now bears his name and divides the scala vestibuli from the scala media, showing anatomically that the membranous labyrinth is a closed system. Fol lowing this observation there has been much speculation concerning the characteristics of the endolymphatic and perilymphatic fluids. In 1927 Stacy Guild 3 performed an experiment which he felt fur nished sufficient evidence to indicate the nature of fluid flow within the scala media.Through a small pipette Guild injected a solution of potassium ferrocyanide and iron ammonium citrate into the scala media of sev eral living guinea pigs. After the lapse of various time intervals, the animals were sacrificed and the acid in the fixation fluid precipitated prussian blue granules in sites along the scala media. The temporal bones of these animals were then sectioned and mounted serially so that the location of the granules could be studied with the micro scope. In 16 of 20 animals the blue granules were found in the walls of the endolymphatic sac. From this he concluded that the flow of endolymph was from the stria vascularis down the scala media through the canalis reuniens to the saccule ending finally in the endolymphatic
SUMMARY1. Cats anaesthetized with chloralose were used. Potentials evoked by electrical stimulation of the vestibular, cochlear, facial, trigeminal and chorda tympani nerves were recorded with micro-electrodes in the cortex in the anterior syprasylvian sulcus.2. Negative focal potentials with a latency of 3 msec were evoked by stimulation of the contralateral and ipsilateral vestibular nerves. These potentials were located in the lower and upper banks of the sulcus at a level just caudal to the projection of the Group I muscle afferents to the lower bank.3. The cochlear projections were located mainly in the lower bank partially overlapping the vestibular and the Group I fields.4. Trigeminal responses were recorded in both banks of the sulcus but were of largest amplitude and shortest latency rostrally in the upper bank. The potentials evoked by the chorda tympani had a similar distribution but were of low amplitude.5. The hypothesis is suggested, that the cortex in the anterior suprasylvian sulcus plays a role in the orientation of the body and head towards auditory stimuli.
The most widely accepted theory for the explanation of the audi tory effects of Meniere's disease, namely, that the loss of hearing is due to an endolymphatic cochlear hypertension, is a plausible one, but experimental evidence that an increase in pressure in the inner ear can cause a hearing loss has been lacking.Indeed, experiments to date have pointed in the opposite direc tion, but a careful examination of these experimental efforts reveals that they may not have eliminated the possibility of endolymphatic hypertension producing a deafness.To Williams, 1 Békésy's 2 experiments cast doubt on the theory that increased pressure of perilymph and endolymph could produce loss of hearing. Békésy, however, in the experiment cited, demon strated only that by increasing intracochlear pressure, neither the stapedial footplate nor the round window membrane was fixed from within and that hearing loss could not accrue from this. Békésy did not rule out the possibility of hearing loss by interference with or inefficiency of basilar membrane vibration, or of compression of the organ of Corti which might interfere with torsion or bending of the hair cells. Lempert and his co-workers 3 raised the pressure of perilymph in the lateral semicircular canal and found no decrease in
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