Effects of orbital cortical stimulation on facial motoneurons in the cat

EXPERIMENTAL

66, 343-355 (1979)

NEUROLOGY

Effects

of Orbital Cortical Motoneurons

JOSE L. WESSOLOSSKY, Department

ofAnatomy

NOBORU

Stimulation in the Cat

MIZUNO,

AND CARMINE

on Facial

D. CLEMENTE’

and the Brain Research Institute. School qf Medicine, California, Los Angeles. California 90024 Received

May

University

of

4. 1979

Effects of orbital cortical stimulation on the excitability of facial motoneurons were examined in the cat by means of extracellular and intracellular recording techniques. Orbital cortical stimulation induced prolonged changes in the infraorbital facial reflex; an initial phase offacilitation was followed by long-lasting suppression. Cortical effect with the same time course was observed on the antidromic field potential of the facial nucleus. After orbital cortical stimulation, 64.2% of facial motoneurons showed an initial excitatory postsynaptic potential followed by a prolonged hyperpolarizing potential. Both antidromically and orthodromically induced spikes in these cells were facilitated or suppressed, respectively, during the depolarizing or hyperpolarizing phase induced in the motoneurons by stimulating the orbital cortex. The facilitatory or inhibitory effect of cortical stimulation on the infraorbital facial reflex and the antidromic field potential of the facial nucleus showed a close temporal correlation with the cortically induced depolarizing or hyperpolarizing postsynaptic potential in facial motoneurons.

INTRODUCTION Physiologic characteristics of facial motoneurons and the reflexes involving the facial nucleus have been extensively studied in the cat (3,4,6, 15- 18). In the present study, orbital cortical effects on antidromically or reflexly elicited electrical activities of facial motoneurons were examined Abbreviation: EPSP-excitatory postsynaptic potential. 1 Dr. Wessolossky was on leave from the Department of Physiology, Jose Vargas Medical School, Central University of Venezuela, Caracas, Venezuela, but is now deceased. Dr. Mizuno’s present address is Department of Anatomy, Faculty of Medicine, Kyoto University, Kyoto 606. Japan. The authors acknowledge the photographic assistance of Mr. Akira Uesugi. Requests for reprints should be sent to Dr. C. D. Clemente. 343 0014-4886/79/110343-13$02.00/O Copyright 0 1979 by Academic Press, Inc. All rights of reproduction in any form reserved.

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AND

CLEMENTE

in the cat; stimulation of the orbital cortex is known to induce suppressive effects on the monosynaptic masseteric reflex (1,9- 13). METHODS Thirty-three adult cats were used. Tracheotomy and cannulation of the femoral vein were done under ether anesthesia. Artificial respiration was begun immediately after injection of sodium methohexital. All surgical procedures thereafter were carried out under barbiturate anesthesia (initial i.p. doses: 6 mglkg; maintenance doses: 3 mglkg whenever necessary). The ventral branch of the facial nerve was dissected out centrally to its junction with the dorsal branch, which was also dissected out in a similar way. After cutting all other small branches of the facial nerve the stem of the facial nerve was isolated from the surrounding tissue to a point 10 to 15 mm distal to the stylomastoid foramen; the dissected nerve was 25 to 30 mm in length. The cat was then placed in a stereotaxic instrument and all pressure points and wound edges were infiltrated with 2% xylocaine. After enucleation the infraorbital nerve was dissected from the orbital floor; the exposed nerve was 10 to 15 mm in length. The frontal region of the brain was exposed and the dura was removed. The spinal cord was transected at level C2 after local injection of 0.5 ml of 2% xylocaine. Subsequently, the cat was placed in a supine position. The ventral surface of the brain stem was exposed by ventral approach between the tympanic bullae. The dura was removed and the brain stem was covered with 1.5% agar in Tyrode’s solution. The cat was kept warm by an infrared light and a heat pad through which warm water circulated. A bilateral pneumothorax was made and gallamine triethiodide was injected intravenously. The facial nerve, mounted on a bipolar silver wire electrode with 4-mm interpolar distance, was kept in a pool of warm mineral oil placed between the masseter muscle and the skin. This electrode was used to record the infraorbital facial reflex responses, as well as the antidromic stimulation of the facial motoneurons. A collar-type bipolar stimulating electrode with 4-mm interpolar distance was implanted on the infraorbital nerve and fixed in position. This electrode was covered with cotton soaked in Vaseline to avoid current spread. Cortical stimulation was delivered through two silver ball electrodes spaced 2 mm apart and insulated except for the tips. Electrical stimulation was delivered from pulse generators (Tektronix Type 161), and responses were displayed on a cathode ray oscilloscope (Tektronix Type 565). Glass micropipets for extracellular and intracellular recordings were filled with either 3 M KC1 or 2 M K-citrate; tip resistance was 10 to 20 Ma. The micropipets were inserted vertically into the brain stem with a hydraulic micromanipulator (Mechanical Developments Co.). Stereotaxic coordinates for placing the

CORTICAL

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MOTONEURONS

recording electrode were obtained from the stereotaxic atlases and the landmarks on the surface of the brain stem (the exit point of the abducens nerve: P 6.0). Intracellular and extracellular potentials were displayed on the oscilloscope through a neutralized input capacity amplifier (Bioelectric Instruments Type DS2C) and a DC amplifier (Tektronix Type 3A74). All recordings began at least 3 h after the last injection of the barbiturate. RESULTS Effects of Cortical Stimulation on the Infraorbital Facial Reflex. Stimulation of the infraorbital nerve induced a reflex response in the facial nerve with a latency of 4.3 ms (Figs. lA, D). This reflex response with several peaks of activity was decreased in amplitude by stimulation of the infraorbital nerve at frequencies greater than 1 Hz; at 20 Hz the amplitude was less than half that of the control response. This polysynaptic infraorbital facial reflex was modified by stimulating the rostra1 part of the orbital gyrus and its vicinity. The conditioning stimuli, usually a train of three pulses of from 5 to 10 V, were delivered ipsilaterally to the orbital gyrus at a frequency of 50/s. When the conditioning-test stimulus interval was between 6 and 17 ms after the first cortical shock, the amplitude of the reflex was increased (Fig. 1B). This facilitatory phase was followed by a long-lasting suppressive phase (Fig. IE). The changes of the voltage amplitude of the reflex were plotted against the time interval between the first cortical shock and the stimulus artifact applied to the infraorbital nerve

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cortical effects on the infraorbital facial reflex. A and D-control records by stimulation ofthe infraorbital nerve (5 V. 1 .O ms). B and E-conditioning Small evoked responses are seen in the facial nerve after stimulation the ipsilateral orbital gyrus. C and F-facilitation(C) and suppression(F) by conditioning orbital cortical stimulation (10 V, 0.3 ms, 500/s).

of of of

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MIZUNO,

AND CLEMENTE

(Fig. 6A); the reflex was facilitated in the initial phase (6 to 17 ms) and suppressed for more than 100 ms after returning to the control value. Similar effects on the infraorbital facial reflex were also observed after stimulation of other orbital cortical areas (Fig. 2); six cortical areas were arbitrarily demarcated around the orbital sulcus (Fig. 2A), and the effect of stimulation of each area on the infraorbital facial reflex was examined. When the conditioning-test interval was longer than 40 ms, contralateral stimulation was less effective in suppressing the test reflex than ipsilateral stimulation (Fig. 2B). Stimulation of area 3 or 6 was less effective in eliciting the facilitatory phase than that of area 1,2,4, or 5 (Figs. 2C, D). The duration of the suppressive phase elicited by stimulation of area 2,4,5, or 6 was shorter than that elicited by stimulation of area 1 or 3 (Figs. 2C, D). Antidromic Field Potential of the Facial Nucleus. While stimulating the facial nerve continuously at a rate of l/s (2 V, 0.1 ms), the microelectrode was lowered into the brain stem. A localized negative potential of 2 to 4 mV was recorded at a depth of 2 mm from the ventral surface of the brain stem (Fig. 3). This negativity was usually preceded by a small positivity of short duration and followed by a prolonged positivity. The peak latency of the main negative potential was consistent in each cat: 2.1 t 0.4 ms. This negative potential was not diminished substantially at frequencies to 40 to 50/s. These findings indicate that this negative potential was the antidromic field potential of the facial nucleus. Stimulation of the rostra1 part of the orbital gyrus induced an initial facilitatory and then a long-lasting suppressive effect on the antidromic field potential of the facial nucleus (Fig. 4). The time course of this sequence of facilitation-suppression was approximately the same as that observed in the infraorbital facial reflex after the same conditioning cortical stimuli (Fig. 6B). Intracellular Recording of the Antidromic Spike Potential from Facial Motoneurons. Facial motoneurons were identified by the antidromic spike potential elicited by stimulation of the facial nerve (Fig. 5A). Identification of the antidromic spike potential was based on the following criteria: (i) the FIG. 2. Time course of the cortical effects on the infraorbital facial reflex. A-schematic representation of the lateral surface ofthe cat brain, where six areas are arbitrarily demarcated around the orbital sulcus. The orbital gyrus is divided into areas 1 and 3. Area 3 corresponds to the area rostra1 to the orbital gyrus. Areas 5,4, and 6 are situated, respectively, in the rostra], middle, and caudal parts of the coronal gyrus. B-effects of ipsilateral and contralateral orbital cortical stimulation. C and D-cortical effects on the reflex elicited by stimulation of the ipsilateral areas 1, 2, and 3 (C) and 4, 5, and 6 (D). In B, C, and D, suprathreshold stimulation for maximal amplitude of the reflex response was applied to the infraorbital nerve. All data in this figure were obtained from the same cat. Cortical stimulation: three shocks, 10 V, 0.3 ms, 500/s.

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of orbital cortical stimulation on the antidromic field potential of the facial FIG. 4. Effects nucleus. A-control record of conditioning cortical stimulation applied ipsilaterally to the rostra1 part of the orbital gyrus (10 V, 0.3 ms. 500/s). B-control record of the antidromic field potential elicited by facial nerve stimulation (1 V. 0.1 ms). C and D-facilitation (C) and suppression (D) of the antidromic field potential induced by the orbital cortical stimulation. Calibration line for each record of A-D indicates 2 ms. Negativity downward.

latency of spike was constant in each cat; (ii) it arose directly from the baseline without preceding depolarization; and (iii) it followed a repetitive stimulation to as long as 40 s. Based on these criteria, a total of 39 facial motoneuron cells was identified. The antidromic spike potentials were 40 to 101 mV (mean ? SD, 53.9 + 11.8 mV), and the mean duration was 1.7 -+ 0.3 ms. The mean latency was 1.1 2 0.4 ms, and the peak latency was 1.9 t 0.6 ms. In addition to the antidromic spike, an excitatory postsynaptic potential (EPSP) with a longer latency was induced in 5 of 39 cells by stimulating the facial nerve. This EPSP triggered the second spike (Fig. 51). The latency of the second spike was variable in different cells, but constant within each cell. The second spike was considered to be orthodromic, triggered by afferent fibers in the facial nerve (4-6, 15). The impaled motoneurons also responded to stimulation of the infraorbital nerve with a depolarizing potential, which usually triggered one to three spikes (Fig. 5E). The latency of the depolarizing potential was 3.0 ms and the duration about 10 ms. Postsynaptic of the Orbital

Potentials in Facial Motoneurons Induced by Stimulation Cortex. Stimulation of the rostra1 part of the orbital gyrus

induced ipsilaterally

in facial motoneurons

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field potentials in the facial nuclear region evoked by stimulation of the FIG. 3. Antidromic facial nerve. A-ventrodorsal distribution pattern of the field potentials evoked by stimulation of the facial nerve (2 V, 0.1 ms. 2/s). Each record consists of 20 superimposed traces (negativity downward). Numbers indicate distances in micrometers of the recording points from the ventral surface ofthe brain stem. B-amplitudes ofthe negative component of the antidromic field potentials (ordinate) are plotted against the distance from the ventral surface of the brain (abscissa).

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5 msec FIG. 5. Orbital cortical effects on the membrane potential of facial motoneurons. A-an antidromic spike potential induced by facial nerve stimulation (5 V, 0.1 ms). B-control record of conditioning cortical stimulation applied ipsilaterally to the rostral part of the orbital gyrus (10 V, 0.3 ms, 400/s). C and D-suppression of the antidromic spike potential with conditioning orbital cortical stimulation. E-orthodromic spike potential induced by infraorbital nerve stimulation (2.5 V, 0.1 ms). F-conditioning cortical stimulation applied ipsilaterally to the rostra1 part of the orbital gyrus (8 V, 0.3 ms, 500/s). G and H-suppression of the orthodromic spike potential with conditioning orbital cortical stimulation. Arrows in E, G, and H indicate the artifacts of stimulation applied to the infraorbital nerve. I-intracellular recording of a “double spike” (an antidromic, followed by an orthodromic spike) from a facial motoneuron evoked by stimulation of the facial nerve (5 V, 0.1 ms).

membrane potential followed by a prolonged hyperpolarization (Tables 1, 2, Fig. 6C). The initial depolarization induced one or two spikes (Figs. 5B-D, F, H). In 34 facial motoneurons tested with conditioning cortical stimulation, 28 cells responded to the cortical stimulation; 18 (64.2%) cells showed an initial depolarization followed by hyperpolarization; 7 (25%) showed only a depolarizing potential; and 3 (10.7%) responded only with a hyperpolarizing potential.

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1

Mean Values of Latencies of Depolarizing and Hyperpolarizing Potentials Induced in Facial Motoneurons by Stimulation Applied Ipsilaterally to the Rostra1 Part of the Orbital Gyrus” Number of cortical shocks

Depolarizing potential Latency (ms) Peak latency (ms) Hyperpolarizing potential Latency (ms) Peak latency (ms)

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5.0 9.0

6.8 11.8

8.0 9.5

16.0 36.0

17.5 32.0

23.8 44.6

18.0 33.5

a One to five shocks, 10 v, 0.5 ms, 500 to 777/s

Stimulation of the rostra1 part of the orbital gyrus was more effective in inducing spikes than stimulation of the more caudal parts of the gyrus (Fig. 7); stimulation of the caudal parts of the gyrus induced an initial depolarization only when it was strong, such as five shocks at 10 V. Effects of Cortical Stimulation on Antidromic and Orthodromic Spike Potentials of Facial Motoneurons. Antidromic and orthodromic spike induction in facial motoneurons was facilitated during the period of cortically induced depolarization, and suppressed partially or completely during the cortically induced hyperpolarizing phase; these effects were observed whether or not a spike was evoked by cortical conditioning stimuli (Fig. 5). The time course of the sequence of facilitation and suppression of the infraorbital facial reflex and the antidromic field potential in the facial TABLE

2

Latencies, Peak Amplitudes, and Durations of Postsynaptic Potentials Induced in Facial Motoneurons by Three Shocks Applied Ipsilaterally to the Rostra1 Part of the Orbital Cortex” Depolarizing Latency (ms) Peak latency (ms) Peak amplitude (mV) Duration (ms)

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I smv FIG. 6. Time course of changes in excitability of facial motoneurons induced by orbital cortical stimulation. A-amplitudes of the infraorbital facial reflex (ordinate) are plotted against the time intervals between the first cortical shock applied ipsilaterally to the rostra1 part of the orbital gyrus (10 V, 0.3 ms, 500/s) and the stimulation of the infraorbital nerve (1 V, 0.1 ms). The circle with vertical bars indicates the control value of the reflex potential (? 1 SD). B-amplitudes of antidromic field potentials in the facial nucleus are plotted against the time intervals between the conditioning cortical stimulation applied ipsilaterally to the rostra1 part

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FIG. 7. Postsynaptic membrane potential (PSP) changes of facial motoneurons induced by orbital cortical stimulation. A and B-PSPs recorded in a facial motoneuron after stimulation of the rostra1 (A) or caudal (B) part of the ipsilateral orbital gyrus (10 V, 0.5 ms. 500/s). C, D. and E-changes of the membrane potential elicited by stimulation applied ipsilaterally to the caudal part of the orbital gyrus (10 V, 0.3 ms, 500 to 7771s). The excitatory PSP was elicited only when five shocks were applied to the cortical area(E). Records C-E were obtained from the same cell.

nucleus after orbital cortical stimulation were closely correlated with the time course of the postsynaptic membrane potential changes recorded intracellularly from facial motoneurons (Fig. 6). DISCUSSION Mapping of the antidromic field potential in the facial nucleus showed that the potential decreased in amplitude in some part of the nuclear region (Fig. 3B). Because the facial nucleus is known to be divided into several subnuclei [for review, cf. (7)], the electrode was considered to be located in the “vacant” region between these subnuclei. Electrical stimulation of the rostra1 part of the orbital gyrus induced a postsynaptic potential within the facial motoneurons. It consisted of an initial period of depolarization followed by a prolonged period of hyperpolarization. During this hyperpolarizing phase, antidromic and orthodromic spikes recorded intracellularly from facial motoneurons were suppressed. This suppression of antidromic spikes was encountered at of the orbital gyrus (10 V, 0.2 ms. 500/s) and the stimulation of the facial nerve (4 V.O.1. ms). The circle with vertical bars indicates the control value of the antidromic field potential (t 1 SD). C-a postsynaptic potential recorded intracellularly in a facial motoneuron after stimulation of the rostra1 part of the ipsilateral orbital gyrus (10 V, 0.3 ms, 500/s). The time scale is the same in A, B, and C.

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short conditioning-test intervals. The orbital cortical stimulation also induced a sequence of facilitation and suppression of the infraorbital facial reflex as well as of the antidromic field potential in the facial nucleus. The time course of the facilitation and suppression sequence of the infraorbital facial reflex and the antidromic field potential in the facial nucleus induced by orbital cortical stimulation was closely correlated with the time course of the sequence of postsynaptic depolarizing and hyperpolarizing membrane potential changes induced in the facial motoneurons by orbital cortical stimulation. Therefore, we concluded that the cortically induced sequence of facilitation and suppression of the infraorbital facial reflex and the antidromic field potential of the facial nucleus was mainly due to the sequence of depolarization and hyperpolarization of facial motoneurons. Nakamura ef al. (9) described a masseteric reflex inhibition induced by stimulation of the rostra1 part of the orbital gyrus. They found that the suppression of the masseteric reflex was due primarily to postsynaptic inhibition. The suppression phase of the infraorbital facial reflex observed in the present study, however, lasted more than 100 ms; it was much longer than the hyperpolarizing potential induced in facial motoneurons by orbital cortical stimulation. Darian-Smith and Yokota (2) reported that primary afferent depolarization of the central terminals of trigeminal cutaneous afferents was elicited by stimulation of the coronal, anterior ectosylvian, or anterior sigmoid gyrus in the cat; it lasted longer than 150 ms. A smiliar effect was also induced in the central terminals of the infraorbital nerve by stimulating the rostra1 part of the orbital gyrus (11). Based on the data described above, it was assumed that both postsynaptic and presynaptic inhibitory mechanisms were involved in the cortically induced prolonged suppression of the infraorbital facial reflex. Mizuno et al.@) reported that, after ablation of the rostra1 part of the orbital gyrus and its vicinity, degeneration fibers were traced from the internal capsule to the lower brain stem, and that degenerated fibers terminated chiefly in the spinal trigeminal nuclei as well as in the brain stem reticular nuclei. It was also reported that both pontine and medullary neurons were involved in the pathways mediating orbital cortical effects to masseteric motoneurons (11, 14). The inhibitory postsynaptic potential recorded in masseteric motoneurons after orbital cortical stimulation had a latency of about 6 ms (9); on the other hand, the latency of the initial EPSP recorded in facial motoneurons after the orbital cortical stimulation was about 7 ms. The difference in the polarity of the initial phase of the orbital cortically induced postsynaptic potentials between masseteric and facial motoneurons suggested that, in interneurons activated initially by orbital cortical stimulation, those sending their axons to facial motoneurons were different from those giving rise to axons terminating on masseter motoneurons.

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REFERENCES 1. CLEMENTE, C. D., M. H. CHASE, T. K. KNAUSS, E. K. SAUERLAND. AND M. B. STERMAN. 1966. Inhibition of a monosynaptic reflex by electrical stimulation of the basal forebrain or the orbital gyrus in the cat. Experientia 22: 844-845. 2. DARIAN-SMITH, I., AND T. YOKOTA. 1966. Cortically evoked depolarization of trigeminal cutaneous afferent fibers in the cat. J. Neuruphysiol. 29: 170-184. 3. GREEN, J. D., J. DEGROOT, AND J. SUTIN. 1957. Trigemino-bulbar reflex pathways. Am. J. Physiol. 189: 384-388. 4. IWATA, N., S. T. KITAI, AND S. OLSON. 1972. Afferent component of the facial nerve: its relation to the spinal trigeminal and facial nucleus. Bruin Res. 43: 662-667. 5. KITAI. S. T., T. AKAIKE, T. BANDO, T. TANAKA, N. TSUKAHARA. AND H. Yu. 1971. Antidromic and synaptic activation of the facial nucleus of cat. Brain Reg. 33: 227-232. 6. KI~AI, S. T.. T. TANAKA, N. TSUKAHARA, AND H. Yu. 1972. The facial nucleus of cat: antidromic and synaptic activation and peripheral nerve representation. E.wp. Bruin Res. 16: 161-183. 7. KUME. M., M. UEMURA, K. MATSUDA, R. MATSUSHIMA. AND N. MIZUNO. 1978. Topographical representation of peripheral branches of the facial nerve within the facial nucleus: a HRP study in the cat. Neurosci. Left. 8: 5-8. 8. MIZUNO, N.. E. K. SAUERLAND, AND C. D. CLEMENTE. 1968. Projections from the orbital gyrus in the cat. I. To brain stem structures. 1. Comp. Neural. 133: 463-476. 9. NAKAMURA, Y.. L. J. GOLDBERG, AND C. D. CLEMENTE. 1967. Nature of suppression of the masseteric monosynaptic reflex induced by stimulation of the orbital gyrus of the cat. Bruin Res. 6: 184- 198. 10. NAKAMURA, Y., T. MURAKAMI, M. KIKUCHI. Y. KUBO. AND S. ISHIMINE. 1977. Primary afferent depolarization in the trigeminal spinal nucleus of cats. E.up. Bruin Res. 29: 45-56. 11. NAKAMURA, Y., AND S. NOZAKI. 1978. A brain stem mechanism responsible for cortical control of trigeminal motoneurons. Pages 207-208 in M. Ito. Ed., The Zntegrutive Control Functions of the Bruin. Vol. 1. Kodansha Scientific, Tokyo, and Elsevier. Amsterdam. 12. SAUERLAND, E. K., T. KNAUSS. Y. NAKAMURA, AND C. D. CLEMENTE. 1967. Inhibition of monosynaptic and polysynaptic reflexes and muscle tone by electrical stimulation of the cerebral cortex. Exp. New-o/. 17: 159- 171. 13. SAUERLAND, E. K.. AND N. MIZUNO. 1969. Cortically induced presynaptic inhibition of trigeminal proprioceptive afferents. Bruin Res. 13: 556-568. 14. SAUERLAND. E. K.. Y. NAKAMURA. AND C. D. CLEMENTE. 1967. The role of the lower brain stem in cortically induced inhibition of somatic reflexes in the cat. Bruin Res. 6: 164- 180. 15. TANAKA, T. 1977. Synaptic activation of facial afferents on the facial neurons of the cat. Bruin Res. 123: 378-383. 16. TANAKA. T. 1977. Further electrophysiological analysis of a spinofacial pathway in the cat. Bruin Res. 138: 545-549. 17. TANAKA, T., H. Yu, AND S. T. KITAI. 1971. Trigeminal and spinal input to the facial nucleus. Bruin Res. 33: 504-508. 18. Yu. H., J. F. DEFRANCE, N. IWATA, S. T. KITAI, AND T. TANAKA. 1972. Rubral inputs to the facial motoneurons in cat. Bruin Res. 42: 220-224.