Input patterns and pathways from the six semicircular canals to motoneurons of neck muscles. I. The multifidus muscle group

1994 ◽  
Vol 72 (6) ◽  
pp. 2691-2702 ◽  
Author(s):  
Y. Shinoda ◽  
Y. Sugiuchi ◽  
T. Futami ◽  
N. Ando ◽  
T. Kawasaki

1. The pattern of connections between the six semicircular canals and neck motoneurons of the multifidus muscle group was investigated by recording intracellular potentials from motoneurons in the upper cervical cord of anesthetized cats. 2. Synaptic potentials were recorded in motoneurons of the rectus capitis posterior (RCP) muscle at C1, the obliquus capitis inferior (OCI) muscle at C1 and C2, and the cervical multifidus muscle (Multi) at C4 in response to electrical stimulation of individual ampullary nerves of the six semicircular canals. Excitatory or inhibitory postsynaptic potentials (EPSPs or IPSPs, respectively) were evoked by separate stimulation of individual ampullary nerves in all of the neck motoneurons. Virtually all of the neck motoneurons received convergent inputs from the six ampullary nerves. 3. Motoneurons that supplied a single muscle had a homogeneous pattern of input from the six semicircular canals. There were two patterns of input from the six semicircular canals to motoneurons of the multifidus muscle group. RCP and Multi motoneurons were excited by stimulation of the bilateral anterior canal nerves (ACNs) and the contralateral lateral canal nerve (LCN) and inhibited by stimulation of the bilateral posterior canal nerves (PCNs) and the ipsilateral LCN. This input pattern is similar to that previously observed in other dorsal extensor muscles, whereas the other input pattern observed in OCI motoneurons is entirely new. OCI motoneurons at C1 and C2 were excited by stimulation of the ipsilateral ACN, PCN, and the contralateral LCN and inhibited by stimulation of the contralateral ACN, PCN, and the ipsilateral LCN. 4. Most postsynaptic potentials (PSPs) were disynaptic, but there were trisynaptic inhibitory connections between the contralateral ACN and PCN and OCI motoneurons, and between the contralateral PCN and RCP motoneurons. 5. The pathways for mediating these inputs from different semicircular canals to neck motoneurons were determined by making lesions in the lower medulla. Transection of the ipsilateral medial longitudinal fascicle (MLF) abolished the following potentials: all disynaptic PSPs in RCP motoneurons except the disynaptic EPSPs from the ipsilateral ACN, and in OCI motoneurons, disynaptic PSPs from the bilateral LCNs, and disynaptic IPSPs from the contralateral PCN. Complete bilateral section of the MLF did not affect the disynaptic EPSPs from the ipsilateral ACN in RCP motoneurons, the disynaptic EPSPs from the ipsilateral ACN and PCN in OCI motoneurons, nor the trisynaptic IPSPs from the contralateral ACN and PCN in COI motoneurons and from the contralateral PCN in RCP motoneurons.(ABSTRACT TRUNCATED AT 400 WORDS)

1997 ◽  
Vol 77 (3) ◽  
pp. 1234-1253 ◽  
Author(s):  
Y. Shinoda ◽  
Y. Sugiuchi ◽  
T. Futami ◽  
N. Ando ◽  
J. Yagi

Shinoda, Y., Y. Sugiuchi, T. Futami, N. Ando, and J. Yagi. Input patterns and pathways from the six semicircular canals to motoneurons of neck muscles. II. The longissimus and semispinalis muscle groups. J. Neurophysiol. 77: 1234–1253, 1997. To reveal patterns of input from the six semicircular canals to motoneurons of various neck muscles and their relationship to the mechanical actions of individual neck muscles, patterns of input to neck motoneurons of the longissimus and the semispinalis muscle groups were investigated in the upper cervical spinal cord of anesthetized cats. Intracellular potentials were recorded from motoneurons of the longissimus muscle group (obliquus capitis superior muscle, OCS; splenius muscle, SPL; longissimus muscle, LONG) and the semispinalis muscle group (biventer cervicis muscle, BIV; complexus muscle, COMP), and effects of separate electrical stimulation of the six ampullary nerves on them were analyzed in each preparation. Neck motoneurons usually received convergent inputs from all of the six ampullary nerves, and motoneurons that supplied a particular muscle had a homogeneous pattern of input from the six ampullary nerves. Two different patterns of input were identified for motoneurons of these two muscle groups; one pattern for motoneurons of the longissimus muscle group and the other pattern for motoneurons of the semispinalis muscle group. Motoneurons of the OCS, the SPL, and the LONG muscles received excitation from the three contralateral ampullary nerves and inhibition from the three ipsilateral ampullary nerves. BIV and COMP motoneurons received excitation from the bilateral anterior canal nerves (ACNs) and the contralateral lateral canal nerve (LCN) and inhibition from the bilateral posterior canal nerves (PCNs) and the ipsilateral LCN. Latencies of postsynaptic potentials (PSPs) evoked by stimulation of each of the six ampullary nerves indicated that the earliest component of excitatory PSPs (EPSPs) and inhibitory PSPs (IPSPs) was disynaptic in these motoneurons. However, trisynaptic IPSPs were evoked by stimulation of the contralateral PCN in a considerable number of BIV and COMP motoneurons. In OCS, SPL, and LONG motoneurons, all of the excitation from the contralateral and all of the inhibition from the ipsilateral ampullary nerves were mediated through the ipsilateral medial longitudinal fascicle (MLF). In BIV and COMP motoneurons, disynaptic excitation from the contralateral ACN and LCN and disynaptic inhibition from the ipsilateral LCN and bilateral PCNs were mediated through the ipsilateral MLF, whereas disynaptic excitation from the ipsilateral ACN was mediated through the ipsilateral lateral vestibulospinal tract. The patterns of semicircular canal input to neck motoneurons of these two muscle groups are related closely to the mechanical actions of individual neck muscles and the optimal stimulus to the semicircular canals such that the connections will tend to stabilize head position in response to head perturbations.


1996 ◽  
Vol 76 (4) ◽  
pp. 2439-2446 ◽  
Author(s):  
N. Isu ◽  
D. B. Thomson ◽  
V. J. Wilson

1. Previous studies of vestibular effects on the upper cervical cord have concentrated on the lateral and medial vestibulospinal tracts and on the actions that they exert on neck motoneurons and other neurons in the ventral horn. It is known, however, that both the rostral and the caudal areas of the vestibular nuclei (VN) give rise to axons that are located in the dorsal and dorsolateral funiculi and that terminate in the dorsal horn. A primary goal of our experiments was to investigate the effect of VN stimulation on neurons dorsal to lamina VII. 2. In decerebrate cats with the caudal cerebellar vermis removed, we stimulated different areas of the VN with an array of electrode. The area of stimulation extended from the caudal tip of the descending nucleus to Deiters' nucleus, and was divided into rostral and caudal halves with the use of the descending nucleus as a reference. For control purposes some stimulating points were placed in the external cuneate nucleus and restiform body. 3. We tested the effects of VN stimulation on spontaneously firing neurons in the ipsilateral C2 and C3 segments. For purposes of classification the gray matter was divided into four zones corresponding approximately to laminae 1-IV, V-VI, VII, and VIII of Rexed. Overall, the activity of 39 of 84 neurons was influenced from one or more stimulating sites. For six cells there was some possibility of current spread to the external cuneate nucleus or to the underlying reticular formation. 4. VN-evoked effects could consist of facilitation, or, less often, inhibition. In the majority of facilitated neurons conditioning stimuli evoked a synchronized, short-latency, increase in firing probability. When evoked by single stimuli this facilitation was considered monosynaptic. Facilitation that was diffuse, or that was only evoked by two or more stimuli, presumably involved more complex pathways. The latency of inhibition could not be measured, but was short. 5. Stimulation of either the rostral or caudal VN had no effect on neurons in laminae I-IV. Electrodes placed rostrally had little effect on neurons in laminae V-VI, but influenced more than half the neurons in laminae VII-VIII. Conversely, electrodes placed caudally were most effective on cells in laminae V-VII, although they also influenced some neurons in lamina VIII. 6. Stimulation of the dorsal rami influenced most neurons in laminae V-VI, and about a quarter of the neurons in laminae VII-VIII. When tested, there was often convergence between vestibulospinal and peripheral inputs. 7. Our results provide physiological evidence that vestibulospinal fibers influence neurons not only in laminae VII and VIII, but also as far dorsally as lamina V. Fibers that influence neurons in laminae V and VI originate primarily in the caudal areas of the VN. As suggested previously on anatomic grounds, the projection to the dorsal laminae, which is predominantly facilitatory, often converges with afferent input and can therefore modulate its influence on spinal neurons.


1999 ◽  
Vol 82 (5) ◽  
pp. 2092-2107 ◽  
Author(s):  
Harumitsu Hirata ◽  
James W. Hu ◽  
David A. Bereiter

Corneal-responsive neurons were recorded extracellularly in two regions of the spinal trigeminal nucleus, subnucleus interpolaris/caudalis (Vi/Vc) and subnucleus caudalis/upper cervical cord (Vc/C1) transition regions, from methohexital-anesthetized male rats. Thirty-nine Vi/Vc and 26 Vc/C1 neurons that responded to mechanical and electrical stimulation of the cornea were examined for convergent cutaneous receptive fields, responses to natural stimulation of the corneal surface by CO2 pulses (0, 30, 60, 80, and 95%), effects of morphine, and projections to the contralateral thalamus. Forty-six percent of mechanically sensitive Vi/Vc neurons and 58% of Vc/C1 neurons were excited by CO2 stimulation. The evoked activity of most cells occurred at 60% CO2 after a delay of 7–22 s. At the Vi/Vc transition three response patterns were seen. Type I cells ( n = 11) displayed an increase in activity with increasing CO2 concentration. Type II cells ( n = 7) displayed a biphasic response, an initial inhibition followed by excitation in which the magnitude of the excitatory phase was dependent on CO2 concentration. A third category of Vi/Vc cells (type III, n = 3) responded to CO2 pulses only after morphine administration (>1.0 mg/kg). At the Vc/C1 transition, all CO2-responsive cells ( n = 15) displayed an increase in firing rates with greater CO2 concentration, similar to the pattern of type I Vi/Vc cells. Comparisons of the effects of CO2 pulses on Vi/Vc type I units, Vi/Vc type II units, and Vc/C1 corneal units revealed no significant differences in threshold intensity, stimulus encoding, or latency to sustained firing. Morphine (0.5–3.5 mg/kg iv) enhanced the CO2-evoked activity of 50% of Vi/Vc neurons tested, whereas all Vc/C1 cells were inhibited in a dose-dependent, naloxone-reversible manner. Stimulation of the contralateral posterior thalamic nucleus antidromically activated 37% of Vc/C1 corneal units; however, no effective sites were found within the ventral posteromedial thalamic nucleus or nucleus submedius. None of the Vi/Vc corneal units tested were antidromically activated from sites within these thalamic regions. Corneal-responsive neurons in the Vi/Vc and Vc/C1 regions likely serve different functions in ocular nociception, a conclusion reflected more by the difference in sensitivity to analgesic drugs and efferent projection targets than by the CO2 stimulus intensity encoding functions. Collectively, the properties of Vc/C1 corneal neurons were consistent with a role in the sensory-discriminative aspects of ocular pain due to chemical irritation. The unique and heterogeneous properties of Vi/Vc corneal neurons suggested involvement in more specialized ocular functions such as reflex control of tear formation or eye blinks or recruitment of antinociceptive control pathways.


1996 ◽  
Vol 781 (1 Lipids and Sy) ◽  
pp. 264-274 ◽  
Author(s):  
Y. SHINODA ◽  
Y. SUGIUCHI ◽  
T. FUTAMI ◽  
S. KAKEI ◽  
Y. IZAWA ◽  
...  

1988 ◽  
Vol 59 (4) ◽  
pp. 1204-1219 ◽  
Author(s):  
S. B. McMahon ◽  
P. D. Wall

1. Lamina I cells were recorded in the lumbar dorsal horn of decerebrate rats. Their projecting axons were mainly located in the contralateral dorsolateral funiculus (DLF) in the upper cervical cord. 2. The effect on these cells of short and long trains of stimuli applied to the upper cervical DLF was examined by measuring the ongoing activity of the cells, their response to peripheral stimuli, and the size of their receptive fields. 3. The presence of tonic descending influences from brain stem to spinal cord was investigated by measuring the properties of the lamina I cells before and during block of descending impulses. 4. The results of DLF stimulation and of cord block show that substantial and prolonged excitation affected many cells, whereas some were inhibited for shorter periods of time. 5. The experiments were repeated with stimulation of the DLF caudal to chronic section to eliminate descending fibers. The results suggest that the changes of excitability in intact animals were partly produced by stimulation of descending fibers and partly by the invasion of collaterals activated by the antidromic stimulation of the axons projecting from the lamina I cells. 6. Although long trains of DLF stimuli generally excited lamina I cells, only inhibitions were seen in the deep dorsal horn. Moreover, stimulation rostral to an acute unilateral DLF lesion was without effect on lamina I cells but inhibited deep cells. 7. It is proposed that the lamina I cells might activate brain stem circuits, which in turn influence deep dorsal horn cells.


1989 ◽  
Vol 62 (6) ◽  
pp. 1225-1236 ◽  
Author(s):  
S. M. Gurahian ◽  
S. H. Chandler ◽  
L. J. Goldberg

1. The effects of repetitive stimulation of the nucleus pontis caudalis and nucleus gigantocellularis (PnC-Gi) of the reticular formation on jaw opener and closer motoneurons were examined. The PnC-Gi was stimulated at 75 Hz at current intensities less than 90 microA. 2. Rhythmically occurring, long-duration, depolarizing membrane potentials in jaw opener motoneurons [excitatory masticatory drive potential (E-MDP)] and long-duration hyperpolarizing membrane potentials [inhibitory masticatory drive potentials (I-MDP)] in jaw closer motoneurons were evoked by 40-Hz repetitive masticatory cortex stimulation. These potentials were completely suppressed by PnC-Gi stimulation. PnC-Gi stimulation also suppressed the short-duration, stimulus-locked depolarizations [excitatory postsynaptic potentials (EPSPs)] in jaw opener motoneurons and short-duration, stimulus-locked hyperpolarizations [inhibitory postsynaptic potentials (IPSPs)] in jaw closer motoneurons, evoked by the same repetitive cortical stimulation. 3. Short pulse train (3 pulses; 500 Hz) stimulation of the masticatory area of the cortex in the absence of rhythmical jaw movements activated the short-latency paucisynaptic corticotrigeminal pathways and evoked short-duration EPSPs and IPSPs in jaw opener and closer motoneurons, respectively. The same PnC-Gi stimulation that completely suppressed rhythmical MDPs, and stimulus-locked PSPs evoked by repetitive stimulation to the masticatory area of the cortex, produced an average reduction in PSP amplitude of 22 and 17% in jaw closer and opener motoneurons, respectively. 4. PnC-Gi stimulation produced minimal effects on the amplitude of the antidromic digastric field potential or on the intracellularly recorded antidromic digastric action potential. Moreover, PnC-Gi stimulation had little effect on jaw opener or jaw closer motoneuron membrane resting potentials in the absence of rhythmical jaw movements (RJMs). PnC-Gi stimulation produced variable effects on conductance pulses elicited in jaw opener and closer motoneurons in the absence of RJMs. 5. These results indicate that the powerful suppression of cortically evoked MDPs in opener and closer motoneurons during PnC-Gi stimulation is most likely not a result of postsynaptic inhibition of trigeminal motoneurons. It is proposed that this suppression is a result of suppression of activity in neurons responsible for masticatory rhythm generation.


1969 ◽  
Vol 24 (2) ◽  
pp. 310-324 ◽  
Author(s):  
Carlo Desole ◽  
Eugenio A. Pallestrini

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