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Division of Cardiovascular Medicine, Departments of Internal Medicine and Human Physiology, University of California, Davis, California 95616
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In decerebrate paralyzed cats, we examined the effects of two central motor commands (fictive locomotion and scratching) on the discharge of dorsal horn neurons receiving input from group III and IV tibial nerve afferents. We recorded the impulse activity of 74 dorsal horn neurons, each of which received group III input from the tibial nerve. Electrical stimulation of the mesencephalic locomotor region (MLR), which evoked fictive static contraction or fictive locomotion, inhibited the discharge of 44 of the 64 dorsal horn neurons tested. The mean depth from the dorsal surface of the spinal cord of the 44 neurons whose discharge was inhibited by MLR stimulation was 1.77 ± 0.04 mm. Fictive scratching, evoked by topical application of bicuculline to the cervical spinal cord and irritation of the ear, inhibited the discharge of 22 of the 29 dorsal horn neurons tested. Fourteen of the twenty-two neurons whose discharge was inhibited by fictive scratching were found to be inhibited by MLR stimulation as well. The mean depth from the dorsal surface of the cord of the 22 neurons whose discharge was inhibited by fictive scratching was 1.77 ± 0.06 mm. Stimulation of the MLR or the elicitation of fictive scratching had no effect on the activity of 22 dorsal horn neurons receiving input from group III and IV tibial nerve afferents. The mean depth from the dorsal surface of the cord was 1.17 ± 0.07 mm, a value that was significantly (P < 0.05) less than that for the neurons whose discharge was inhibited by either MLR stimulation or fictive scratching. We conclude that centrally evoked motor commands can inhibit the discharge of dorsal horn neurons receiving thin fiber input from the periphery.
group III and IV afferents; cats; exercise; spinal cord
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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BOTH STATIC AND MODERATELY intense dynamic exercise increase mean arterial pressure, heart rate, and ventilation. Two neural mechanisms are believed to be responsible for these effects, namely central command (52) and the exercise pressor reflex (30). Central command is activated at the onset of exercise and is defined as the parallel activation of the central neural circuits controlling cardiovascular, ventilatory, and motor function (20, 52). The exercise pressor reflex is evoked by both mechanical and metabolic stimuli (15, 33). Its sensory arm is comprised of group III and IV muscle afferents (33).
During exercise, the probability is high that both central command and the muscle reflex are engaged. Studies measuring arterial pressure, heart rate, and phrenic nerve discharge in anesthetized cats have shown that simultaneous activation of both mechanisms evoked responses that added nonalgebraically (44, 53). Specifically, the sum of the responses evoked by each mechanism separately was significantly more than the responses evoked by activating both mechanisms simultaneously.
One explanation for this nonalgebraic summation is that central command suppressed the muscle reflex. The dorsal horn of the spinal cord may be an important site for this suppression to occur. For example, previous work has shown that stimulation of hypothalamic and midbrain sites, which caused analgesia, suppressed the responses of dorsal horn neurons to nociceptive input from hindlimb skin (13, 14). These findings raised the possibility that the central command to exercise, part of which can arise from the mesencephalic locomotor region (MLR), may suppress the discharge of dorsal horn cells receiving input from group III and IV muscle afferents.
In the experiments described, we recorded the discharge of dorsal horn neurons receiving group III and IV afferent input from the hindlimb, whereas two central commands, fictive locomotion and scratching, were evoked in paralyzed cats. Fictive locomotion was evoked by electrical stimulation of the MLR, which is located in the cuneiform nucleus of the midbrain (20, 48, 49). Fictive scratching was evoked by irritating the ear after bicuculline, a GABA antagonist, was applied topically to the cervical spinal cord (7, 9, 47). We tested the hypothesis that either of these two central commands to exercise would inhibit the discharge of dorsal horn neurons receiving group III and IV afferent inputs. Support for this hypothesis might provide an electrophysiological basis for the nonalgebraic summation of the cardiovascular and ventilatory responses to simultaneous elicitation of central command and the muscle reflex.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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General. Adult cats (n = 30) of either sex (2.2-3.5 kg) were anesthetized with a mixture of halothane (3-4%) and oxygen. Once anesthetized, the cats breathed the anesthetic gas mixture through a nose cone, while the trachea, one common carotid artery, and the left jugular vein were cannulated. The lungs were then ventilated with the anesthetic gas mixture through the tracheal cannula. The remaining carotid artery was ligated in preparation for the decerebration (see below). Body temperature was maintained near 37°C with a heating pad and lamp. The cat was placed in a Kopf stereotaxic and spinal unit. The right hindlimb was extensively denervated and the following muscle nerves were dissected free, cut, and their central ends mounted on bipolar stainless steel recording electrodes: posterior biceps-semitendinosus, semimembranosus anterior biceps, and tibialis anterior and extensor digitorum longus (i.e., deep peroneal nerve). The tibial nerve was dissected free and mounted on a stimulating electrode. The ipsilateral triceps surae muscles were exposed, and the ipsilateral calcaneal (Achilles) tendon was cut. A laminectomy exposing spinal segments L4-S2 was performed and was followed by a precollicular postmammillary decerebration. All neural tissue rostral to the section was removed, bleeding was controlled, and the cranial vault was filled with agar. After the decerebration procedure was completed, the lungs were ventilated with a mixture of room air and oxygen. Skin flaps surrounding the spinal cord and the hindlimb nerves were used to construct warm (37°C) mineral oil pools. The dorsal surface of the first two cervical segments was exposed by opening the dura after removal of the dorsal arches of the C1 and C2 vertebrae. Arterial blood gases were measured and maintained within normal limits by either adjusting ventilation or injecting sodium bicarbonate (8.5% iv).
A stainless steel monopolar electrode was placed into the MLR (coordinates: P2, L4, HC
1) for delivery of monophasic
electrical pulses (parameters of stimulation: 25-50 Hz;
0.1-0.5 ms; 80-120 µA). The optimal position of the MLR
electrode was judged by the appearance of efferent activity in
peripheral nerves with a low intensity of stimulation. The cord dorsum
potential (CDP) was recorded with a monopolar silver ball electrode
near the dorsal root entry zone at the L6-L7 border; the indifferent
electrode was placed distant to the ball electrode. The intensity of
the current applied to the tibial nerve was expressed in multiples of
the threshold current needed to evoke a CDP. Extracellular impulses
from dorsal horn neurons were recorded from either L7 or S1 spinal
segments with tungsten microelectrodes (FHC) having tip impedances at
1,000 Hz of 4-12 M
. The electrodes were connected to a
high-impedance probe, which in turn was connected to a preamplifier (PBA-1, Frederick Haer). Filters were set at 100-5,000 Hz. The electrodes recording efferent discharge from the muscle nerves and the
CDP were connected to a high-impedance probe (Grass, HIP 511), which in
turn was connected to a preamplifier (Grass, 511). Filters were set at
100-3,000 Hz. Arterial blood pressure was measured from the
carotid arterial cannula, which in turn was connected to a Statham
transducer (P23XL). All signals were written on a chart recorder
(Gould) and also recorded on videotape after being digitized (Vetter).
Activity from the dorsal horn was displayed on a storage oscilloscope.
Extracellular records and recording of CDP were superimposed offline
using an RC-Electronics program. We measured latency of responses of
the dorsal horn neurons to electrical stimulation of the tibial nerve
from stimulus onset.
Protocols. The cats were first paralyzed with vecuronium bromide (0.1 mg/kg iv), which was supplemented every 30 min. Then, the activity of dorsal horn neurons that received group III and IV afferent input were identified. To accomplish this task, we stimulated electrically (1 Hz, 0.5 ms) the tibial nerve at current intensities that were 10-20 times threshold while advancing the recording electrode through the dorsal horn. In this way, we searched for both spontaneously active and silent neurons. If we found a dorsal horn cell that was activated by tibial nerve stimulation at current intensities of 10-20 times threshold, we increased the intensity to 200 times threshold. A minimum of 20 stimulus presentations were recorded if a neuron was suspected of receiving group III and/or IV afferent input from the tibial nerve. We considered a neuron as receiving group III afferent input if the latency of response was at least 6-7 ms and the intensity for activation was >10 times threshold. We considered a neuron as receiving group IV afferent input if the latency of response was >60 ms and the intensity for activation was >50 times threshold. Group III afferents are known to be stimulated by currents equal to 10 times motor threshold, and given that the conduction distance between stimulating and recording electrode was ~150 mm, dorsal horn neurons receiving group III inputs should respond with a latency of at least 6 ms. Likewise, group IV afferents are stimulated often by currents equal to 50 times motor threshold, and given the above conduction distance, neurons receiving group IV input should respond with a latency of at least 60 ms (43). In some experiments, we used mechanical activation of group III and IV afferents by stretching the calcaneal tendon or noxious pinching of the ipsilateral triceps surae muscles as a test for the identification of muscle afferent input to the dorsal horn neurons.
Next, the effect of the electrical stimulation of the MLR on the discharge of the neurons was examined. Typically, the MLR was stimulated for 5-30 s. If an effect on discharge of the cell was observed, the stimulus was turned off for 2-3 min and then repeated. The sequence was repeated two to four times until a clear pattern of effect emerged. Stimulation of the MLR evoked two different types of responses from muscle nerves. The first was fictive locomotion, which was identified by oscillating bursts of multiunit impulses with a frequency of ~0.5-2 Hz. The second response consisted of tonic discharge in the muscle nerves (duration 2-20 s). In some instances, the effect of fictive scratching on cellular activity in the dorsal horn was examined. This motor pattern was evoked by placing onto the cervical spinal cord a small piece of cotton wool that was soaked in bicuculline methiode (1-2 mg/ml). Approximately 0.6-0.8 ml of bicuculline solution was placed onto the cotton wool, after which the ear was irritated by the experimenter's fingers. Fictive scratching was identified by oscillating bursts of discharges in the muscle nerves with a frequency of ~4-6 Hz. We used a conditioning-test protocol to determine the time course and efficacy of the MLR-induced inhibition of dorsal horn neuronal discharge. The conditioning stimulus was a brief train of 3-11 pulses (250-300 Hz) applied to the MLR. The test response was evoked from the dorsal horn neuron by stimulating the tibial nerve with a current intensity of at least 10 times threshold. At least five single stimuli (1 Hz) were applied to the tibial nerve to determine the firing index, which was calculated as the average number of impulses discharged by the dorsal horn neuron in response to tibial nerve stimulation. The ratio of the firing index of the neuron with and without the conditioning stimuli was used as a measure of the inhibition of the dorsal horn neuron's responses to tibial nerve stimulation by the MLR. The conditioning-testing interval was the time period between the first pulse applied to the MLR and the pulse applied to the tibial nerve. Because the dorsal horn neurons could respond to tibial nerve stimulation after a long latent period, the conditioning stimulus to the MLR was applied both before and after the onset of tibial nerve stimulation. When the MLR stimulus preceded the tibial nerve stimulus, the conditioning-testing interval was a positive number. When the tibial nerve stimulus preceded the MLR stimulus, the conditioning-testing interval was a negative number. Silent neurons were activated electrically by stimulating the tibial nerve at 1 Hz. The current intensities and pulse duration were the same as those used when the neurons were initially identified. At the end of the experiment, electrolytic lesions were made to mark the position of recording electrodes, and electrode localizations were verified histologically. Values are reported as means ± SE. When appropriate, we performed paired t-tests to determine statistical significance. The criterion level was set at P < 0.05.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We recorded the impulse activity of 74 dorsal horn neurons
receiving input from group III and IV afferents in the tibial nerve. The current intensity of the electrical pulse applied to the tibial nerve that was required to activate these dorsal horn neurons was at
least 10 times threshold for the most excitable fibers in the dorsal
roots; their latency to activation was at least 6 ms (Fig.
1A). The mean latency and
current threshold of these dorsal horn neurons averaged 26.1 ± 5.0 ms and 23.6 ± 2.3 times that for the most excitable fibers in
the dorsal roots. When the current applied to the tibial nerve was
increased, a second and later response was evoked from 26 of these
neurons. This second response had a mean latency of 39.4 ± 7.5 ms
and a current threshold of 44.3 ± 5.7 times that for the most
excitable fibers, respectively (Fig. 1B).
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We calculated that seven dorsal horn neurons with a latency of activation of >60 ms received only group IV afferent input from the tibial nerve. Two additional neurons probably received input from both group III and IV afferents. Each of the other 65 neurons received input from group III tibial afferents whose conduction velocities ranged from 2.5 to 30 m/s.
Of the 74 dorsal horn neurons, 50 discharged spontaneously with a mean rate of 2.3 ± 0.52 impulses/s. The remaining 24 neurons were silent and were activated by electrical stimulation (>10× threshold) of the tibial nerve when we examined the effect of MLR stimulation or fictive scratching on their discharge. Of the 74 dorsal horn neurons, 64 were tested with MLR stimulation and 29 were tested with fictive scratching. Twenty-two were tested with both.
Inhibition by MLR stimulation.
MLR stimulation inhibited the discharge of 44 of the 64 dorsal
horn neurons tested (Figs.
2-5).
For 30 of the 44 neurons whose discharge was inhibited by MLR
stimulation, the pattern of efferent discharge recorded from hindlimb
muscle nerves was suggestive of static muscular contraction (Fig. 2).
For the remaining 14 neurons, MLR stimulation evoked a pattern of
efferent discharge indicative of fictive locomotion (Figs. 3 and 5). In
every case (i.e., n = 44), the inhibition ceased when
efferent discharge stopped. We did not find any dorsal horn neurons
displaying phasic modulation of their activity during fictive
locomotion. Seven of the sixty-four neurons received group IV afferent
input from the tibial nerve; MLR stimulation inhibited the discharge of
each of the seven.
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Inhibition by fictive scratching.
Fictive scratching inhibited the discharge of 22 of the 29 dorsal horn
neurons tested (Figs. 5 and 7). We did
not find any dorsal horn neurons displaying phasic modulation of
activity during fictive scratching. In every case (i.e.,
n = 22), the inhibition of dorsal horn neuronal
discharge ceased when efferent discharge (i.e., fictive scratching)
stopped. The pressor response evoked by fictive scratching (Figs. 5 and
7) started several seconds after the onset of inhibition of activity by
the dorsal horn neuron.
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Receptive fields. For 27 of the neurons whose activity was inhibited by either MLR stimulation or fictive scratching, we searched for receptive fields in the ipsilateral triceps surae muscles. Fourteen of the twenty-seven neurons tested responded to stretching the calcaneal tendon. Three others responded to noxious pinching of these muscles. For the remaining 10 neurons, we could not find a receptive field in the triceps surae muscles.
Neurons showing no effect from either MLR stimulation or fictive locomotion. Stimulation of the MLR or the elicitation of fictive scratching had no effect on the activity of 22 dorsal horn neurons receiving input from thin fiber tibial nerve afferents. These neurons were found at depths from the dorsal surface of the spinal cord ranging from 0.75 to 1.88 mm (Fig. 6D). The mean depth was 1.17 ± 0.07 mm, which was significantly less than that for the neurons whose activity was inhibited by either MLR stimulation or by fictive scratching (P < 0.05). Their locations were evenly distributed in the medial, central, and lateral parts of the dorsal horn. The mean onset latency to stimulation of the tibial nerve was 16.1 ± 2.7 ms (n = 22). For 8 of the 22 neurons, we searched for receptive fields in the triceps surae muscles. Three of the eight neurons were found to discharge in response to stretching the calcaneal tendon. None of the eight neurons responded to pinching the triceps surae muscles in a noxious manner.
Conditioning-testing protocol.
The minimum conditioning-testing interval that evoked maximum MLR
induced inhibition of dorsal horn neuronal responsiveness to tibial
nerve stimulation averaged 28.7 ± 1.4 ms and ranged from 25 to 34 ms (n = 6; Figs. 8 and
9). The duration of this MLR-induced
inhibition averaged 80.0 ± 19.1 ms (n = 6; Fig.
9). As a consequence, the time between the conditioning stimulus
applied to the MLR and the recovery of responsiveness to tibial nerve stimulation averaged 108.7 ± 18.9 ms (n = 6). In
two neurons, the strength of the MLR induced-inhibition of the
responses of the dorsal horn neurons to tibial nerve stimulation were
decreased as the number of pulses and their frequency comprising the
conditioning stimulus were decreased. Each of the six neurons received
only group III input from the tibial nerve; two were found to have a
receptive field in the triceps surae muscles.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We have shown in decerebrate paralyzed cats that the activation of two central motor commands causing either fictive locomotion or fictive scratching inhibited the discharge of dorsal horn neurons receiving input from thin fiber afferents innervating the hindlimb. We have also shown that activation of a motor command representative of static muscular contraction inhibited this discharge as well. This inhibition occurred well before the pressor responses that always accompanied the central motor commands evoked in our experiments. As a consequence, the inhibition of dorsal horn discharge by central motor commands was unlikely to have been secondary to the baroreceptor reflex. Nevertheless, we cannot exclude the possibility that the baroreflex may have contributed to some of the sustained inhibition after arterial pressure increased. In addition, this inhibition often occurred before or simultaneously with the onset of rhythmic neural activity, an effect that is similar to that reported by Shefchyk et al. (45) for L4 dorsal horn interneurons that received group II muscle afferent input.
An important issue that arises when interpreting our findings concerns
the types of hindlimb afferents that impinged onto the dorsal horn
neurons whose activity was inhibited by central motor commands. The
evidence we have provided strongly suggests that these dorsal horn
neurons were receiving input from mostly A-
(group III) fibers. This
suggestion is based on two findings. First, electrical stimulation of
the tibial nerve activated these neurons with onset latencies that were
consistent with A- fiber stimulation. Second, the minimum current
required to activate the neurons was 10 times threshold, a level that
is needed to recruit A- (group III) fibers. In a few instances,
however, we found evidence that C fibers (group IV) were also impinging
onto these dorsal horn neurons. This evidence consisted of long-onset latencies to activation when the tibial nerve was electrically stimulated and when the minimum current required for activation with
these latencies was 100 times threshold.
One limitation of our study is that the origins of the thin fiber afferents impinging onto the dorsal horn neurons whose activity we recorded is not clear. The endings of the tibial afferent fibers stimulated in our experiments could have been located in the hindlimb skin, muscle, or joints. Nevertheless, we were able to show that some of the dorsal horn neurons tested were stimulated by stretching the calcaneal tendon, a maneuver that activates group III afferents in the triceps surae muscles (31). Some were stimulated by noxious pinching of this muscle group, a maneuver that activates group IV afferents (31). Obviously, these dorsal horn neurons could have received converging inputs from cutaneous and joint afferents, a possibility that was not tested in our experiments.
In general, we found that the elicitation of central motor commands inhibited the discharge of neurons located in the deep part of the dorsal horn but had no effect on the discharge of those located in the shallow part. In general, the location of the inhibited neurons corresponds to laminae V and VI, whereas that of the noneffected neurons corresponds to laminae II, III, and IV (41). These locations are consistent with what is known about the termination of group III and IV muscle afferents in the lumbar dorsal horn. Specifically, group III afferents innervating the gastrocnemius muscle have been shown electrophysiologically to project both monosynaptically and polysynaptically to laminae I, IV, and V (22, 26, 40). In addition, group IV afferents innervating this muscle have been shown anatomically to project to laminae I and V, but not to laminae II-IV (16, 34).
In our experiments, the neural mechanism and neurotransmitters
responsible for inhibiting dorsal horn neuronal discharge when central
motor commands were activated remain to be identified. Nevertheless,
some useful parallels can be drawn from the pain literature. For
example, there is evidence that the postsynaptic action of
norepinephrine, serotonin, and opioids can inhibit the discharge of
dorsal horn neurons receiving noxious input (24, 29, 54). On the other hand, there is evidence
that presynaptic action of these neurotransmitters can raise the
electrical threshold of the spinal terminals of A- and C fiber
afferents in the sural nerve (12).
The pathway from the MLR to the dorsal horn that caused the inhibition of discharge from neurons receiving input from group III and IV tibial afferents is not known. This pathway might involve the spinal circuitry causing locomotion; alternatively, it might bypass these locomotor circuits. Our finding that the MLR-induced inhibition of dorsal horn neuronal discharge occurred before the appearance of rhythmic neuronal activity in the hindlimb nerves, and our data with conditioning-test intervals are consistent with the hypothesis that, in at least some instances, the spinal locomotor circuitry was bypassed.
The MLR, which is defined operationally, is located in the caudal part of the cuneiform nucleus of the midbrain. Depression of transmission from the group II muscle afferents by electrical stimulation of the caudal part of the cuneiform nucleus (i.e., MLR) was demonstrated in anesthetized cats (37). Field potentials recorded in the dorsal horn and evoked by stimulation of group II afferents were reduced when the test stimuli applied to peripheral nerves were preceded by conditioning stimulation of the cuneiform nucleus. The depression occurred at conditioning-testing intervals of 20-400 ms and was maximal at intervals of 32-72 ms. In addition, intracellular potentials were recorded from three dorsal horn cells receiving group II input. Stimulation of the cuneiform nucleus evoked inhibitory postsynaptic potentials (IPSPs) in these cells with latencies of 15-20 ms. We have extended these findings (37) by showing that the discharge of dorsal horn cells receiving groups III and IV muscle afferent input was inhibited by a central motor command from the MLR.
Anatomic studies have shown that the cuneiform nucleus has connections with the medial reticular formation (5, 21, 23, 51), the locus ceruleus (19, 50), and the raphe nuclei (8, 19, 51). The pathway from the MLR to the medial reticular formation appears to be responsible for initiating locomotion (38, 39), but its role in the inhibition of dorsal horn discharge by central motor commands is unknown. We note with interest that the time course of the inhibition of the discharge of dorsal horn neurons receiving nociceptive input caused by electrical stimulation of these brain stem structures (21, 35) was similar to that reported by us when we stimulated the MLR. This similarity leads us to speculate that either a reticulospinal pathway (21) or a monoaminergic pathway (1, 27, 28, 42) might be the anatomic substrate for our findings.
In our experiments, the inhibition of discharge of dorsal horn neurons by stimulation of the MLR could also have been caused by segmental inhibitory interneurons. The pathways involved in the activation of segmental inhibitory interneurons are not known. Nevertheless, we can speculate that reticulospinal pathways involved in the activation of spinal locomotor circuits could activate a population of inhibitory segmental interneurons that, in turn, would inhibit dorsal horn neurons receiving input from thin fiber muscle afferents. The appearance of not only disynaptic excitatory postsynaptic potentials, but also trisynaptic IPSPs recorded from spinal motoneurons during fictive locomotion induced by MLR stimulation (17, 46), shows that this stimulation can activate a population of inhibitory interneurons in the lumbosacral cord.
The pathway from the scratching pattern generator to the dorsal horn neurons whose discharge was inhibited by the application of bicuculline to the cervical spinal cord is also not known. However, anatomic studies have demonstrated propriospinal projections from the cervical cord to the lumbosacral cord, (10, 32, 36). Moreover, electrophysiological studies have shown that cervical cord neurons inhibit the discharge of dorsal horn neurons in the lumbar cord (11, 18, 25). Similar to the MLR, descending propriospinal inhibitory systems of the cervical spinal segments may directly inhibit the discharge of dorsal horn neurons or they may act via an inhibitory interneuron.
Our findings concerning locomotion confirm and extend those reported by Baev et al. (6). This group of investigators showed that spontaneous fictive locomotion in decerebrate cats inhibited the discharge of a few lumbar dorsal horn neurons. Nevertheless, the small number of neurons recorded in this study prevented Baev et al. (6) from making a distinction between the locations within the dorsal horn of inhibited vs. noneffected neurons. Moreover, receptive fields for the neurons whose activity was recorded were not identified.
Likewise, our findings concerning fictive scratching confirm and extend those reported previously. Baev et al. (7), found that fictive scratching inhibited the discharge of dorsal horn neurons receiving input mostly from group II but also from a few rapidly conducting group III muscle afferents. We have extended these findings to show that dorsal horn neurons receive input from slowly conducting group III muscle afferents as well as from one group IV afferent. In addition, we have shown that two central motor commands, namely fictive scratching and locomotion, converged to inhibit the discharge of the same dorsal horn neurons.
Arshavsky et al. (2) found that the responses of neurons in the lateral reticular nucleus (LRN) to high-intensity electrical stimulation of the radial nerve were suppressed during actual locomotion. This finding might be explained by postulating that the MLR inhibits transmission from thin fiber afferents to spinoreticular neurons. Likewise, the findings of Arshavsky et al. (3, 4) that LRN cells and ventral spinocerebellar tract cells responded with similar discharge rates to both fictive and actual scratching, might also be explained by postulating that the scratching generator inhibited transmission to both spinoreticular and spinocerebellar neurons.
Our findings provide an electrophysiological basis for the finding that the cardiovascular and ventilatory responses to central command and the exercise pressor reflex, evoked simultaneously, added in a nonalgebraic manner (44, 53). Moreover, our findings are consistent with the notion that this nonalgebraic summation is initiated in laminae V and VI of the dorsal horn of the spinal cord. This particular effect may result in central command, when activated by electrical stimulation of the MLR, in preventing the full expression of the autonomic and ventilatory components of the exercise pressor reflex.
Perspectives
One interpretation of our findings is that central command arising from the MLR overrides the exercise pressor reflex and that the anatomic substrate for this interaction is the deep laminae of the dorsal horn. Such an interpretation, however, would overlook our other finding, namely, that central command had no effect on thin fiber input into the superficial dorsal horn. Consequently, we hesitate to draw any firm conclusions from our data. Nevertheless, some speculation might be in order. The inhibition by the MLR of thin fiber muscle afferent input into the deep dorsal horn might be a mechanism to prevent an excess level of sympathetically induced vasoconstriction, which, in turn, would restrict blood flow to exercising skeletal muscles. Conceivably, this excess vasoconstriction could overwhelm metabolic vasodilation and thus decrease the threshold level of O2 consumption whereby blood supply and demand in the exercising muscles are mismatched.| |
ACKNOWLEDGEMENTS |
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We appreciate the technical assistance of Rachel Smith.
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FOOTNOTES |
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This work was supported by National Heart, Lung, and Blood Institute Grant HL-30710.
Address for reprint requests and other correspondence: A. M. Degtyarenko, Division of Cardiovascular Medicine, TB 172, Bioletti Way, Univ. of California, One Shields Ave., Davis, CA 95616.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Received 22 November 1999; accepted in final form 23 February 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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