Stimulation-induced setting of postural muscle tone in the decerebrate rat

These studies demonstrate the presence of pontomedullary areas in the rat brainstem which, when stimulated electrically, serve to set postural muscle tone in the hindlimbs. Low amplitude stimulation of the dorsal tegmental field (DTF) was found to inhibit postural muscle tone and, in some rats, was found to decrease mean arterial pressure. Low amplitude stimulation of the ventral tegmental field (VTF) was found to increase postural muscle tone and, in all cases tested, was found to increase mean arterial pressure.     

Parallel suppression of extensor muscle tone and respiration by stimulation of pontine dorsal tegmentum in decerebrate cat

This paper describes the pontine brainstem area responsible for the suppression of postural muscle tone as well as of respiration in acute precollicular-postmammillary decerebrate (mesencephalic) cats. Stimulation of the dorsal part of the pontine tegmentum (DTF) along the midline (P4-P7, H-5 to H-6) decreased the bilateral tone of the hindlimb extensor muscles and the diaphragmatic activity. Tonic discharges of the extensor muscles were suppressed by DTF stimulation and the suppression of muscle activity continued for more than 5 min after termination of the stimulation. In contrast, the suppression of the diaphragmatic activity, which resulted in apnea in some of the animals tested, resumed in spite of the continuation of the stimulation. However, the rebound augmentation of the diaphragmatic activity appeared immediately after the termination of the stimulation. The existence of such a rebound phenomenon suggested that the suppressive effects on the diaphragmatic activity persisted during the entire period of the stimulation. The recovery of respiratory movements during the stimulation led us to suggest that the strong respiratory drives emerge to overcome the exerted DTF-elicited suppressive effects on respiration. In the paralyzed and vagotomized animal, the DTF-elicited suppressive effects on phrenic neural discharges were minimal when the end-tidal pCO2 was set at a higher level than during spontaneous breathing.     

Two different inhibitory effects on respiration by thin-fiber muscular afferents in cats

In anesthetized, vagotomized, paralyzed, and artificially ventilated cats, respiratory responses to electrical stinulation of the gastrocnemius muscle nerve were studied by recording the phrenic nervous discharges. Besides intensity-dependent facilitation of respiration, electrical stimulation of the thin-fiber muscular afferents caused two different types of respiratory suppression, during and after the stimulation. The first suppressive phase (‘initial suppression’) was observed immediately after the start of stimulation above A-δ fiber threshold, and usually accompanied by a fall of blood pressure. The other suppressive phase (‘after suppression’) was observed within several minutes after the cessation of the stimulation. The intensity of stimulation required to evoke the ‘after suppression’ was much higher than that for the ‘initial suppression’, and was usually in the C fiber stimulation range. Naloxone did not affect the ‘initial suppression’, but abolished the ‘after suppression’.     

Thermoregulatory responses of decerebrate and spinal cats

Cooling the spinal cord of the unanesthetized cat elicited shivering, piloerection, and vasoconstriction. A high-level decerebration abolished these effects. Lowering the decerebration to the level of the lower pons or medulla reinstated these responses to spinal cord cooling. In unanesthetized chronic spinal cats, cooling the spinal cord below the level of a T6 transection produced similar thermoregulatory effects limited to the hind limbs, although it was of less intensity and without piloerection. A high-level decerebration abolished shivering in the forelimbs to whole body cooling, while permitting shivering below the level of transection to spinal cord cooling. Lowering the level of decerebration to the lower pons or medulla reinstated shivering, vasoconstriction, and piloerection in the forelimbs. The data suggest that there is a region in the midbrain and upper pontine tegmentum which exerts tonic inhibition on lower regions in the lower pons, medulla, and spnal cord. When released from inhibition these lower regions are capable of facilitating thermoregulatory responses. Such an organization resolves contradictory reports on the abolition of thermoregulation after decerebration and answers the question of why spinal cord cooling produces shivering in spinal preparations but not in decerebrate preparations.     

Radiofrequency cordotomy for the relief of spasticity in decerebrate cats

The effectiveness of radiofrequency (RF) cordotomy of segmental motoneurone pools of the lumbosacral cord in reducing spasticity of decerebrate cats is evaluated. The need for a new form of therapy for clinical spasticity is based upon the limitations of contemporary methods, including surgical and pharmacological techniques. In man, spasticity of spinal origin may be treated effectively by intrathecal administration of hyperbaric phenol solutions. The advantages and disadvantages are described. Difficulty in controlling the lesion is emphasized. Tension and EMG-length curves of the spastic triceps surae muscle in acute and chronic animals show that RF lesions (fixed amperage and duration) of the segmental motoneurone pools reduces myotatic reflex activity in accordance with the number of segments cordotomized. Clinical examination including cinematography and electromyography complement the physiological interpretation. RF lesions of the internuncial pool induce spontaneous EMG discharges. This finding is related to similar observations of EMG discharges and alterations in muscle tone after asphyxiation of the spinal cord.     

Descending pathways eliciting forelimb stepping in the lateral funiculus: Experimental studies with stimulation and lesion of the cervical cord in decerebrate cats

The funicular pathways that elicit forelimb stepping were investigated with stimulation and lesion of the cervical white matter in decerebrate cats with the lower thoracic cord transected. We localized cross-sectional areas where stimulation evoked rhythmic motor-nerve discharges imitating those of stepping (fictive locomotion) in the immobilized animal, and further examined whether or not lesions made in the corresponding areas abolished actual locomotor movements. Stimulation of the C3 lateral funiculus (LF) produced fictive locomotion in the ipsilateral forelimb. The effective areas of stimulation were located separately in the dorsolateral funiculus (DLF) and in the ventrolateral funiculus (VLF), while the VLF was more effective than the DLF. Effective stimuli were pulse trains with a frequency of about 30 Hz, with a rather wide pulse duration of about 0.5 ms. Blocking axonal conduction through the lower thoracic cord by cooling reproducibly facilitated fictive locomotion in both amplitude and frequency. In the lesion experiments, forelimb locomotor movements were elicited spontaneously or by stimulation of the mesencephalic locomotor region (MLR). The locomotor movements were abolished by complete lesions of the C2-C3 LFs on both sides, but these remained when either the DLF or the VLF was intact on one side. These findings together suggested that the descending pathways for the activation of the spinal locomotor network of the single forelimb are located ipsilaterally in the DLF as well as in the VLF. Both the DLF and the VLF pathways can initiate locomotion, while the VLF pathways have a higher potential for its initiation. Lesion experiments further showed that cats can walk with both forelimbs, even though the spinal locomotor network of the single forelimb was deprived of its main descending input by unilateral lesions of the LF. However, when the unilateral lesion extended to the medial part of the LF, the bilateral walking was abolished; the limb on the lesioned side showed only rhythmic extension movements without active flexion movements, which was out of phase with the stepping movements on the intact side. This finding suggested that the medial part of the LF is important for producing flexion movements during the swing phase of stepping.     

Two methods of measuring muscle tone applied in patients with decerebrate rigidity.

Two methods were used to measure muscle tone in patients with decerebrate rigidity. In the first method forces of square waveform were applied and the calculated compliance of the joint was used as an index of rigidity. Oscillatory transients were seen at the same frequency as the physiological tremor. The range of normal variation in compliance was large and the values measured in the patients flucuated markedly which limited the value of this index. In the second method, where forces of sinusoidal waveform were employed, the resonant frequency of the joint was measured and used as an index of rigidity. This index proved reliable and reproducible.     

Descending pathways controlling visually guided updating of reaching in cats

This study uses a previously described paradigm (Pettersson et al., 1997) to investigate the ability of cats to change the direction of ongoing reaching when the target is shifted sideways; the effect on the switching latency of spinal cord lesions was investigated. Large ventral lesions transecting the ventral funicle and the ventral half of the lateral funicle gave a 20-30 ms latency prolongation of switching in the medial (right) direction, but less prolongation of switching directed laterally (left), and in one cat the latencies of switching directed laterally were unchanged. It may be inferred that the command for switching in the lateral direction can be mediated by the dorsally located cortico- and rubrospinal tracts whereas the command for short-latency switching in the medial direction is mediated by ventral pathways. A restricted ventral lesion transecting the tectospinal pathway did not change the switching latency. Comparison of different ventral lesions revealed prolongation of the latency if the lesion included a region extending dorsally along the ventral horn and from there ventrally as a vertical strip, so it may be postulated that the command for fast switching, directed medially, is mediated by a reticulospinal pathway within this location. A hypothesis is forwarded suggesting that the visual control is exerted via ponto-cerebellar pathways.     

Evocation of postural atonia and respiratory depression by pontine carbachol in the decerebrate rat.

To study mechanisms underlying the postural muscle atonia and respiratory depression associated with rapid eye movement (REM) sleep, the cholinergic agonist, carbachol, was microinjected into the pontine reticular formation in decerebrate, spontaneously breathing rats. Carbachol injection led to a simultaneous depression of neck and tonic intercostal EMG activity (lasting 14.5 min +/- 7.6 (S.D.)) and a reduction of the respiratory rate. Phasic inspiratory intercostal activity was not consistently depressed. After a spontaneous recovery from the atonia and respiratory depression, subsequent carbachol injections at the same site produced similar responses. Thus, the decerebrate rat may provide a useful model for studies of the inhibitory neural mechanisms activated by the increased acetylcholine levels in the pons that occur in REM sleep. Pontine carbachol effects in rats differ from those described in cats in a manner analogous to differences in the patterns of natural REM sleep in these two species.     

Suppression of the recurrent inhibitory pathway in lumbar cord segments during locus coeruleus stimulation in cats

The present study revealed a consistent reduction of ventral root-induced recurrent inhibition of monosynaptic reflexes in both extensor (gastrocnemius-soleus) and flexor (common peroneal) motonuclei upon delivery of preconditioning stimuli to the locus coeruleus (LC) in decerebrate cats. The magnitudes of the LC-induced decrease in recurrent inhibition, functionally disinhibition, and of recurrent inhibition were significantly correlated. Direct recordings from Renshaw cells have indicated that LC conditioning stimuli cause a decrease in the number of spikes and the duration of firing in response to single antidromic (ventral root) volleys. These results suggest that the LC depression of the recurrent inhibitory pathway is attributed, in part at least, to inhibition of Renshaw cell activity.     

Cardiovascular reflexes arising from the gallbladder and pancreas in spinal and in decerebrate cats

Cardiovascular responses to chemical stimulation of thin-fiber afferents from the gallbladder and pancreas were determined before and after C₁ transection of the spinal cord in cats. Additional cats were studied before and after decerebration. Stimulation of gallbladder and pancreatic afferents caused significant increases in arterial pressure and heart rate in all groups; however, smaller responses often occurred in spinal cats. These results demonstrate that spinal circuitry alone can generate cardiovascular responses to visceral stimulation and that supraspinal, though not necessarily suprapontine areas, are involved in producing the full response.     

Effect of spontaneous exercise on reflex slowing of the heart in decerebrate cats

Exercise has been shown to reduce the ability of the baroreflex to slow the heart, and signals arising from cerebral cortex may cause this reduction. To test whether signals arising from the cerebral cortex are required to cause this inhibition, reflex slowing of the heart was assessed in decerebrate cats during rest and spontaneous walking. This reflex was quantified by the relation between systolic blood pressure and the subsequent heart beat interval or its inverse, beat to beat heart rate, during transient rises in pressure caused by injections of phenylephrine. Reflex slowing of the heart was reduced during spontaneous exercise compared to rest. Exercise may inhibit reflex cardiac slowing by activating beta-adrenoceptors that inhibit vagal effects on the heart. To test whether activation of beta-adrenoceptors caused the inhibition of reflex cardiac slowing produced by spontaneous walking in these decerebrate cats, the ability of the baroreflex to slow the heart during blockade of beta-receptors by propranolol was tested in 3 cats. Propranolol did not abolish the inhibitory effect of spontaneous walking on this reflex. These data indicate that the cerebral cortex and beta-adrenoceptors are not required for exercise to inhibit reflex cardiac slowing.     

Effects of naloxone on the cardiovascular responses to muscular contraction in decerebrate cats

The action of baclofen, a GABA analog, was studied at the crayfish neuromuscular junction (NMJ). Baclofen depressed the amplitude of excitatory junction potentials (ejps) without affecting muscle input resistance and reduced the frequency of spontaneous miniature ejps without affecting their size. Thus, baclofen may mediate presynaptic inhibition by depressing transmitter release from the excitatory nerve. The site of baclofen's effect at the crayfish NMJ may parallel its site of action in the vertebrate nervous system.     

Morphine effects in brainstem-transected cats: II. Behavior and sleep of the decerebrate cat

Previous studies have shown that opiates suppress both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Furthermore, during the induced insomnia period, characteristic species-specific behaviors occur which are associated with high voltage slow waves in the EEG. This paper investigates the lower brainstem mechanisms involved in the generation of these effects, and describes the action of single morphine doses (0.5, 2.0 or 3.0 mg/kg, i.p.) on the behavior and REM sleep of chronic decerebrate cats. The effects of morphine in the decerebrate cat followed a 3-stage time course similar to that seen in intact cats: (1) autonomic manifestations (3-8 min postdrug); (2) a quiet state (10-60 min postdrug) with behavioral signs of NREM; and (3) a state of activated behavior (1-6 h postdrug), including motor activity and variations in muscle tone. The decerebrate cats also showed a dose-dependent suppression of REM sleep. The present results indicate that: (1) the lower brainstem provides the basic mechanisms for the behavioral deactivation-activation and the autonomic effects of the drug; (2) hypnogenic and synchronizing influences arising from the brainstem might induce the high voltage, slow burst EEG produced by opiates; (3) REM sleep suppression originates only partially in the lower brainstem; (4) the subsidiary action of the prosencephalon seems to be required for the full expression of the drug's effect on behavior and the EEG.