[Time course of descending inhibition of monosynaptic and polysynaptic reflexes in local tetanus].
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Test subjects exposed to altitude decompression without preliminary denitrogenization showed in 65-75% of cases stability or reduction of the amplitude of the H-response of a leg with subsequent painful sensations and in increase of the amplitude of the H-response in the other leg as long as they were raised to an altitude of 11,000 m. When bends developed in a leg the amplitude of the H-response in that leg decreased and in the opposite leg increased. During the descent and disappearance of painful sensations changes in the amplitude of the H-response were just the opposite. It is assumed that a decrease of the amplitude of the H-response during altitude decompression was associated with oxygen deficiency of nerve afferents and an increase--with the descending activating supraspinal effect.
A heteronymous group I oligosynaptic reflex from the common peroneal nerve to vastus medialis muscle was compared with a group I homonymous monosynaptic reflex to soleus, using electrical stimulation of peripheral nerve trunks in two groups of healthy men, mean ages 22 and 65 years. The oligosynaptic reflex was still elicitable with age, its magnitude decreasing similarly to the monosynaptic reflex. A further group of older subjects, mean age 75 years, showed similar results. Clearly, the oligosynaptic reflex is not lost with healthy aging. The motor interneuronal pool may at least partially avoid the age-related cell loss of motoneuronal pools, with consequent maintenance of segmental participation for movements such as gait. The slowing of conduction velocities, for these proprioceptive reflex arcs, may reduce the effectiveness of autoregulation of the gait.
Intrapontine microinjections of serotonin in acutely decerebrated cats resulted in the bilateral augmentation of the postural muscle tone of the hindlimbs. Optimal injection sites were located in the dorsomedial part of the rostral pontine reticular formation corresponding to the nucleus reticularis pontis oralis (NRPo). In this study, attempts were made to elucidate the cellular basis for the serotoninergically induced augmentation of postural muscle tone by recording the electromyographic (EMG) activity of hindlimb extensor muscles, the monosynaptic reflex responses evoked by electrical stimulation of group Ia muscle afferent fibres and the membrane potentials of hindlimb alpha-motoneurons (MNs). Serotonin injections resulted not only in the augmentation of the EMG activity of gastrocnemius soleus muscles, but also in the restoration of EMG suppression, which was induced by previous injection of carbachol into the NRPo. Extensor and flexor monosynaptic reflex responses were facilitated by serotonin injections into the NRPo. Such reflex facilitation was not induced by serotonin injections into the mesencephalic or the medullary reticular formation. Intrapontine serotonin injections resulted in membrane depolarization of extensor and flexor MNs with decreases in input resistance and rheobase. Spontaneous depolarizing synaptic potentials (EPSPs) increased in both frequency and amplitude. Peak voltage of Ia monosynaptic EPSPs also increased. Serotonin injections which followed carbachol injections resulted in membrane depolarization of MNs along with an increase in the frequency of spontaneous EPSPs and a decrease in carbachol-induced inhibitory postsynaptic potentials. Following pontine carbachol injections, antidromic and orthodromic responses in MNs were suppressed. Discharges of MNs evoked by intracellular current injections were also suppressed, but were restored following serotonin injections. These results indicate that postsynaptic excitation, presynaptic facilitation and disinhibition (withdrawal of postsynaptic inhibition) simultaneously act on the hindlimb MNs during serotonin-induced postural augmentation and restoration.
1. The time course of the changes in presynaptic inhibition of Ia fibres to soleus motoneurones has been investigated during a voluntary ramp-and-hold plantar flexion. 2. Monosynaptic Ia facilitation of the soleus H reflex was evoked by stimulation of the inferior soleus (homonymous) and femoral (heteronymous) nerves. Changes in presynaptic inhibition of the Ia fibres mediating the conditioning volleys were inferred from changes in the amount of reflex facilitation evoked by such constant conditioning stimulations. 3. At the beginning of the voluntary contraction, both homonymous and heteronymous Ia facilitations were markedly increased with respect to their rest values. Then, they dropped abruptly in the middle of the ramp, whatever the ramp duration. 4. The stronger the contraction at the end of the ramp, the larger the initial increase in reflex facilitation. 5. These results indicate that presynaptic inhibition of Ia terminals on motoneurones of the contracting muscle is decreased during the first half of the ramp and then returns to its rest level. It is argued that these changes in presynaptic inhibition are centrally programmed, and it is suggested that, under certain conditions, presynaptic inhibition can be modulated according to both the strength and timing of the contraction. 6. The functional role of the resulting changes in the gain of the stretch reflex is discussed.
Studies in rats have shown that the polysynaptic flexor reflex (FR) but not the monosynaptic reflexes are affected by N-methyl-D-aspartate (NMDA) receptor antagonists. Theoretically, the suppression of FR might be caused by an alteration of the spinal nociceptive neurons. To investigate, whether the non-competitive NMDA receptor antagonist memantine interferes with nociception in man, we studied both its effect on pain perception and on FR. In a double-blind study 14 male subjects were randomly assigned to either placebo or memantine (30 mg p.o.) treatment. H-reflex (HR) and FR as well as pain and tolerance threshold were determined prior to and 6 h after drug intake. Contrary to expectations, there were no differential treatment effects either on FR threshold and magnitude or on pain and tolerance thresholds or the HR amplitude.
The ganglionic blocking effects of the secondary and tertiary amines, mecamylamine and pempidine, on the spinal reflex of cats of both sexes were investigated. These blocking effects were then compared with findings in the quaternary ammonium compounds such as tetraethylammonium (TEA) and decamethonium (C10). Mecamylamine (5 mg/kg) and pempidine (1 mg/kg) inhibited spinal reflex potentials such as the monosynaptic reflex (MSR), the polysynaptic reflex (PSR) and the dorsal root reflex (DRR). Maximal inhibition occurred 40 min after intravenous administration these drugs. In the case of mecamylamine, the inhibited potentials recovered gradually after reaching the maximum inhibition. However, the inhibitory effect of pempidine was prolonged, and recovery of the potentials did not occur for 6 min or longer. Although 10 mg/kg of C10 and 0.025 mg/kg of nicotine transiently inhibited the MSR and PSR, these compounds had no effect on the DDR. TEA produced prolonged inhibition of the MSR and PSR, and slightly enhanced the DRR. These results demonstrated the differences in DRR responses to secondary and tertiary amines, and quaternary ammoniums.
The properties and development of the stretch reflex pathway were investigated in new-born and fetal rats using the isolated spinal cord-hind limb preparation. Muscle afferent discharge was elicited by small stretch of the triceps surae muscle in the new-born rat and in the fetus. It appeared as early as embryonic day 18.5. Ramp-and-hold stretch elicited only phasic discharges in most afferent fibres. A phasic reflex response was evoked in the triceps surae muscle by brief or ramp-and-hold stretch of the muscle in the new-born rat. The threshold stretch required for evoking the reflex response was close to that for eliciting the afferent discharge. A reflex response in the triceps surae muscle was also evoked by electrical stimulation of the triceps surae muscle nerve or the sciatic nerve in the new-born rat. Excitatory post-synaptic potentials (e.p.s.p.s) in the triceps surae motoneurones were evoked by stimulation of the muscle nerve in the new-born rat. The amplitude of the e.p.s.p.s was large enough to generate spike potentials. Homonymous e.p.s.p.s were significantly larger than heteronymous e.p.s.p.s. The amplitudes of the e.p.s.p.s were very susceptible to the rate of stimulus repetition. At a stimulus frequency of 10 Hz they were depressed to less than 10% of the control value. Presynaptic impulses evoked by stimulation of afferents in the muscle nerve appear in the motor nucleus less than 1.0 ms before the onset of synaptically evoked field potentials. The interval between the arrival of impulses evoked by dorsal root stimulation and the onset of e.p.s.p.s in motoneurones was 0.56 +/- 0.16 ms, indicating monosynaptic transmission from the primary afferents to the motoneurones. In the fetus, a reflex response in the triceps surae muscle was observed following a small stretch of the muscle (or electrical stimulation of the sciatic nerve) in all preparations at embryonic day 20.5 and in about half of those examined at embryonic day 19.5. Neither stimulation evoked a reflex response at embryonic day 18.5. Latencies of the reflex responses evoked by muscle stretch or by nerve stimulation were similar to those in the new-born rat. It is concluded that the monosynaptically evoked stretch reflex response in the triceps surae muscle first appear at embryonic day 19.5. Natural and electrical stimulation of the plantar skin evoked a reflex response with long latencies in flexor muscles. Such a cutaneous reflex was first present at embryonic day 17.5, two days earlier than the onset of the stretch reflex.