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Notes: Modulation of responses of four types of ascending tract cells by noradrenaline and serotonin was compared in order to investigate how information forwarded by these cells may be gated by monoaminergic tract neurons. Spinocervical tract, postsynaptic dorsal column and dorsal spinocerebellar tract neurons located in Clarke's column and in the dorsal horn were identified by their axonal projections. Noradrenaline and serotonin were applied ionophoretically close to a selected neuron, and their effects were tested on extracellularly recorded responses of this neuron to electrical stimulation of low-threshold skin afferents and group II muscle spindle afferents. The modulatory actions of noradrenaline and serotonin were estimated from changes in the number of responses evoked by 30 successive stimuli, the minimal latencies of these responses, and their firing frequency. All four populations of ascending tract neurons investigated were modulated by serotonin and noradrenaline, but not in the same way. The responses were most often depressed by noradrenaline and facilitated by serotonin, but in some types of neuron they were affected in the same direction. Transmission from low-threshold skin and group II muscle afferents changed in the same direction in some types of neuron but in the opposite direction in other types. The results indicate that transfer of information from skin and group II muscle afferents to supraspinal centres may be gated by descending monoaminergic pathways in a highly differentiated manner, and is adjusted to the requirements of various behavioural situations.

Notes: Abstract The effects of short trains of electrical stimuli applied within the cuneiform nucleus and the subcuneiform region were examined on transmission from group I and group II muscle afferents to first-order spinal neurons. Variations in the effectiveness of transmission from these afferents were assessed from changes in the sizes of the monosynaptic component of extracellular field potentials evoked following stimulation of muscle nerves. Field potentials evoked from group II muscle afferents in the dorsal horn of the midlumbar and sacral segments and in the intermediate zone of the midlumbar segments were reduced when the test stimuli applied to peripheral nerves were preceded by conditioning stimulation of the cuneiform nucleus or the subcuneiform region. The depression occurred at conditioning-testing intervals of 20–400 ms, being maximal at intervals of 32–72 ms for dorsal horn potentials and 40–100 ms for intermediate zone potentials. At the shortest intervals, both group II and group I field potentials in the intermediate zone were depressed. Conditioning stimulation of the cuneiform nucleus depressed group II field potentials nearly as effectively as conditioning stimulation of the coerulear or raphe nuclei. We propose that the nonselective depression of transmission from group I and II afferents at short intervals is due to the activation of reticulospinal pathways by cells or fibers stimulated within the cuneiform area. We also propose that the selective depression of transmission from group II afferents at long intervals is mediated at least partly by monoaminergic pathways, in view of the similarity of the effects of conditioning stimulation of the cuneiform nucleus and of the brainstem monoaminergic nuclei and by directly applied monoamines (Bras et al. 1990). In addition, it might be caused by primary afferent depolarization mediated by non-monoaminergic fibers (Riddell et al. 1992).

Notes: Abstract  The possibility of collateral segmental actions of spinocervical tract (SCT) neurones upon interneurones with input from cutaneous and group II muscle afferents was investigated in deeply anaesthetized cats. To this end, intracellular and/or extracellular recordings were made from 35 dorsal horn and 15 intermediate zone interneurones in midlumbar segments of the spinal cord and effects of stimulation of the ipsilateral dorso-lateral funiculus (DLF) at C3 and C1 levels, i.e. below and above the lateral cervical nucleus where axons of SCT cells terminate, were compared. The stimuli applied at the C3 segment were within the range of stimuli (50–100 μA) required for antidromic activation of SCT neurones in the same experiment. Those applied at the C1 segment (200–500 μA) were at least 3 times stronger than C3 stimuli. Under the same experimental conditions, long ascending and descending tract neurones (dorsal spino-cerebellar and rubro-spinal tract neurones) with axons in the DLF were activated at similar thresholds from the C1 and C3 segments. Intracellular recordings were made from 29 interneurnoes of which 19 (65%) were dorsal horn and 10 (35%) were intermediate zone interneurones. Excitatory postsynaptic potentials (EPSPs) evoked by single stimuli applied at the C3 segment, but not the C1 segment, were found in 14 (48%) of those interneurones; their latencies (3.0–5.7 ms) and frequency following with only minimal temporal facilitation were as required for potentials being evoked monosynaptically by the fastest conducting SCT neurones. Extracellular recordings were made from 30 interneurones (24 dorsal horn and 6 intermediate zone interneurones), and in these neurones spike potentials induced from the C3, but not from the C1 segment, were evoked only by short trains of stimuli. However, their latencies from the first effective stimulus (4.3–5.4 ms) were compatible with mono- or oligosynaptically mediated collateral actions of SCT neurones. They were found in 10 (33%) of the 30 investigated interneurones. Similar effects of C3 stimuli were found in similar proportions of dorsal horn interneurones and intermediate zone interneurones. Indications were also found for synaptic actions evoked by C3 stimuli that could not be attributed to direct collateral actions of SCT neurones. In some intracellularly recorded dorsal horn interneurones, short-latency EPSPs were evoked from the C3 segment by the 2nd or 3rd stimulus in the train, but not by single stimuli. In other dorsal horn and intermediate zone interneurones, inhibitory postsynaptic potentials (IPSPs) were evoked from the C3 segment at minimal latencies (2.7–3.2 ms), which might be too short to allow their mediation via SCT neurones. We conclude that SCT neurones might be used to forward information from muscle group II and cutaneous afferents not only to neurones in the lateral cervical nucleus and via them to thalamus and cerebral cortex but also to interneurones in spinal reflex pathways. Thereby reflex actions evoked from group II and cutaneous afferents might be co-ordinated with responses mediated by supraspinal neurones. We conclude also that dorsal horn and intermediate zone mid-lumbar interneurones might contribute to the previously reported di-and poly-synaptic excitation or inhibition of postsynaptic dorsal column (PSDC), spinothalamic tract (STT) and spinomesencephalic tract (SMT) neurones by collateral actions of SCT cells. Thereby these interneurones might contribute to the co-ordination of responses mediated by various populations of supraspinal neurones.

Notes: Abstract Antispastic effects of the noradrenaline and dopamine precursor l-3,4-dihydroxyphelanine (l-dopa) were investigated in 11 subjects in which exaggerated stretch reflexes developed after spinal cord injuries. The effects were evaluated from changes in the electromyographic (EMG) response of the quadriceps muscle during tendon jerks evoked by standardized taps over the patellar tendon, in clonus and in resistance to passive movements of the limb. After administration of l-dopa, EMG responses occurring 30–150 ms after the tendon tap decreased to about 50% of control, and clinical tests revealed a marked decrease in the resistance to muscle stretches and in the degree of clonus. The effects were maximal within about 1 h. The depressive actions of l-dopa are interpreted as being exerted primarily at the spinal level, since they were evoked in paraplegics and tetraplegics. The results support the previous hypothesis that group II muscle afferents contribute to the exaggerated stretch reflex in spastic patients because l-dopa depresses transmission from group II but not from group I muscle afferents. They also indicate the possibility of using l-dopa in the treatment of spastic patients.