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Neurons in the primary somatosensory cortex (S1) respond to peripheral stimulation with synchronised bursts of spikes, which lock to the macroscopic 600 Hz EEG waves. The mechanism of burst generation and synchronisation in S1 is not yet understood. Using models of single-neuron responses fitted to unit recordings from macaque monkeys, we show that these synchronised bursts are the consequence of correlated synaptic inputs combined with a refractory mechanism. In the presence of noise these models reproduce also the observed trial-to-trial response variability, where individual bursts represent one of many stereotypical temporal spike patterns. When additional slower and global excitability fluctuations are introduced the single-neuron spike patterns are correlated with the population activity, as demonstrated in experimental data. The underlying biophysical mechanism of S1 responses involves thalamic inputs arriving through depressing synapses to cortical neurons in a high-conductance state. Our findings show that a simple feedforward processing of peripheral inputs could give rise to neuronal responses with non-trivial temporal and population statistics. We conclude that neural systems could use refractoriness to encode variable cortical states into stereotypical short-term spike patterns amenable to processing at neuronal time scales (tens of milliseconds).Significance statementNeurons in the hand area of the primary somatosensory cortex respond to repeated presentation of the same stimulus with variable sequences of spikes, which can be grouped into distinct temporal spike patterns. In a simplified model, we show that such spike patterns are product of synaptic inputs and intrinsic neural properties. This model can reproduce both single-neuron and population responses only when a private variability in each neuron is combined with a multiplicative gain shared over whole population, which fluctuates over trials and might represent the dynamical state of the early stages of sensory processing. This phenomenon exemplifies a general mechanism of transforming the ensemble cortical states into precise temporal spike patterns at the level of single neurons.

International audience; The present studies are designed to further characterise the interneuronal pathway mediating the disynaptic reciprocal group I inhibition between flexors and extensors at the wrist and the elbow levels in humans. In the first series of experiments, we compared the electrical threshold of the reciprocal group I inhibition at the wrist and the elbow level after a prolonged vibration aimed at raising the electrical threshold of the antagonistic activated Ia afferents. Prolonged vibration to the 'conditioning' tendon, which raised significantly the electrical threshold of the inhibition at the elbow level, did not alter it at the wrist level. These results suggest that the dominant input to the relevant interneurones is Ia in origin at the elbow level but Ib in origin at the wrist level. In the second series of experiments, using the spatial facilitation method, we compared the effects on the post-stimulus time histograms of single voluntarily activated motor units of two volleys delivered both separately and together to group I afferents in the nerves supplying the homonymous and antagonistic muscles. At the wrist, but not at the elbow level, the peak of homonymous monosynaptic group I excitation was reduced on combined stimulation, although the antagonistic IPSP was just at the threshold. Because the suppression did not involve the initial bins of the peak, it is argued that the suppression is not due to presynaptic inhibition of Ia terminals, but probably reflects convergence between the homonymous and antagonistic volleys onto the interneurones mediating the disynaptic inhibition. Taken together with the previously reported effects of recurrent inhibition on reciprocal inhibition, these results suggest that inhibition between flexors and extensors is differently organised at the elbow (reciprocal Ia inhibition) and the wrist (non-reciprocal group I inhibition) levels. It is argued that the particular connectivity at the wrist level might correspond to some functional requirements at this ball joint.

International audience; OBJECTIVE: Spinal reflexes from hand to wrist muscles were investigated in writer's cramp. METHODS: Stimulus-triggered rectified EMG averages after ulnar nerve and cutaneous stimulation, in wrist flexors and extensors during tonic contraction, were compared in 18 controls and 19 patients. RESULTS: On the patient dystonic side, ulnar-induced EMG suppression was decreased in wrist extensors, and facilitation in wrist flexors modified dependent on the dystonic wrist posture during writing. No change was found on the patient non-dystonic side. Cutaneous stimulation increased wrist flexor EMG on both sides of the patients with normal wrist posture during writing, but had no effect in controls and patients with abnormal wrist posture. CONCLUSIONS: Comparison between cutaneous and mixed nerve stimuli suggests that spindle afferents from intrinsic hand muscles may mediate patients' ulnar-induced EMG modulations. Abnormal proprioceptive control was only observed on dystonic side, while bilateral unusual cutaneous control was found in patients. Changes in spinal transmission were partly related to the dystonic wrist posture, suggesting that systems involved in sensory processing can be differentially altered in writer's cramp. SIGNIFICANCE: Changes in spinal transmission, probably related to peripheral and/or cortical inputs, might either take part in primary or adaptive mechanisms underlying writer's cramp.

International audience; Effects of electrical stimulation of ulnar and median nerves at wrist level were investigated in post-stimulus time histograms (PSTHs) of single motor units from both flexors and extensors in human arm and forearm. Stimulation of ulnar nerve produced late (mean extra time-after monosynaptic group Ia excitation-10.7 +/- 0.1 ms) high-threshold (>1.2 x motor threshold, MT) excitation, which was not reproduced by purely cutaneous stimulation, in all the investigated motor nuclei except in Extensor Carpi Radialis. Stimulation of median nerve, and of the skin of fingers II and III (at palmar side level), produced short latency inhibition (mean extra time 3.8 +/- 0.3 ms), which was most often truncated or followed by late excitation (mean extra time 11.8 +/- 0.3 ms); both effects were of low threshold (0.8 x MT). Short latency inhibition was very strong, and late excitation was rare and weak in almost all the investigated motor units except in those supplying flexors in forearm, in which the main effect was the late facilitation (stronger than in other motoneurones). Since extra time was not more than 13 ms, it is suggested that the late effects may be mediated through spinal pathways, at least during their 3-5 first ms. Based on the electrophysiological results and on the anatomical characteristics of ulnar and median nerves, it is assumed that ulnar-induced late high-threshold peak in PSTHs might reflect group II excitation in spinal motoneurones, and median-induced modifications in motor unit discharge, mainly cutaneous control of motoneurone discharge. Since the central delay of median-induced inhibition is longer the more caudal the motoneurone, inhibitory propriospinal-like interneurones are supposed to mediate cutaneous inhibitory control from hand upon muscles in arm and forearm. Potential roles of proprioceptive and cutaneous control from hand to more proximal musculature, provided by ulnar and median nerve, respectively, during precise hand movements are discussed.

International audience; Repetitive pairing of a peripheral stimulation with a magnetic transcortical stimulation (PAS) is widely used to induce plastic changes in the human motor cortex noninvasively. Based on the contrast between PAS-induced increase of corticospinal excitability and absence of PAS-induced increase of the spinal F wave size, it has been generally accepted that PAS-induced plasticity is cortical in origin. Here, instead of F waves, we used H reflex recruitment curves to assess spinal excitability, and we demonstrate that PAS induces parallel changes in cortical and spinal excitability.