Introduction Since the outbreak of coronavirus disease 2019 (COVID-19), more than 3000 (including clinical diagnosis) healthcare workers (HCWs) have been infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in China. This study is aimed to investigate the risk perception and immediate psychological state of HCWs in the early stage of the COVID-19 epidemic. Methods This study utilized a cross-sectional survey designed on a convenient sample of 4357 HCWs in China. Its data were collected using anonymous structured questionnaires distributed through social software. 6 questions were set to evaluate the participants' risk perception of COVID-19, and a General Health Questionnaire was used to identify the participants' immediate psychological status. Descriptive statistics were used for data analysis. Risk perception and psychological status were compared by demographic characteristics and COVID-19 exposure experiences. Result A total of 4,600 questionnaires were distributed, and 4,357 qualified ones (94.7%) were collected. The main concerns of HCWs are: infection of colleagues (72.5%), infection of family members (63.9%), protective measures (52.3%) and medical violence (48.5%). And 39.1% of the HCWs had psychological distress, especially working in Wuhan, participating in frontline treatments, having been isolated and having family members or colleagues infected. Conclusions The finding indicating that, faced with the COVID-19 epidemic, HCWs, especially in Wuhan, were worried about the risks of infection and protective measures, resulting in psychological distress, so further actions should be taken.

Spike frequency adaptation (SFA) is a fundamental property of repetitive firing in motoneurones (MNs). Early SFA (occurring over several hundred milliseconds) is thought to be important in the initiation of muscular contraction. To date the mechanisms underlying SFA in spinal MNs remain unclear. In the present study, we used both whole-cell patch-clamp recordings of MNs in lumbar spinal cord slices prepared from motor functionally mature mice and computer modelling of spinal MNs to investigate the mechanisms underlying SFA. Pharmacological blocking agents applied during whole-cell recordings in current-clamp mode demonstrated that the medium AHP conductance (apamin), BK-type Ca 2+ -dependent K + channels (iberiotoxin), voltage-activated Ca 2+ channels (CdCl 2 ), M-current (linopirdine) and persistent Na + currents (riluzole) are all unnecessary for SFA. Measurements of Na + channel availability including action potential amplitude, action potential threshold and maximum depolarization rate of the action potential were found to correlate with instantaneous firing frequency suggesting that the availability of fast, inactivating Na + channels is involved in SFA. Characterization of this Na + conductance in voltage-clamp mode demonstrated that it undergoes slow inactivation with a time course similar to that of SFA. When experimentally measured parameters for the fast, inactivating Na + conductance (including slow inactivation) were incorporated into a MN model, SFA could be faithfully reproduced. The removal of slow inactivation from this model was sufficient to remove SFA. These data indicate that slow inactivation of the fast, inactivating Na + conductance is likely to be the key mechanism underlying early SFA in spinal MNs.

Electrical stimulation of the brainstem in paralysed decerebrate cats evokes a centrally generated pattern of motor output (fictive locomotion) that has many of the characteristics of overground locomotion in adult quadripedal mammals (see Rossignol, 1996). During fictive locomotion, motoneurones innervating limb muscles receive alternating excitatory and inhibitory synaptic currents from the central pattern generator (CPG) for locomotion (Jordan, 1983). These result in the rhythmic fluctuations of membrane potential (locomotor drive potentials, LDPs) that underlie the patterned activation of motoneurones during locomotion. The transformation of rhythmic excitatory drive into trains of action potentials is governed by the passive and active membrane properties of motoneurones. It is now known that some of these properties are altered during locomotion. For example, the post-spike afterhyperpolarization (AHP) is reduced in motoneurones during fictive locomotion (Brownstone et al. 1992;Schmidt, 1994) and there is the appearance of a voltagedependent excitatory current (Brownstone et al. 1994). This voltage-dependent excitation results in non-linear responses of motoneurones to depolarizing currents, which may facilitate the recruitment of motoneurones, or augment motoneuronal output evoked by reflex or central excitation (Brownstone et al. 1994;McCrea et al. 1997;Bennett et al. 1998). These changes in motoneurone membrane properties result in increased motoneuronal firing in response to intracellular current injection during fictive locomotion (Brownstone et al. 1992;. The fictive locomotor state thus appears to include processes that increase the excitability of hindlimb motoneurones.The membrane potential at which action potentials are initiated in response to sufficient depolarizing currents (the voltage threshold, V th ) is not a fixed value in motoneurones. For example, V th tends to be higher (more depolarized) in higher rheobase motoneurones (Gustafsson & Pinter, 1984) 1. Experiments were conducted on decerebrate adult cats to examine the effect of brainstemevoked fictive locomotion on the threshold voltage (V th ) at which action potentials were initiated in hindlimb motoneurones. Measurements of the voltage threshold of the first spike evoked by intracellular injection of depolarizing ramp currents or square pulses were compared during control and fictive locomotor conditions. The sample of motoneurones included flexor and extensor motoneurones, and motoneurones with low and high rheobase currents.2. In all 38 motoneurones examined, action potentials were initiated at more hyperpolarized membrane potentials during fictive locomotion than in control conditions (mean hyperpolarization _8.0 ± 5.5 mV; range _1.8 to _26.6 mV). Hyperpolarization of V th occurred immediately at the onset of fictive locomotion and recovered in seconds (typically < 60 s) following the termination of locomotor activity.3. The V th of spikes occurring spontaneously without intracellular current injection was also reduced during loc...

Key points• Locomotor training of rats held in an upright posture has been used recently to restore locomotion after spinal cord injury. Our results show that the upright posture alone improves locomotor recovery in spinal rats.• This improvement is reversed by the removal of cutaneous afferent feedback from the paw, showing that sensory feedback from the foot facilitates the spinal central pattern generator (CPG) for locomotion.• 5-HT 2 and 5-HT 1A/7 agonists improve locomotion in the horizontal posture but can impair locomotion in the upright posture, suggesting that a proper balance of afferent feedback from the foot and 5-HT receptor activation is necessary for optimal locomotor recovery.• Our results provide new insights into the organization of the CPG for locomotion and the evolution of hominid bipedalism. The potent effects of cutaneous afferents from the paw revealed here must be taken into account in the design of strategies to restore locomotion after spinal cord injury.Abstract Recent studies on the restoration of locomotion after spinal cord injury have employed robotic means of positioning rats above a treadmill such that the animals are held in an upright posture and engage in bipedal locomotor activity. However, the impact of the upright posture alone, which alters hindlimb loading, an important variable in locomotor control, has not been examined. Here we compared the locomotor capabilities of chronic spinal rats when placed in the horizontal and upright postures. Hindlimb locomotor movements induced by exteroceptive stimulation (tail pinching) were monitored with video and EMG recordings. We found that the upright posture alone significantly improved plantar stepping. Locomotor trials using anaesthesia of the paws and air stepping demonstrated that the cutaneous receptors of the paws are responsible for the improved plantar stepping observed when the animals are placed in the upright posture. We also tested the effectiveness of serotonergic drugs that facilitate locomotor activity in spinal rats in both the horizontal and upright postures. Quipazine and (±)-8-hydroxy-2-(dipropylamino)tetralin hydrobromide (8-OH-DPAT) improved locomotion in the horizontal posture but in the upright posture either interfered with or had no effect on plantar walking. Combined treatment with quipazine and 8-OH-DPAT at lower doses dramatically improved locomotor activity in both postures and mitigated the need to activate the locomotor CPG with exteroceptive stimulation. Our results suggest that afferent input from the paw facilitates the spinal CPG for locomotion. These potent effects of afferent input from the paw should be taken into account when interpreting the results obtained with rats in an upright posture and when designing interventions for restoration of locomotion after spinal cord injury.

Evidence is presented that one locus of adaptation in the "neural adaptations to training" is at the level of the alpha-motoneurons. With increased voluntary activity, these neurons show evidence of dendrite restructuring, increased protein synthesis, increased axon transport of proteins, enhanced neuromuscular transmission dynamics, and changes in electrophysiological properties. The latter include hyperpolarization of the resting membrane potential and voltage threshold, increased rate of action potential development, and increased amplitude of the afterhyperpolarization following the action potential. Many of these changes demonstrate intensity-related adaptations and are in the opposite direction under conditions in which chronic activity is reduced. A five-compartment model of rat motoneurons that innervate fast and slow muscle fibers (termed "fast" and "slow" motoneurons in this paper), including 10 active ion conductances, was used to attempt to reproduce exercise training-induced adaptations in electrophysiological properties. The results suggest that adaptations in alpha-motoneurons with exercise training may involve alterations in ion conductances, which may, in turn, include changes in the gene expression of the ion channel subunits, which underlie these conductances. Interestingly, the acute neuromodulatory effects of monoamines on motoneuron properties, which would be a factor during acute exercise as these monoaminergic systems are activated, appear to be in the opposite direction to changes measured in endurance-trained motoneurons that are at rest. It may be that regular increases in motoneuronal excitability during exercise via these monoaminergic systems in fact render the motoneurons less excitable when at rest. More research is required to establish the relationships between exercise training, resting and exercise motoneuron excitability, ion channel modulation, and the effects of neuromodulators.