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Spreading depression (SD) is a neurophysiological phenomenon which occurs in the grey substance of the central nervous system. SD is characterised by a wave-like spread of depressed neuronal activity, by large ion shifts between intra- and extracellular space, by cellular depolarization, and by altered optical properties of the tissue giving rise to an intrinsic optical signal (IOS). In the shadow of SD further waves are difficult to trigger and such waves spread at lower velocity than usual. In this paper we examine the temperature dependence of the duration of this recovery (refractory) period and the temperature dependence of the duration of the IOS in the chicken retina. It is shown that these SD accompanying events are strongly dependent on temperature and that they are likely to depend on the metabolic rate in the tissue. The observed correlation of the duration of the IOS with the duration of the refractory period suggests that the IOS is a good indicator for the duration of the tissue recovery. Such a correlation would be of great value to the experimentalist who must know about the duration of the refractory period: while the latter is laborious to determine, recording the IOS is convenient. [ABSTRACT FROM AUTHOR]

Motor learning is a process that extends beyond training sessions. Specifically, physical practice triggers a series of physiological changes in the CNS that are regrouped under the term 'consolidation' (Stickgold and Walker ). These changes can result in between-session improvement or performance stabilization (Walker ). In a series of three experiments, we tested whether consolidation also occurs following observation. In Experiment 1, participants observed an expert model perform a sequence of arm movements. Although we found evidence of observation learning, no significant difference was revealed between participants asked to reproduce the observed sequence either 5 min or 24 h later (no between-session improvement). In Experiment 2, two groups of participants observed an expert model perform two distinct movement sequences (A and B) either 10 min or 8 h apart; participants then physically performed both sequences after a 24-h break. Participants in the 8-h group performed Sequence B less accurately compared to participants in the 5-min group, suggesting that the memory representation of the first sequence had been stabilized and that it interfered with the learning of the second sequence. Finally, in Experiment 3, the initial observation phase was replaced by a physical practice phase. In contrast with the results of Experiment 2, participants in the 8-h group performed Sequence B significantly more accurately compared to participants in the 5-min group. Together, our results suggest that the memory representation of a skill learned through observation undergoes consolidation. However, consolidation of an observed motor skill leads to distinct behavioural outcomes in comparison with physical practice. [ABSTRACT FROM AUTHOR]

It has been postulated that the central nervous system (CNS) can tune the mechanical behavior of a joint by altering reflex stiffness in a task-dependant manner. However, most of the evidence supporting this hypothesis has come from the analysis of H-reflexes or electromyogram (EMG) responses. Changes in overall stiffness have been documented but, as yet, there is no direct evidence that the CNS can control reflex stiffness independently of the intrinsic stiffness. We have used a novel identification algorithm to estimate intrinsic and reflex stiffness and feed it back to subjects in real-time. Using this biofeedback, subjects could learn to control reflex stiffness independently of intrinsic stiffness. At low torque levels, subjects could vary their reflex stiffness gain by a factor of 4, while maintaining elastic stiffness and torque constant. EMG measurements confirmed that the contraction levels of the ankle muscles remained constant. Further experiments showed that subjects could change their reflexes rapidly on command. Thus, we conclude that the CNS can control reflex stiffness independently and so has great flexibility in adjusting the mechanical properties of a joint to meet functional requirements. [ABSTRACT FROM AUTHOR]

We studied Fos expression in the central nociceptive pathways at different sedative levels in order to clarify the central mechanism of propofol’s nociceptive action. Sprague–Dawley rats received propofol (PRO) or pentobarbital (PEN) and were divided into two groups with different doses of drug administration (light and deep sedative levels) based on the electroencephalogram analysis. Rats at each sedative level received heat stimulation to their face and Fos immunohistochemistry was performed at various brain sites. We also infused lidocaine into the jugular vein to test whether PRO directly activated nociceptors distributed in the vein. Fos expression in two major ascending pain pathways (lateral and medial systems) and descending modulatory system were precisely analyzed following intravenous (i.v.) administration of PRO or PEN. Many Fos protein-like immunoreactive (Fos protein-LI) cells were expressed in the trigeminal spinal nucleus caudalis (Vc), parabrachial nucleus, parafascicular nucleus, a wide area of the primary somatosensory cortex, anterior cingulate cortex, amygdala, periaqueductal gray, solitary tract nucleus, and lateral hypothalamus following heating of the face during PRO or PEN infusion. The number of Fos protein-LI cells was significantly greater in many Central nervous system regions during PRO infusion compared with PEN. Fos expression was significantly greater in the Vc and Periaqueductal gray following greater amount of PRO infusions compared, whereas they were significantly smaller in the Vc in the rats with PEN infusion. The Fos expression was significantly depressed following i.v. infusion of lidocaine before PRO administration. The present findings suggest that PRO is involved in the enhancement of Vc activity through direct activation of the primary afferent fibers innervating veins, resulting in pain induction during infusion. [ABSTRACT FROM AUTHOR]