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Ghrelin, a gastrointestinal hormone, is a modulator of the sense of smell. The main source of ghrelin in the central nervous system has been mainly observed in specific populations of hypothalamic neurons. An increasing number of studies have reported ghrelin synthesis and its effect on neurons outside the hypothalamus. Ghrelin and its receptors are expressed in the olfactory bulbs and in other centres of the brain, such as the amygdala, for processing olfactory signals, pyramidal neurons of the cerebral cortex and the dorsal vagal complex of the medulla oblongata. It is known that ghrelin is involved in cognitive mechanisms and eating behaviours, in fact, its expression increases in anticipation of food intake. In order to identify the existence of centrifugal direct afferents from the main olfactory bulb to the medial amygdala and the hypothalamus arcuate nucleus, in this work we used two retrograde tracers, Dil and Fluoro Gold, and immunohistochemical procedure to visualize positive ghrelin neurons. Our paper provides neuroanatomic support for the ghrelin modulation of smell. Our results show that ghrelin neuron projections from mitral cells of bulbs can transmit olfactory information via branching connections to the amygdala and the hypothalamus. This pathway could play an important role in regulating feeding behaviour in response to odours. [ABSTRACT FROM AUTHOR]

In this paper, we outline some important milestones in the history of the term “plasticity” in reference to the nervous system. Credit is given to William James for first adopting the term to denote changes in nervous paths associated with the establishment of habits; to Eugenio Tanzi for first identifying the articulations between neurons, not yet called synapses, as possible sites of neural plasticity; to Ernesto Lugaro for first linking neural plasticity with synaptic plasticity; and to Cajal for complementing Tanzi’s hypothesis with his own hypothesis of plasticity as the result of the formation of new connections between cortical neurons. Cajal’s early use of the word plasticity is demonstrated, and his subsequent avoidance of the term is tentatively accounted for by the fact that other authors extended it to mean neuronal reactions partly pathological and no doubt quite different from those putatively associated with normal learning. Evidence is furnished that in the first two decades of the twentieth century the theory was generally accepted that learning is based on a reduced resistance at exercized synapses, and that neural processes become associated by coactivation. Subsequently the theory fell in disgrace when Lashley’s ideas about mass action and functional equipotentiality of the cortex tended to outmode models of the brain based on orthodox neural circuitry. The synaptic plasticity theory of learning was rehabilitated in the late 1940s when Konorski and particularly Hebb argued successfully that there was no better alternative way to think about the modifiability of the brain by experience and practice. Hebb’s influential hypothesis about the mechanism of adult learning contained elements strikingly similar to the early speculations of James, Tanzi and Cajal, but Hebb did not acknowledge specifically these roots of his thinking about the brain, though he was fully aware that he had resurrected old ideas wrongly neglected for a long time. Lately the concept of neural plasticity has been complicated by attributing considerably different meanings to it. A scholarly paper by Paillard is used to show how an analysis in depth can clarify some confusion engendered by an unrestricted use of the concept and term of neural plasticity. [ABSTRACT FROM AUTHOR]

When using visual and proprioceptive information to plan a reach, it has been proposed that the brain combines these cues to estimate the object and/or limb's location. Specifically, according to the maximum-likelihood estimation (MLE) model, sensory inputs are combined such that more reliable inputs are assigned a greater weight (Ernst and Banks in Nature 415:429-433, ). In this paper, we examined if the brain is able to adjust which sensory cue it weights the most. Specifically, we asked if the brain changes how it weights sensory information when the availability of a visual cue is manipulated. Twelve healthy subjects reached to visual (V), proprioceptive (P), or visual + proprioceptive (VP) targets under different visual delay conditions (e.g., on V and VP trials, the visual target was available for the entire reach; it was removed with the go signal, or it was removed 1 s before the go signal). To establish which sensory cue subjects weighted the most, we compared endpoint positions achieved on V and P reaches to VP reaches. Results indicated that subjects combined visual and proprioceptive cues in accordance with the MLE model when reaching to VP targets. Moreover, subjects' reaching errors to visual targets increased with longer visual delays (particularly in the vertical direction). However, there was no change in reach variability with longer delays, and subjects did not reweight visual information as the availability of visual information was manipulated. Thus, a change in visual environment is not sufficient to cause the brain to reweight how it processes sensory information. [ABSTRACT FROM AUTHOR]

In the companion paper utilizing a quantitative model of optimal motor coordination (Part I, Rand and Shimansky, in Exp Brain Res 225:55-73, ), we examined coordination between X and Y movement directions (XYC) during reaching movements performed under three prescribed speeds, two movement amplitudes, and two target sizes. The obtained results indicated that the central nervous system (CNS) utilizes a two-phase strategy, where the initial and the final phases correspond to lower and higher precision of information processing, respectively, for controlling goal-directed reach-type movements to optimize the total cost of task performance including the cost of neural computations. The present study investigates how two different well-known concepts used for describing movement performance relate to the concepts of optimal XYC and two-phase control strategy. First, it is examined to what extent XYC is equivalent to movement trajectory straightness. The data analysis results show that the variability, the movement trajectory's deviation from the straight line, increases with an increase in prescribed movement speed. In contrast, the dependence of XYC strength on movement speed is opposite (in total agreement with an assumption of task performance optimality), suggesting that XYC is a feature of much higher level of generality than trajectory straightness. Second, it is tested how well the ballistic and the corrective components described in the traditional concept of two-component model of movement performance match with the initial and the final phase of the two-phase control strategy, respectively. In fast reaching movements, the percentage of trials with secondary corrective submovement was smaller under larger-target shorter-distance conditions. In slower reaching movements, meaningful parsing was impossible due to massive fluctuations in the kinematic profile throughout the movement. Thus, the parsing points determined by the conventional submovement analysis did not consistently reflect separation between the ballistic and error-corrective components. In contrast to the traditional concept of two-component movement performance, the concept of two-phase control strategy is applicable to a wide variety of experimental conditions. [ABSTRACT FROM AUTHOR]

A quantitative model of optimal transport-aperture coordination (TAC) during reach-to-grasp movements has been developed in our previous studies. The utilization of that model for data analysis allowed, for the first time, to examine the phase dependence of the precision demand specified by the CNS for neurocomputational information processing during an ongoing movement. It was shown that the CNS utilizes a two-phase strategy for movement control. That strategy consists of reducing the precision demand for neural computations during the initial phase, which decreases the cost of information processing at the expense of lower extent of control optimality. To successfully grasp the target object, the CNS increases precision demand during the final phase, resulting in higher extent of control optimality. In the present study, we generalized the model of optimal TAC to a model of optimal coordination between X and Y components of point-to-point planar movements (XYC). We investigated whether the CNS uses the two-phase control strategy for controlling those movements, and how the strategy parameters depend on the prescribed movement speed, movement amplitude and the size of the target area. The results indeed revealed a substantial similarity between the CNS's regulation of TAC and XYC. First, the variability of XYC within individual trials was minimal, meaning that execution noise during the movement was insignificant. Second, the inter-trial variability of XYC was considerable during the majority of the movement time, meaning that the precision demand for information processing was lowered, which is characteristic for the initial phase. That variability significantly decreased, indicating higher extent of control optimality, during the shorter final movement phase. The final phase was the longest (shortest) under the most (least) challenging combination of speed and accuracy requirements, fully consistent with the concept of the two-phase control strategy. This paper further discussed the relationship between motor variability and XYC variability. [ABSTRACT FROM AUTHOR]

The central nervous system uses stereotypical combinations of the three wrist/forearm joint angles to point in a given (2D) direction in space. In this paper, we first confirm and analyze this Donders' law for the wrist as well as the distributions of the joint angles. We find that the quadratic surfaces fitting the experimental wrist configurations during pointing tasks are characterized by a subject-specific Koenderink shape index and by a bias due to the prono-supination angle distribution. We then introduce a simple postural model using only four parameters to explain these characteristics in a pointing task. The model specifies the redundancy of the pointing task by determining the one-dimensional task-equivalent manifold (TEM), parameterized via wrist torsion. For every pointing direction, the torsion is obtained by the concurrent minimization of an extrinsic cost, which guarantees minimal angle rotations (similar to Listing's law for eye movements) and of an intrinsic cost, which penalizes wrist configurations away from comfortable postures. This allows simulating the sequence of wrist orientations to point at eight peripheral targets, from a central one, passing through intermediate points. The simulation first shows that in contrast to eye movements, which can be predicted by only considering the extrinsic cost (i.e., Listing's law), both costs are necessary to account for the wrist/forearm experimental data. Second, fitting the synthetic Donders' law from the simulated task with a quadratic surface yields similar fitting errors compared to experimental data. [ABSTRACT FROM AUTHOR]

The goal of this paper was to determine if trunk antagonist activation is associated with impaired neuromuscular performance. To test this theory, we used two methods to impair neuromuscular control: strenuous exertions and fatigue. Force variability (standard deviation of force signal) was assessed for graded isometric trunk exertions (10, 20, 40, 60, 80% of max) in flexion and extension, and at the start and end of a trunk extensor fatiguing trial. Normalized EMG signals for five trunk muscle pairs ( RA rectus abdominis, EO external oblique, IO internal oblique, TE thoracic erector spinae, and LE lumbar erector spinae) were collected for each graded exertion, and at the start and end of a trunk extensor fatiguing trial. Force variability increased for more strenuous exertions in both flexion ( P < 0.001) and extension ( P < 0.001), and after extensor fatigue ( P < 0.012). In the flexion direction, both antagonist muscles (TE and LE) increased activation for more strenuous exertions ( P < 0.001). In the extension direction, all antagonist muscles except RA increased activation for more strenuous exertions ( P < 0.05) and following fatigue ( P < 0.01). These data demonstrate a strong relationship between force variability and antagonistic muscle activation, irrespective of where this variability comes from. Such antagonistic co-activation increases trunk stiffness with the possible objective of limiting kinematic disturbances due to greater force variability. [ABSTRACT FROM AUTHOR]

The present paper introduces an original biofeedback system for improving human balance control, whose underlying principle consists in providing additional sensory information related to foot sole pressure distribution to the user through a tongue-placed tactile output device. To assess the effect of this biofeedback system on postural control during quiet standing, ten young healthy adults were asked to stand as immobile as possible with their eyes closed in two conditions of No-biofeedback and Biofeedback. Centre of foot pressure (CoP) displacements were recorded using a force platform. Results showed reduced CoP displacements in the Biofeedback relative to the No-biofeedback condition. The present findings evidenced the ability of the central nervous system to efficiently integrate an artificial plantar-based, tongue-placed tactile biofeedback for controlling control posture during quiet standing. [ABSTRACT FROM AUTHOR]

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]