1,721,129 research outputs found

    KINETIC ENERGY RECOVERY DEVICE FOR A VEHICLE AND VEHICLE COMPRISING SUCH A KINETIC ENERGY RECOVERY DEVICE

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    A kinetic energy recovery device (10; 110) for a vehicle provided with at least of one wheel (4) having a hub (6), it comprises at least one elastic accumulator (11; 111), which is configured for accumulating kinetic energy in the form of elastic energy, and comprises a mobile portion (20; 120, 127, 128); and at least one driving device (12; 112), which is coupled to the mobile portion (20, 120, 127, 128) of the elastic accumulator (11; 111) and the hub (6) and is configured to convert the movement of the mobile portion (20; 120, 127, 128) of the elastic accumulator. (11; 111) into a rotary motion of the hub (6) in the direction of travel of the vehicle (1); the driving device (12; 112) is provided with a first cable (75) provided with a first head (78) coupled to the mobile portion (20, 120, 127, 128) of the elastic accumulator (11; 111); and a free-wheeling element (76), which is coupled to a second head (79) of the first cable (75) and is configured in such a way that winding the first cable in a first sense (Ml) without transmitting a rotary motion to the hub (6) and to unwind the first cable (75) in a second sense (M2) opposite the first sense (Ml) and to transmit a rotary motion to the hub ( 6)

    Error signals as powerful stimuli for the operant conditioning-like process of the fictive respiratory output in a brainstem–spinal cord preparation from rats

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    Proprioceptive input induced operant conditioning-like process on respiratory activity in vitro. Afferences contingent on respiratory bursts increase their frequency and amplitude. Long and short term effects are described. Diaphragmatic proprioceptive inputs represent unconditioned stimuli with hedonic features. A forward model is assumed to interpret the results

    Error signals as powerful stimuli for the operant conditioning-like process of the fictive respiratory output in a brainstem-spinal cord preparation from rats

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    Abstract Respiratory neuromuscular activity needs to adapt to physiologic and pathologic conditions. We studied the conditioning effects of sensory fiber (putative Ia and \{II\} type from neuromuscular spindles) stimulation on the fictive respiratory output to the diaphragm, recorded from \{C4\} phrenic ventral root, of in-vitro brainstem-spinal cord preparations from rats. The respiratory burst frequency in these preparations decreased gradually (from 0.26 ± 0.02 to 0.09 ± 0.003 burst s−1 ± SEM) as the age of the donor rats increased from zero to 4 days. The frequency greatly increased when the pH of the bath was lowered, and was significantly reduced by amiloride. \{C4\} low threshold, sensory fiber stimulation, mimicking a stretched muscle, induced a short-term facilitation of the phrenic output increasing burst amplitude and frequency. When the same stimulus was applied contingently on the motor bursts, in an operant conditioning paradigm (A 500 ms pulse train with a delay of 700 ms from the beginning of the burst) a strong and persistent (> than 1 hour) increase in burst frequency was observed (from 0.10 ± 0.007 to 0.20 ± 0.018 burst s−1). Conversely, with random stimulation burst frequency increased only slightly and declined again within minutes to control levels after stopping stimulation. A forward model is assumed to interpret the data, and the notion of error signal, i.e. the sensory fiber activation indicating an unexpected stretched muscle, is re-considered in terms of the reward/punishment value. The signal, gaining hedonic value, is reviewed as a powerful unconditioned stimulus suitable in establishing a long-term operant conditioning-like process

    Inhibitory action of acetylcholine, baclofen and GTP-gamma-S on calcium channels in adult rat sensory neurons

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    High- and low-voltage activated calcium channel currents (HVA and LVA) were inhibited by acetylcholine (10-100-mu-M) and baclofen (10-mu-M) in adult rat sensory neurons. This modulatory effect was present on dihydropyridine (nifedipine 1-mu-M) and/or omega-conotoxin (3.2-mu-M, 2-5 h incubation) insensitive components and was insensitive to holding potentials (V(h) -50 to -90 mV). GTP-gamma-S (100-mu-M) prolonged calcium channel current activation in a time- and voltage-dependent manner. On the other hand, the current amplitude reduction induced by muscarinic and GABA(B) receptor activation, was not relieved by a 50-ms conditioning prepulse to +50 mV. This suggests the possibility of an alternative voltage-independent modulation mechanism

    Prefazione alla prima edizione italiana

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    Prefazione alla prima edizione italiana di Sviluppo del Sistema Nervos

    Effects of extracellular Ca2+ on membrane and seal resistance in patch-clamped rat thalamic and sensory ganglion neurons

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    We studied the effects of [Ca2+]ext changes on seal resistance in patch-clamp experiments. Recordings were made on rat peripheral and thalamic neurons. Increasing [Ca2+]ext from 0.5 to 4.5 mM, reduced the ionic currents evoked at potentials from -100 to +50 mV, in cell-attached recordings, in all the neurons tested. The effect was greater at negative potentials. The change in seal conductance (deltaG) decreased with higher resistance seals and became very low over 1 Gohm (<0.5 nS). However, the ratio deltaG/G(0.5 Ca2+) rose from close to 0 up to 0.6, indicating that Ca2+ has a stronger effect when the microelectrode and the membrane are sealed more tightly. These findings suggest that changes in seal resistance may be misleading in experiments in which extracellular Ca2+ changes are used

    Colture cellulari e loro applicazioni in neurobiologia

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    La comprensione delle complesse interazioni tra il genoma e l'ambiente, che portano alla formazione di un nuovo individuo e quindi del suo sistema nervoso, e la fisiologia di quest'ultimo, a maturazione completata, è condizione indispensabile per affrontare lo studio delle malattie neurologiche e probabilmente anche per la comprensione di alcune patologie psichiatrich
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