Journal of neurophysiology
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We investigated the hypoxia-induced disturbance of cytosolic sodium concentration ([Na+]i) and of cytosolic calcium concentration ([Ca2+]i) in dopamine neurons of the substantia nigra pars compacta in rat midbrain slices, by combining whole cell patch-clamp recordings and microfluorometry. Transient hypoxia (3-5 min) induced an outward current (118.7 +/- 15.1 pA, mean +/- SE; VH = -60 mV). The development of this outward current was associated with an elevation in [Na+]i and in [Ca2+]i. ⋯ Decreasing the concentration of extracellular Na+ to 19.2 mM depressed the hypoxia-induced outward current and resulted in a decrease in resting [Na+]i. Under this condition hypoxia still increased [Na+]i, albeit to levels not exceeding those of resting [Na+]i observed under control conditions. We conclude that 1) a major component of the hypoxia-induced outward current of these cells is caused by a depletion of intracellular ATP in combination with an increase in [Na+]i, 2) that the [Na+]i and [Ca2+]i responses are not mediated by glutamate receptors, 3) that the [Na+]i and [Ca2+]i responses are not depressed by activation of sulfonylurea receptors, and 4) that the rise in [Na+]i induced by short-lasting hypoxia is not due to a ATP depletion-induced failure of Na+ extrusion.
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Physiological survey of medullary raphe and magnocellular reticular neurons in the anesthetized rat.
The present study was designed to provide a detailed and quantitative description of the physiological characteristics of neurons in the medullary raphe magnus (RM) and adjacent nucleus reticularis magnocellularis (NRMC) under anesthetized conditions. The background discharge and noxious stimulus-evoked responses of RM and NRMC neurons were recorded in rats lightly anesthetized with isoflurane. All cells that were isolated successfully were studied. ⋯ Although many cells discharged too infrequently to be classified, units with physiological properties that were different from those described above were rare. In conclusion, most RM and NRMC cells belong to three nonserotonergic physiological cell classes that can be distinguished from each other by the consistency, not the magnitude, of their responses to repeated noxious thermal stimulation. Because most of the heat-evoked change in and cell discharge occurs after the conclusion of the initial motor withdrawal, ON and OFF cells are likely to principally modulate the response to subsequent noxious insults.
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Neurons in the central nucleus of the inferior colliculus (ICc) typically respond with phase-locked discharges to low rates of sinusoidal amplitude-modulated (SAM) signals and fail to phase-lock to higher SAM rates. Previous studies have shown that comparable phase-locking to SAM occurs in the dorsal nucleus of the lateral lemniscus (DNLL) and medial superior olive (MSO) of the mustache bat. The studies of MSO and DNLL also showed that the restricted phase-locking to low SAM rates is created by the coincidence of phase-locked excitatory and inhibitory inputs that have slightly different latencies. ⋯ In none of the cells that we tested did the application of AP5 by itself, or in combination with bicuculline, cause an increase in the range of SAM rates that evoked phase-locking. These results illustrate that the same response property, phase-locking restricted to low SAM rates, is formed in more than one way in the auditory brain stem. In the MSO and DNLL, the mechanism is coincidence of phase-locked excitation and inhibition, whereas in ICc the same response feature is formed by a different but unknown mechanism.
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To characterize muscle synergy organization underlying multidirectional control of stance posture, electromyographic activity was recorded from 11 lower limb and trunk muscles of 7 healthy subjects while they were subjected to horizontal surface translations in 12 different, randomly presented directions. The latency and amplitude of muscle responses were quantified for each perturbation direction. Tuning curves for each muscle were examined to relate the amplitude of the muscle response to the direction of surface translation. ⋯ The results suggest that neither a simple reflex mechanism nor a fixed muscle synergy organization is adequate to explain the muscle activation patterns observed in this postural control task. Our results are consistent with a centrally mediated pattern of muscle latencies combined with peripheral influence on muscle magnitude. We suggest that a flexible continuum of muscle synergies that are modifiable in a task-dependent manner be used for equilibrium control in stance.
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Whole cell voltage- and current-clamp recordings were carried out to investigate the effects of clonidine, an alpha 2-adrenoceptor agonist, in L4 and L5 dorsal root ganglion (DRG) neurons of the rat. In voltage-clamp mode, application of 20 microM clonidine reversibly reduced the inward current evoked by hyperpolarizing voltage steps. The "clonidine-sensitive current" was obtained by subtracting the current during clonidine application from the control current, and its properties were as follows. 1) It was a slowly activating inward current evoked by hyperpolarization. 2) The reversal potential in the standard extracellular solution ([K+]o = 5 mM, [Na+]o = 151 mM) was -38.3 mV, and reduction of [Na+]o shifted it to a more negative potential, whereas an increase of [K+]o shifted it to a more positive potential, indicating that the current was carried by Na+ and K+ (PNa/PK = 0.22). 3) The relationship between the chord conductance underlying the clonidine-sensitive current and voltage could be fitted by a Boltzmann equation. ⋯ Injection of a hyperpolarizing current pulse produced time-dependent rectification in DRG neurons that exhibited Ih, and clonidine blocked this rectification in all intact and transected neurons tested. These results suggest that inhibition of Ih due to alpha 2-adrenoceptor activation contributes to modulation of DRG neuronal activity in rats. On the basis of our findings, we discuss the possible mechanisms whereby sympathetically released norepinephrine modulates the abnormal activity of DRG neuronal cell bodies after nerve injury.