16 research outputs found

    Diminution of Voltage Threshold Plays a Key Role in Determining Recruitment of Oculomotor Nucleus Motoneurons during Postnatal Development

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    The size principle dictates the orderly recruitment of motoneurons (Mns). This principle assumes that Mns of different sizes have a similar voltage threshold, cell size being the crucial property in determining neuronal recruitment. Thus, smaller neurons have higher membrane resistance and require a lower depolarizing current to reach spike threshold. However, the cell size contribution to recruitment in Mns during postnatal development remains unknown. To investigate this subject, rat oculomotor nucleus Mns were intracellularly labeled and their electrophysiological properties recorded in a brain slice preparation. Mns were divided into 2 age groups: neonatal (1–7 postnatal days, n = 14) and adult (20–30 postnatal days, n = 10). The increase in size of Mns led to a decrease in input resistance with a strong linear relationship in both age groups. A well-fitted inverse correlation was also found between input resistance and rheobase in both age groups. However, input resistance versus rheobase did not correlate when data from neonatal and adult Mns were combined in a single group. This lack of correlation is due to the fact that decrease in input resistance of developing Mns did not lead to an increase in rheobase. Indeed, a diminution in rheobase was found, and it was accompanied by an unexpected decrease in voltage threshold. Additionally, the decrease in rheobase co-varied with decrease in voltage threshold in developing Mns. These data support that the size principle governs the recruitment order in neonatal Mns and is maintained in adult Mns of the oculomotor nucleus; but during postnatal development the crucial property in determining recruitment order in these Mns was not the modifications of cell size-input resistance but of voltage threshold

    Cortico-fugal output from visual cortex promotes plasticity of innate motor behaviour

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    The mammalian visual cortex massively innervates the brainstem, a phylogenetically older structure, via cortico-fugal axonal projections. Many cortico-fugal projections target brainstem nuclei that mediate innate motor behaviours, but the function of these projections remains poorly understood. A prime example of such behaviours is the optokinetic reflex (OKR), an innate eye movement mediated by the brainstem accessory optic system, that stabilizes images on the retina as the animal moves through the environment and is thus crucial for vision. The OKR is plastic, allowing the amplitude of this reflex to be adaptively adjusted relative to other oculomotor reflexes and thereby ensuring image stability throughout life. Although the plasticity of the OKR is thought to involve subcortical structures such as the cerebellum and vestibular nuclei, cortical lesions have suggested that the visual cortex might also be involved. Here we show that projections from the mouse visual cortex to the accessory optic system promote the adaptive plasticity of the OKR. OKR potentiation, a compensatory plastic increase in the amplitude of the OKR in response to vestibular impairment, is diminished by silencing visual cortex. Furthermore, targeted ablation of a sparse population of cortico-fugal neurons that specifically project to the accessory optic system severely impairs OKR potentiation. Finally, OKR potentiation results from an enhanced drive exerted by the visual cortex onto the accessory optic system. Thus, cortico-fugal projections to the brainstem enable the visual cortex, an area that has been principally studied for its sensory processing function, to plastically adapt the execution of innate motor behaviours

    Rotational Responses of Vestibular–Nerve Afferents Innervating the Semicircular Canals in the C57BL/6 Mouse

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    Extracellular recordings were made from vestibular–nerve afferents innervating the semicircular canals in anesthetized C57BL/6 mice ranging in age from 4–24 weeks. A normalized coefficient of variation was used to divide afferents into regular (CV* < 0.1) and irregular (CV* > 0.1) groups. There were three overall conclusions from this study. First, mouse afferents resemble those of other mammals in properties such as resting discharge rate and dependence of response dynamics on discharge regularity. Second, there are differences in mouse afferents relative to other mammals that are likely related to the smaller size of the semicircular canals. The rotational sensitivity of mouse afferents is approximately threefold lower than that reported for afferents in other mammals. One consequence of the lower sensitivity is that mouse afferents have a larger linear range for encoding head velocity. The long time constant of afferent discharge, which is a measure of low-frequency response dynamics, is shorter in mouse afferents than in other species. Third, juvenile mice (age 4–7 weeks) appear to lack a class of low-sensitivity, highly irregular afferents that are present in adult animals (age 10–24 weeks). By analogy to studies in the chinchilla, these irregular afferents with low sensitivities for lower rotational frequencies correspond to calyx-only afferents. These findings suggest that, although the calyx ending on to type I hair cells is morphologically complete in mice by the age of about 1 month, the physiological response properties in these juvenile animals are not equivalent to those in adults
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