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  • 1995-1999  (2)
  • 1
    ISSN: 1573-899X
    Keywords: Long-term potentiation ; motor cortex ; somatosensory cortex (SCx) ; thalamus ; ventrolateral nucleus (VL) ; cat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Experiments on anesthetized cats were used to study the activity of motor cortex neurons (field 4γ) in response to separate and simultaneous stimulation of the ventrolateral nucleus of the thalamus and the somatosensory cortex (field 2) of the brain. Long-term potentiation of motor cortex neuron activity in response to simultaneous stimulation of the ventrolateral nucleus and somatosensory cortex arose only in regions receiving corticocortical projections from the stimulation site in the somatosensory cortex of the brain, while regions lacking corticocortical projections from the somatosensory cortex showed no such effect. Experiments demonstrated that the duration of increased motor cortex neuron activity following stimulation of the ventrolateral nucleus of the thalamus and somatosensory cortex was greater than one hour after recording was started. These data led to the conclusion that simultaneous stimulation of corticocortical and thalamocortical afferents can alter the level of neuronal activity in the motor cortex only in regions with convergent sensory inputs from the thalamus and somatosensory cortex of the brain.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary  Although surfactant-secreting type II alveolar cells have been shown to be damaged during influenzavirus pneumonia, little is known about the effects of surfactant replacement therapy. We have developed a mouse influenza model, in which viral infection can be localized to the upper respiratory tract or to both the upper and lower respiratory tract depending on the volume (rather than infectious dose) of intranasal inocula of influenzavirus. In this model, only mice infected with a large inocula die with massive infection in the lung. Using this model, we unexpectedly found that intranasal administration of surfactant dramatically exacerbated influenzavirus infection causing fatal disease even in mice inoculated with a small inocula. This exacerbation resulted from enhancement of intrabronchial and intraalveolar spread of virus, as confirmed by immunohistochemical detection of viral antigen in lungs. Assuming this experimental model in mice recapitulates naturally occurring disease in humans, extreme caution is warranted in surfactant-replacement treatment of influenzavirus pneumonia in humans.
    Type of Medium: Electronic Resource
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