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  • Cuneate nucleus  (1)
  • thalamic intralaminar nuclei  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 39 (1980), S. 327-340 
    ISSN: 1432-1106
    Keywords: Slow waves ; Unitary activity ; Cuneate nucleus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Depth profiles of averaged evoked potentials (AEPs) and simultaneously generated unitary activity have been recorded from the cuneate nucleus of the rat in response to controlled tactile stimulation of the ipsilateral forepaw. Four separate components of the AEPs were isolated, N1, N2, P, and N3. N1corresponds to the classical N wave previously described by other workers; four fractions of N1 are described. The classical P wave which follows N1 reverses at 150–350 μm depth to become a negative wave of identical time course, the N2 wave, at deeper locations. N2 peaks deeper than N1 within the non-relay portion of the cuneate nucleus, or below in the subnuclear reticular førmation where it is the only significant evoked component. Its strong susceptibility to high Mg++ C.S.F. superperfusion suggests a polysynaptic origin. It is argued that the depth distribution and time course of N2 does not support its function relating to depolarisation of primary afferents (PAD) in the vicinity of synaptically driven cuneate cells. Alternative possibilities for its origin are discussed. An additional sustained component of the AEP, the N3 component, is described and evaluated. N3 is co-extensive with N1, has a long time course and simple exponential decay, and is the component most resistant to high Mg++ C.S.F. superperfusion. A similar component to N3 has been described by previous workers in the spinal cord, where it has been shown to arise from glia depolarised by K+ effluxing from discharging afferents and cells. A similar origin for N3 is suggested, and its possible involvement with PAD discussed.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Metabolic brain disease 3 (1988), S. 91-124 
    ISSN: 1573-7365
    Keywords: thiamine deficiency ; thalamic intralaminar nuclei ; neocortex ; synchronous burst spontaneous activity ; excitotoxic brain lesions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Dietary thiamine deficiency, enhanced by pyrithiamine administration in adult rats, produces overt lesions in the brain that are especially prominent in the thalamus. The present study was undertaken to determine whether the thalamic lesions could be correlated with alterations in the physiological properties of neurons in the thalamus and somatosensory cortex. The regimen for experimentally inducing thiamine deficiency produced large lesions in the thalamus of every case; the lesions included most, if not all, of the neurons in the intralaminar thalamic nuclei. The extent of the lesion in the intralaminar thalamus was highly correlated with the loss of bilaterally synchronous spontaneous activity in the cerebral cortex. This correlation was seen in animals analyzed as early as 1–18 hr after the appearance of opisthotonus, the crisis state of thiamine deficiency, and as late as 2–9 weeks of recovery following thiamine replacement therapy. The loss of bilateral synchronous bursting neuronal activity following intralaminar thalamic lesions is consistent with the proposed role of the intralaminar thalamus as a pacemaker for rhythmic cortical activity (Armstrong-Jameset al.,Exp. Brain Res., 1985; Fox and Armstrong-James,Exp. Brain Res. 63: 505–518, 1986). The location and size of the central lesions within the thalamus suggest that the observed neuronal loss could result from a nonhemorrhagic infarction in the ventromedial branches of the superior cerebellar arteries. Experimental thiamine deficiency also produced alterations in the receptive field properties of the somatosensory cortex neurons in all animals examined. Changes in cortical receptive field properties were correlated with the destruction of sensory relay neurons in the thalamic ventrobasal complex. The loss of the central lateral thalamic input to the cortex and the loss of somatosensory relay neurons in the ventrobasal thalamus in experimental thiamine deficiency produce alterations in cortical function which may contribute to deficits in memory and cognition analogous to those which characterize Korsakoff's psychosis in humans.
    Type of Medium: Electronic Resource
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