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  • Cochlear nerve  (1)
  • Potassium channel  (1)
  • genetically-engineered cells  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Anatomy and embryology 195 (1996), S. 15-30 
    ISSN: 1432-0568
    Keywords: Key words Morphogenesis ; Neurofibrils ; Cochlear nerve ; Cochlear nuclei ; Inferior colliculus ; Antigen retrieval
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Morphological, electrophysiological and behavioral evidence indicates that the onset of rapid, synchronized conduction of auditory impulses occurs in the human brainstem during the 28th–29th fetal weeks. This implies that axonal connections in the brainstem auditory pathway are generated prior to this time. In order to investigate the sequence of axogenic events in the human brainstem pathway, we employed immunohistochemical techniques and an antibody to neurofilament protein. Immunostaining for axonal neurofilaments in an age-graded series of fetal brains demonstrates that a small number of cochlear nerve axons have invaded the ventral cochlear nucleus by the 16th fetal week. By this same time point, a limited number of trapezoid body-lateral lemniscus axons have reached the superior olivary complex and inferior colliculus. Between gestational weeks 16 and 26, there is marked expansion and collateralization of the ascending pathway from cochlear nerve to inferior colliculus. By week 26, ascending axons have begun to form plexuses of terminal neuropil within all of the brainstem auditory nuclei. Beginning in week 22, there is development of commissural axons (dorsal commissure of the lateral lemniscus and commissure of the inferior colliculus) and descending projections (descending collicular axons and olivocochlear bundle). This early establishment of a mature pattern of axonal connections presumably forms the basis for the appearance of myelin, acousticomotor reflexes and recordable brainstem responses by fetal week 29.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 410 (1987), S. 408-412 
    ISSN: 1432-2013
    Keywords: Potassium channel ; Transmitter release ; Nerve terminal excitability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The possibility that multiple K+ conductances are present in mammalian motor nerve terminals was investigated by measuring the differential effects of tetraethyl-ammonium (TEA) and 4-aminopyridine (4-AP) on transmitter release and on nerve terminal excitability in mouse phrenic nerve-diaphram preparations. Neither 4-AP nor TEA alter the spontaneous frequency of miniature end-plate potentials (fmepp) and therefore evidently do not affect calcium channels directly. Both 4-AP and TEA increased the quantal content of end-plate potentials (epps) evoked by nerve stimulation but the effects were not mutually exclusive; TEA continued to act in the presence of a maximally effective concentration of 4-AP. The increase in transmitter release evoked by focal polarisation of the terminal was not effected by 4-AP, whereas TEA exerted an effect consistent with a reduction in membrane conductance. Similary, threshold for nerve terminal action potential generation was not affected by 4-AP, but TEA caused a reduction in threshold and alteration of the ‘accommodation curve’ indicative of a reduction of membrane conductance. Under conditions where one would predict no contribution of calcium K+ conductance, i.e., when release was evoked by Ba2+ in the absence of Ca2+, the different and non-competing effects of TEA and 4-AP were still apparent. It is concluded, therefore, that the motor nerve terminal possesses at least two K+ conductances, not including calcium activatedg K, which may be distinguished pharmacologically.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of thermal analysis and calorimetry 49 (1997), S. 771-783 
    ISSN: 1572-8943
    Keywords: cytochrome b 5 ; genetically-engineered cells ; heat flux ; metabolic burden ; mitochondrial activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract It is claimed, though not without dispute, that genetically engineered mammalian cells grow more slowly than their progenitor cells because the recombinant gene system causes a metabolic burden. This was found to be the case for CHO cells transfected with expression vectors forcytochrome b5. The slower growth was associated with lower metabolic activity measured by heat flux and mitochondrial activity (rhodamine 123 fluorescence). The calorimetric-respirometric ratio was similar for all cell types, implying that the greater fluxes of glucose and glutamine in the recombinant cells was channelled to biosynthesis. This demand probably restricted the supply of pyruvate to the mitochondria in these cells.
    Type of Medium: Electronic Resource
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