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  • 1985-1989  (3)
  • Dopamine  (1)
  • Posterior laminectomy  (1)
  • dopamine  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Activity of tuberoinfundibular dopaminergic neurons and concentrations of serum prolactin in the rat following lithium administration (1988)
    Springer
    Psychopharmacology 94 (1988), S. 92-96 
    Details
    ISSN: 1432-2072
    Keywords: Dopamine ; Prolactin ; Lithium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Maintenance of rats on a lithium-containing diet for 3–21 days resulted in a suppression of prolactin (PRL) secretion in vivo and in vitro. Lithium treatment also resulted in an increase in the activity of tuberoinfundibular dopaminergic neurons, as evidenced by an increased accumulation of dihydroxyphenylalanine (DOPA) in the median eminence after inhibition of DOPA decarboxylase and an increased concentration of dopamine in the anterior pituitary gland. The accumulation of DOPA in the neurointer-mediate lobe of the pituitary gland, the prefrontal cortex, the striatum and the nucleus accumbens was also enhanced by lithium treatment. It is concluded that lithium treatment enhances the synthesis of dopamine in many brain regions and that an increased activity of tuberoinfundibular dopaminergic neurons results in an enhanced inhibitory control of PRL secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00735887
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Marked canal stenosis at the level of the atlas (1989)
    Springer
    Neuroradiology 31 (1989), S. 346-348 
    Details
    ISSN: 1432-1920
    Keywords: Cervical canal stenosis ; Cranio-cervical junction ; Spinal cord atrophy ; Posterior laminectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A 38-year-old man with severe canal stenosis at the level of the atlas is reported. The clinical manifestations were muscular weakness and wasting of the upper limbs and spastic paresis of the lower limbs, which all progressed slowly. The atlas was hypoplastic and its retrodental space was narrow. The spinal cord was markedly compressed between the odontoid process and the posterior arch of the atlas. The clinical manifestations improved after a posterior laminectomy of the atlas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00344180
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Differential effects of haloperidol, clozapine, and fluperlapine on tuberoinfundibular dopamine neurons and prolactin secretion in the rat (1987)
    Springer
    Journal of neural transmission 68 (1987), S. 227-240 
    Details
    ISSN: 1435-1463
    Keywords: Neuroleptics ; dopamine ; prolactin ; hypothalamus ; clozapine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two atypical neuroleptic agents, clozapine and fluperlapine, produced rapid elevations in plasma PRL concentrations that were similar in magnitude to those produced by haloperidol. However, the PRL response to clozapine or fluperlapine was of much shorter duration than that elicited by haloperidol. Clozapine, but neither fluperlapine nor haloperidol, produced a rapid increase in the activity of tuberoinfundibular dopamine (TIDA) neurons, as evidenced by an enhanced accumulation of dihydroxyphenylalanine (DOPA) in the median eminence after the inhibition of DOPA decarboxylase. The clozapine-induced increase in DOPA accumulation was evident within 30 minutes after its administration and persisted for at least 4 hours. The clozapine-induced increase in the activity of TIDA neurons may account, in part, for the abbreviated PRL response to this neuroleptic. In addition, ability to produce a short-lived increase in PRL secretion in the rat appears to be common to the atypicl neuroleptic drugs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02098500
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    Paper (German National Licenses)
    Fulltext
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