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Träfflista för sökning "L773:0165 1838 srt2:(1990-1994)"

Search: L773:0165 1838 > (1990-1994)

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1.
  • Hardebo, Jan Erik, et al. (author)
  • Dynorphin B is present in sensory and parasympathetic nerves innervating pial arteries
  • 1994
  • In: Journal of the Autonomic Nervous System. - : Elsevier BV. - 0165-1838. ; 47:3, s. 171-176
  • Journal article (peer-reviewed)abstract
    • Dynorphin B (dyn B) in trigeminal ganglion cells and in perivascular nerve fibers in pial arteries was demonstrated in rat, guinea-pig, and monkey by immunohistochemistry. The pathway from the trigeminal ganglion, which runs via the nasociliary nerve and ethmoidal foramen to the pial arteries, was shown in rat by retrograde tracer technique and nerve section. In the guinea-pig the peptide was demonstrated to coexist with substance P and calcitonin gene-related peptide in neurons of the trigeminal ganglion and pial nerve fibers, i.e., it was present in cerebrovascular sensory nerves with primarily nociceptive function. Another finding in guinea-pig was a coexistence of dyn B with vasoactive intestinal polypeptide in the pial nerve fibers and neurons of the sphenopalatine ganglion, indicating a presence also in parasympathetic nerves to the cerebral vessels. No vasomotor effect of dyn B could be detected in isolated segments of rat pial arteries, which rules out a direct postsynaptic effect on vascular tone. The peptide did not display a prejunctional modulatory action on the adrenergic nerves present in the vessels. The function of dyn B in the cerebrovascular nerves is discussed.
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2.
  • Suzuki, Norihiro, et al. (author)
  • Central origins of preganglionic fibers to the sphenopalatine ganglion in the rat. A fluorescent retrograde tracer study with special reference to its relation to central catecholaminergic systems
  • 1990
  • In: Journal of the Autonomic Nervous System. - : Elsevier BV. - 0165-1838. ; 30:2, s. 101-109
  • Journal article (peer-reviewed)abstract
    • The brainstem origin of preganglionic fibers to the sphenopalatine ganglion in rat was revealed by the aid of the retrograde axonal tracer True Blue (which does not traverse to a second order neuron) applied deep in the sphenopalatine ganglion or the Vidian nerve on one side. The majority of fibers originate in the ipsilateral lacrimo-muconasal nucleus in the ventrolateral rostral medulla oblongata and caudal pons. A smaller number of fibers originate more dorsomedially and caudally in the medullary reticular formation. After application to the ganglion a third small group of labelled neurons was found more rostrally in the brainstem, in the reticular formation ventrolateral to the caudal part of the dorsal raphe nucleus. Simultaneous visualization of catecholaminergic nerves revealed that the labelled neurons in the lacrimo-muconasal nucleus were heavily innervated by catecholaminergic fibers. It appears from previous studies that the preganglionic neurons may not be cholinergic. None of the labelled neurons in the brainstem stained positively for catecholamines. Thus, further studies are required to elucidate the transmitter(s) used in these neurons.
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3.
  • Andersson, Staffan, et al. (author)
  • Assessment of autonomic nerve function in myotonic dystrophy
  • 1990
  • In: Journal of the Autonomic Nervous System. - : Elsevier BV. - 0165-1838 .- 1872-7476. ; 29:3, s. 187-192
  • Journal article (peer-reviewed)abstract
    • The function of the autonomic nervous system was studied in 23 patients with myotonic dystrophy, from a defined population in northern Sweden with an extremely high prevalence of this disease. Heart rate variability tests showed only minor signs of parasympathetic dysfunction. Blood pressure and plasma noradrenaline measurements in recumbent and upright positions showed no signs of sympathetic neuropathy. Increased plasma levels of noradrenaline was an unexpected finding. Our study does not support the hypothesis that cardiac arrhythmias, orthostatic hypotension, gastrointestinal motility disturbances and urinary bladder dysfunction in myotonic dystrophy are caused by autonomic neuropathy, and we believe that these symptoms should rather be ascribed to a defective function of the target organs
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