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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1998-10-22
pubmed:abstractText
HDs racI Thrombin causes profound metabolic and morphological changes in cultured neural cells via activation of the thrombin receptor, also called protease-activated receptor 1 (PAR1). PAR1 mRNA is present in the rat brain, but the role of this receptor in the nervous system remains elusive. The expression of PAR1 and the potent thrombin inhibitor protease nexin-1 (PN-1) was investigated in the developing rat brain and spinal cord and after peripheral nerve lesion. As seen by in situ hybridization, the PAR1 mRNA signal in the late embryonic and early postnatal nervous system was widespread, but generally of low intensity whereas in the adult it was more pronounced and confined to particular neuronal cells. These include the mesencephalic dopaminergic neurons, several thalamic and brainstem nuclei, the mitral cells in the olfactory bulb and the Purkinje cells in the cerebellum. In the spinal cord, PAR1 mRNA was abundant in motoneurons and a particularly high expression was detected in the preganglionic neurons of the autonomic nervous system. High PAR1 mRNA expression was also found in the dorsal root ganglia. Interestingly, strong immunoreactivity for the protease inhibitor PN-1 was present in spinal motoneuron cell bodies, although its transcript was undetectable there. In response to sciatic nerve transection, the signal intensity of PAR1 mRNA as seen by Northern analysis increased in the proximal and the distal part of the lesioned nerve and in the denervated muscle, whereas the PN-1 mRNA signal strongly increased only in the distal part of the nerve but remained unchanged in the proximal part and in the muscle. After facial nerve transection, PAR1 mRNA expression substantially decreased in facial motoneurons. No PAR1 transcript was detected in reactive astrocytes. Similar to PAR1, PN-1 mRNA which was expressed in interneurons within the facial nucleus was also decreased following facial nerve transection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0953-816X
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1590-607
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:9751132-Amyloid beta-Protein Precursor, pubmed-meshheading:9751132-Animals, pubmed-meshheading:9751132-Carrier Proteins, pubmed-meshheading:9751132-Cells, Cultured, pubmed-meshheading:9751132-Embryonic and Fetal Development, pubmed-meshheading:9751132-Facial Nerve Injuries, pubmed-meshheading:9751132-Nervous System, pubmed-meshheading:9751132-Nervous System Physiological Phenomena, pubmed-meshheading:9751132-Protease Nexins, pubmed-meshheading:9751132-RNA, Messenger, pubmed-meshheading:9751132-Rats, pubmed-meshheading:9751132-Rats, Sprague-Dawley, pubmed-meshheading:9751132-Receptor, PAR-1, pubmed-meshheading:9751132-Receptors, Cell Surface, pubmed-meshheading:9751132-Receptors, Thrombin, pubmed-meshheading:9751132-Sciatic Nerve, pubmed-meshheading:9751132-Serine Proteinase Inhibitors, pubmed-meshheading:9751132-Serpins, pubmed-meshheading:9751132-Spinal Cord
pubmed:year
1998
pubmed:articleTitle
Changes in the expression of protease-activated receptor 1 and protease nexin-1 mRNA during rat nervous system development and after nerve lesion.
pubmed:affiliation
Friedrich Miescher-Institut, Basel, Switzerland.
pubmed:publicationType
Journal Article