title: Upregulation of p75 neurotrophin receptor after stroke in mice does not contribute to differential vulnerability of striatal neurons.
abstract: The survival of different neuron types and the expression of the p75 neurotrophin receptor (p75(NTR)) after focal cerebral ischemia were studied in the mouse striatum using immunocytochemical and histochemical techniques and stereological procedures. As assessed at 1 week after 30 min of middle cerebral artery occlusion, the order of vulnerability was projection neurons > parvalbumin-expressing interneurons > nitric oxide synthase-containing interneurons > cholinergic interneurons. Within the ischemic lesion, projection neurons were almost completely lost whereas cholinergic interneurons were spared. Calretinin-immunoreactive interneurons also seemed resistant to the insult. Expression of p75(NTR) was induced in cholinergic interneurons within the lesioned area, raising the possibility of a protective action. However, the number of cholinergic interneurons was unaffected in p75(NTR) knockout mice subjected to the same ischemic insult. These quantitative data demonstrate that striatal neurons in the mouse are differentially susceptible to ischemic damage and argue against a significant role of p75(NTR) for the high resistance of cholinergic interneurons.
authors.affiliation: Section of Restorative Neurology, Wallenberg Neuroscience Center, University Hospital, SE-221 85 Lund, Sweden.
authors.forename: G
authors.initials: G
authors.lastname: Andsberg
authors.forename: Z
authors.initials: Z
authors.lastname: Kokaia
authors.forename: O
authors.initials: O
authors.lastname: Lindvall
mesh_terms: D000818:Animals; D064032:Calbindin 2; D003342:Corpus Striatum / Q000378:metabolism* / Q000473:pathology; D007839:Functional Laterality; D005786:Gene Expression Regulation; D006801:Humans; D007395:Interneurons / Q000378:metabolism / Q000473:pathology; D002546:Ischemic Attack, Transient / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D020768:Middle Cerebral Artery; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D010320:Parvalbumins / Q000032:analysis; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor / Q000172:deficiency / Q000235:genetics* / Q000502:physiology; D064030:S100 Calcium Binding Protein G / Q000032:analysis; D020521:Stroke / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D015854:Up-Regulation
chemical_list: C576764:CALB2 protein, human; C576511:Calb2 protein, mouse; D064032:Calbindin 2; D010320:Parvalbumins; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor; D064030:S100 Calcium Binding Protein G; D019001:Nitric Oxide Synthase