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Focal cerebral ischemia in rats induces expression of p75 neurotrophin receptor in resistant striatal cholinergic neurons

Kokaia, Z. LU orcid ; Andsberg, G. LU ; Martinez-Serrano, A. and Lindvall, O. LU (1998) In Neuroscience 84(4). p.1113-1125
Abstract

Expression of p75 neurotrophin receptor and survival of medium-sized spiny projection neurons and cholinergic interneurons in the rat striatum were studied using immunocytochemistry at different times after transient, unilateral middle cerebral artery occlusion. Thirty minutes of middle cerebral artery occlusion caused a major loss of projection neurons, identified by their immunoreactivity to dopamine- and adenosine 3':5'- monophosphate-regulated phosphoprotein with a molecular weight of 32,000, in the lateral part of the striatum, as observed at 48 h following the insult with no further change at one week. In contrast, no reduction of the number of choline acetyltransferase-positive, cholinergic interneurons, which also expressed... (More)

Expression of p75 neurotrophin receptor and survival of medium-sized spiny projection neurons and cholinergic interneurons in the rat striatum were studied using immunocytochemistry at different times after transient, unilateral middle cerebral artery occlusion. Thirty minutes of middle cerebral artery occlusion caused a major loss of projection neurons, identified by their immunoreactivity to dopamine- and adenosine 3':5'- monophosphate-regulated phosphoprotein with a molecular weight of 32,000, in the lateral part of the striatum, as observed at 48 h following the insult with no further change at one week. In contrast, no reduction of the number of choline acetyltransferase-positive, cholinergic interneurons, which also expressed TrkA, was detected at either time-point. At 48 h following middle cerebral artery occlusion, expression of p75 neurotrophin receptor was observed in striatal cells which, by the use of double-label immunostaining, were identified as the cholinergic interneurons. No p75 neurotrophin receptor immunoreactivity remained in cholinergic cells after one week of reperfusion. Based on current hypotheses regarding the function of the p75 neurotrophin receptor, the transient expression of this receptor in striatal cholinergic interneurons might contribute to their high resistance to ischemic neuronal death. However, the expression of p75 neurotrophin receptor could also be a first step in a pathway leading to apoptosis, which is inhibited after the present insult due to concomitant activation of TrkA.

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author
; ; and
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Cholinergic interneurons, Immunocytochemistry, Neuronal death, Neurotrophic factor, Striatum
in
Neuroscience
volume
84
issue
4
pages
1113 - 1125
publisher
Elsevier
external identifiers
  • pmid:9578399
  • scopus:0031981458
ISSN
0306-4522
DOI
10.1016/S0306-4522(97)00579-4
language
English
LU publication?
no
id
71e6e8c1-9ad1-40fc-8d0f-3ddb0840b2e7
date added to LUP
2019-09-03 17:05:05
date last changed
2024-04-30 20:11:35
@article{71e6e8c1-9ad1-40fc-8d0f-3ddb0840b2e7,
  abstract     = {{<p>Expression of p75 neurotrophin receptor and survival of medium-sized spiny projection neurons and cholinergic interneurons in the rat striatum were studied using immunocytochemistry at different times after transient, unilateral middle cerebral artery occlusion. Thirty minutes of middle cerebral artery occlusion caused a major loss of projection neurons, identified by their immunoreactivity to dopamine- and adenosine 3':5'- monophosphate-regulated phosphoprotein with a molecular weight of 32,000, in the lateral part of the striatum, as observed at 48 h following the insult with no further change at one week. In contrast, no reduction of the number of choline acetyltransferase-positive, cholinergic interneurons, which also expressed TrkA, was detected at either time-point. At 48 h following middle cerebral artery occlusion, expression of p75 neurotrophin receptor was observed in striatal cells which, by the use of double-label immunostaining, were identified as the cholinergic interneurons. No p75 neurotrophin receptor immunoreactivity remained in cholinergic cells after one week of reperfusion. Based on current hypotheses regarding the function of the p75 neurotrophin receptor, the transient expression of this receptor in striatal cholinergic interneurons might contribute to their high resistance to ischemic neuronal death. However, the expression of p75 neurotrophin receptor could also be a first step in a pathway leading to apoptosis, which is inhibited after the present insult due to concomitant activation of TrkA.</p>}},
  author       = {{Kokaia, Z. and Andsberg, G. and Martinez-Serrano, A. and Lindvall, O.}},
  issn         = {{0306-4522}},
  keywords     = {{Cholinergic interneurons; Immunocytochemistry; Neuronal death; Neurotrophic factor; Striatum}},
  language     = {{eng}},
  number       = {{4}},
  pages        = {{1113--1125}},
  publisher    = {{Elsevier}},
  series       = {{Neuroscience}},
  title        = {{Focal cerebral ischemia in rats induces expression of p75 neurotrophin receptor in resistant striatal cholinergic neurons}},
  url          = {{http://dx.doi.org/10.1016/S0306-4522(97)00579-4}},
  doi          = {{10.1016/S0306-4522(97)00579-4}},
  volume       = {{84}},
  year         = {{1998}},
}