title: Focal cerebral ischemia in rats induces expression of P75 neurotrophin receptor in resistant striatal cholinergic neurons.
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 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.
authors.affiliation: Section of Restorative Neurology, Wallenberg Neuroscience Center, Lund University Hospital, Sweden.
authors.forename: Z
authors.initials: Z
authors.lastname: Kokaia
authors.forename: G
authors.initials: G
authors.lastname: Andsberg
authors.forename: A
authors.initials: A
authors.lastname: Martinez-Serrano
authors.forename: O
authors.initials: O
authors.lastname: Lindvall
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002545:Brain Ischemia / Q000378:metabolism*; D002536:Cerebral Arteries / Q000502:physiology; D002795:Choline O-Acetyltransferase / Q000096:biosynthesis; D051937:Dopamine and cAMP-Regulated Phosphoprotein 32; D007150:Immunohistochemistry; D007395:Interneurons / Q000378:metabolism; D008297:Male; D017072:Neostriatum / Q000166:cytology / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D009474:Neurons / Q000378:metabolism*; D010275:Parasympathetic Nervous System / Q000166:cytology / Q000378:metabolism*; D010750:Phosphoproteins; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D020794:Receptor Protein-Tyrosine Kinases / Q000096:biosynthesis; D020800:Receptor, Nerve Growth Factor; D020917:Receptor, trkA; D017475:Receptors, Nerve Growth Factor / Q000096:biosynthesis*; D005680:gamma-Aminobutyric Acid / Q000502:physiology
chemical_list: D051937:Dopamine and cAMP-Regulated Phosphoprotein 32; D009419:Nerve Tissue Proteins; D010750:Phosphoproteins; D011518:Proto-Oncogene Proteins; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor; D005680:gamma-Aminobutyric Acid; D002795:Choline O-Acetyltransferase; D020794:Receptor Protein-Tyrosine Kinases; D020917:Receptor, trkA