title: Axonal accumulation of p75NTR and TrkA in the septum following lesion of septo-hippocampal pathways.
abstract: Septal cholinergic neurones depend on trophic support by nerve growth factor (NGF) which can rescue them from injury-induced degeneration. Since NGF exerts its effects via p75NTR and TrkA receptors coexpressed in vast majority of these neurones and down-regulated without NGF treatment after injury, in this study we aimed to examine how does the lesion to the cholinergic tracts affect distribution of both types of receptor proteins in damaged fibres. Early changes (two and seven days) were examined immunocytochemically within the septum and supracallosal stria after unilateral lesion to the supracallosal area and cingulum transecting some septal cholinergic efferents. We found accumulation of p75NTR and TrkA immunoreactive material (so-called "pile-up") within axonal segments of distended appearance proximal to the transection at two days postlesion and its translocation towards cell bodies seven days postsurgery. We observed p75NTR pile-up to be more intense than TrkA, which may indicate different cellular concentrations of both receptors. Receptor pile-up resembled acetylcholinesterase pile-up reported previously, suggesting a common response mechanism involving axonal transport disturbances.
authors.affiliation: Department of Neurophysiology, Nencki Institute of Experimental Biology, Warsaw, Poland. mskup@nencki.gov.pl.
authors.forename: M
authors.initials: M
authors.lastname: Skup
authors.forename: A
authors.initials: A
authors.lastname: Bacia
authors.forename: D
authors.initials: D
authors.lastname: Koczyk
authors.forename: W
authors.initials: W
authors.lastname: Jegliński
authors.forename: M
authors.initials: M
authors.lastname: Zaremba
authors.forename: B
authors.initials: B
authors.lastname: Oderfeld-Nowak
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D001370:Axonal Transport; D001369:Axons / Q000378:metabolism* / Q000473:pathology; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D001930:Brain Injuries / Q000473:pathology / Q000503:physiopathology*; D004564:Electrocoagulation; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism*; D020917:Receptor, trkA; D017475:Receptors, Nerve Growth Factor / Q000378:metabolism*; D013997:Time Factors
chemical_list: D011518:Proto-Oncogene Proteins; D017475:Receptors, Nerve Growth Factor; D020794:Receptor Protein-Tyrosine Kinases; D020917:Receptor, trkA; D000110:Acetylcholinesterase