PMID- 8254373
OWN - NLM
STAT- MEDLINE
DCOM- 19940112
LR  - 20191101
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 13
IP  - 12
DP  - 1993 Dec
TI  - Atrophy but not death of adult septal cholinergic neurons after ablation of 
      target capacity to produce mRNAs for NGF, BDNF, and NT3.
PG  - 5263-76
AB  - The effect of unilateral excitotoxic ablation of hippocampal neurons was 
      investigated on (1) the local production of mRNA for NGF and related 
      neurotrophins, (2) the amount of NGF protein in the septal region, and (3) the 
      viability and appearance of afferent septal cholinergic neurons in adult rats. 
      After near complete ablation of hippocampal neurons, total levels of NGF, 
      brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT3) mRNA measured 
      by quantitative Northern blot analysis in the hippocampal remnant fell 
      significantly, to less than 25% of control values by 28 d and to less than 9% by 
      300 d. In the septal region ipsilateral to such lesions, NGF protein levels 
      measured by ELISA fell significantly, to about 35% of control values, but the 
      number of immunohistochemically detected cholinergic neurons did not decline 
      significantly for up to 500 d. Instead, the cholinergic neurons persisted in an 
      atrophied state, exhibiting severe shrinkage and reduced staining for the 
      transmitter-synthesizing enzyme ChAT. The parameters of cell size and ChAT 
      staining intensity correlated significantly with the amount of hippocampal tissue 
      present. These findings indicate that in adult rats, target-derived NGF, BDNF, 
      and NT3 do not regulate the survival of septal cholinergic neurons in proportion 
      to the number of target neurons present. Moreover, the findings suggest that one 
      or more of these target-derived neurotrophins regulate the structural and 
      chemical phenotype of these neurons in the adult.
FAU - Sofroniew, M V
AU  - Sofroniew MV
AD  - Department of Anatomy, University of Cambridge, United Kingdom.
FAU - Cooper, J D
AU  - Cooper JD
FAU - Svendsen, C N
AU  - Svendsen CN
FAU - Crossman, P
AU  - Crossman P
FAU - Ip, N Y
AU  - Ip NY
FAU - Lindsay, R M
AU  - Lindsay RM
FAU - Zafra, F
AU  - Zafra F
FAU - Lindholm, D
AU  - Lindholm D
LA  - eng
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Neurotrophin 3)
RN  - 0 (RNA, Messenger)
RN  - 6384-92-5 (N-Methylaspartate)
SB  - IM
MH  - Animals
MH  - Atrophy
MH  - Brain-Derived Neurotrophic Factor
MH  - *Cell Death
MH  - Cholinergic Fibers/metabolism/pathology
MH  - Female
MH  - Hippocampus/drug effects/metabolism/pathology
MH  - Male
MH  - N-Methylaspartate/pharmacology
MH  - Nerve Growth Factors/*genetics/metabolism
MH  - Nerve Tissue Proteins/*genetics/metabolism
MH  - Neurons, Afferent/metabolism/pathology
MH  - Neurotrophin 3
MH  - RNA, Messenger/*metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Septal Nuclei/*metabolism/*pathology
PMC - PMC6576406
EDAT- 1993/12/01 00:00
MHDA- 1993/12/01 00:01
PMCR- 1994/06/01
CRDT- 1993/12/01 00:00
PHST- 1993/12/01 00:00 [pubmed]
PHST- 1993/12/01 00:01 [medline]
PHST- 1993/12/01 00:00 [entrez]
PHST- 1994/06/01 00:00 [pmc-release]
AID - 10.1523/JNEUROSCI.13-12-05263.1993 [doi]
PST - ppublish
SO  - J Neurosci. 1993 Dec;13(12):5263-76. doi: 10.1523/JNEUROSCI.13-12-05263.1993.