Medial septal cholinergic neurons express c-Jun but do not undergo DNA fragmentation after fornix-fimbria transections

被引:28
作者
Butterworth, NJ [1 ]
Dragunow, M [1 ]
机构
[1] UNIV AUCKLAND,DEPT PHARMACOL & CLIN PHARMACOL,FAC MED & HLTH SCI,AUCKLAND 1,NEW ZEALAND
来源
MOLECULAR BRAIN RESEARCH | 1996年 / 43卷 / 1-2期
关键词
axotomy; programmed cell death; apoptosis;
D O I
10.1016/S0169-328X(96)00143-X
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We investigated the expression of inducible transcription factors (ITFs) and the fate of medial septal (MS) cholinergic neurons following fornix fimbria (FF) transection. c-Jun, but not c-Fos or Krox 24 was induced in nerve growth factor receptor-immunoreactive (NGFr-ir), parvalbumin-negative MS neurons by 48 h and still highly expressed 2 months after transection. JunD was expressed only at 48 h after transection. Levels of choline acetyl transferase immunoreactivity (ChAT-ir) and NGFr-ir decreased substantially 7 and 14 days respectively following FF transection and remained depressed for up to 2 months. We also investigated other measures of nerve cell death and found that there was a time-dependent loss of cresyl violet staining, but no evidence of DNA fragmentation, acidophilia or clusterin expression in the MS region. There was however, good evidence of microglial activation and astrocyte hypertrophy in the MS. These results suggest that axotomized c-Jun-positive septohippocampal neurons lose their cholinergic phenotype but do not die for up to 2 months after FF transection. The function of c-Jun in axotomized MS neurons remains a mystery, but c-Jun expression alone is clearly not sufficient to elicit death of these neurons.
引用
收藏
页码:1 / 12
页数:12
相关论文
共 48 条
  • [1] RESPONSE OF SEPTAL CHOLINERGIC NEURONS TO AXOTOMY
    ARMSTRONG, DM
    TERRY, RD
    DETERESA, RM
    BRUCE, G
    HERSH, LB
    GAGE, FH
    [J]. JOURNAL OF COMPARATIVE NEUROLOGY, 1987, 264 (03) : 421 - 436
  • [2] Beilharz Erica J., 1995, Molecular Brain Research, V29, P1, DOI 10.1016/0169-328X(94)00217-3
  • [3] TRANSECTION OF RAT FIMBRIA-FORNIX INDUCES LASTING EXPRESSION OF C-JUN PROTEIN IN AXOTOMIZED SEPTAL NEURONS IMMUNONEGATIVE FOR CHOLINE-ACETYLTRANSFERASE AND NITRIC-OXIDE SYNTHASE
    BRECHT, S
    MARTINVILLALBA, A
    ZUSCHRATTER, W
    BRAVO, R
    HERDEGEN, T
    [J]. EXPERIMENTAL NEUROLOGY, 1995, 134 (01) : 112 - 125
  • [4] CASTELLAZZI M, 1993, ONCOGENE, V8, P1149
  • [5] OVEREXPRESSION OF C-JUN, JUNB, OR JUND AFFECTS CELL-GROWTH DIFFERENTLY
    CASTELLAZZI, M
    SPYROU, G
    LAVISTA, N
    DANGY, JP
    PIU, F
    YANIV, M
    BRUN, G
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (20) : 8890 - 8894
  • [6] APOPTOSIS - MOLECULAR CONTROL POINT IN TOXICITY
    CORCORAN, GB
    FIX, L
    JONES, DP
    MOSLEN, MT
    NICOTERA, P
    OBERHAMMER, FA
    BUTTYAN, R
    [J]. TOXICOLOGY AND APPLIED PHARMACOLOGY, 1994, 128 (02) : 169 - 181
  • [7] DEFELIPE C, 1994, J NEUROSCI, V14, P2911
  • [8] DEFELIPE C, 1993, ADV NEUROL, V59, P263
  • [9] AXOTOMIZED MEDIAL SEPTAL DIAGONAL BAND NEURONS EXPRESS JUN-LIKE IMMUNOREACTIVITY
    DRAGUNOW, M
    [J]. MOLECULAR BRAIN RESEARCH, 1992, 15 (1-2): : 141 - 144
  • [10] IN-SITU EVIDENCE FOR DNA FRAGMENTATION IN HUNTINGTONS-DISEASE STRIATUM AND ALZHEIMERS-DISEASE TEMPORAL LOBES
    DRAGUNOW, M
    FAULL, RLM
    LAWLOR, P
    BEILHARZ, EJ
    SINGLETON, K
    WALKER, EB
    MEE, E
    [J]. NEUROREPORT, 1995, 6 (07) : 1053 - 1057