Normal inhibitory avoidance learning and anxiety, but increased locomotor activity in mice devoid of PrPC

被引:80
作者
Roesler, R
Walz, R
Quevedo, J
de-Paris, F
Zanata, SM
Graner, E
Izquierdo, I
Martins, VR
Brentani, RR
机构
[1] UFRGS, ICBS, Dept Bioquim, Ctr Memoria, BR-90035003 Porto Alegre, RS, Brazil
[2] Ludwig Inst Canc Res, Sao Paulo Branch, BR-01509010 Sao Paulo, Brazil
[3] Fdn Antonio Prudente, BR-01509010 Sao Paulo, Brazil
来源
MOLECULAR BRAIN RESEARCH | 1999年 / 71卷 / 02期
基金
巴西圣保罗研究基金会;
关键词
prion; PrPC; Prnp(0/0) mice; memory; behavior;
D O I
10.1016/S0169-328X(99)00193-X
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Prions are the causative agents of transmissible spongiform encephalopathies. The transmissible agent (PrPSC) is an abnormal form of PrPC, a normal neuronal protein. The physiological role of PrPC remains unclear. In the present report, we evaluated behavioral parameters in Prnp(0/0) mice devoid of PrPC. Prnp(0/0) mice showed normal short- and long-term retention of a step-down inhibitory avoidance task and normal behavior in an elevated plus maze test of anxiety. During a 5-min exploration of an open field, Prnp(0/0) mice showed normal number of rearings, defecation, and latency to initiate locomotion, but a significant increase in the number of crossings. The results suggest that Prnp(0/0) mice show normal fear-motivated memory, anxiety and exploratory behavior, and a slight increase in locomotor activity during exploration of a novel environment. (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:349 / 353
页数:5
相关论文
共 16 条
[1]   Prion research: the next frontiers [J].
Aguzzi, A ;
Weissmann, C .
NATURE, 1997, 389 (6653) :795-798
[2]   A SYNAPTIC MODEL OF MEMORY - LONG-TERM POTENTIATION IN THE HIPPOCAMPUS [J].
BLISS, TVP ;
COLLINGRIDGE, GL .
NATURE, 1993, 361 (6407) :31-39
[3]   NORMAL DEVELOPMENT AND BEHAVIOR OF MICE LACKING THE NEURONAL CELL-SURFACE PRP PROTEIN [J].
BUELER, H ;
FISCHER, M ;
LANG, Y ;
BLUETHMANN, H ;
LIPP, HP ;
DEARMOND, SJ ;
PRUSINER, SB ;
AGUET, M ;
WEISSMANN, C .
NATURE, 1992, 356 (6370) :577-582
[4]   PRION PROTEIN IS NECESSARY FOR NORMAL SYNAPTIC FUNCTION [J].
COLLINGE, J ;
WHITTINGTON, MA ;
SIDLE, KCL ;
SMITH, CJ ;
PALMER, MS ;
CLARKE, AR ;
JEFFERYS, JGR .
NATURE, 1994, 370 (6487) :295-297
[5]   CHANGES IN THE LOCALIZATION OF BRAIN PRION PROTEINS DURING SCRAPIE INFECTION [J].
DEARMOND, SJ ;
MOBLEY, WC ;
DEMOTT, DL ;
BARRY, RA ;
BECKSTEAD, JH ;
PRUSINER, SB .
NEUROLOGY, 1987, 37 (08) :1271-1280
[6]   Mechanisms for memory types differ [J].
Izquierdo, I ;
Barros, DM ;
Souza, TME ;
de Souza, MM ;
Izquierdo, LA ;
Medina, JH .
NATURE, 1998, 393 (6686) :635-636
[7]   Sequential role of hippocampus and amygdala, entorhinal cortex and parietal cortex in formation and retrieval of memory for inhibitory avoidance in rats [J].
Izquierdo, I ;
Quillfeldt, JA ;
Zanatta, MS ;
Quevedo, J ;
Schaeffer, E ;
Schmitz, PK ;
Medina, JH .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1997, 9 (04) :786-793
[8]  
Katamine S, 1998, CELL MOL NEUROBIOL, V18, P731, DOI 10.1023/A:1020234321879
[9]   Mice deficient for prion protein exhibit normal neuronal excitability and synaptic transmission in the hippocampus [J].
Lledo, PM ;
Tremblay, P ;
Dearmond, SJ ;
Prusiner, SB ;
Nicoll, RA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (06) :2403-2407
[10]   Prion protein is necessary for latent learning and long-term memory retention [J].
Nishida, N ;
Katamine, S ;
Shigematsu, K ;
Nakatani, A ;
Sakamoto, N ;
Hasegawa, S ;
Nakaoke, R ;
Atarashi, R ;
Kataoka, Y ;
Miyamoto, T .
CELLULAR AND MOLECULAR NEUROBIOLOGY, 1997, 17 (05) :537-545