Modifications of open field and novelty behaviours by hippocampal and amygdaloid lesions in two inbred strains of mice: Lack of strain × lesion interactions

Clelia Rossi-Arnaud, Martine Ammassari-Teule

Research output: Contribution to journalArticlepeer-review

Abstract

C57BL/6 (C57) and DBA/2 (DBA) mice with dorsal hippocampus, central amygdala and sham lesions were observed for an eight-minute period, repeated on three consecutive days, in an open field situation with a novel object. Strain-dependent differences emerged when comparing sham lesioned mice; higher rearing and grooming scores as well as more defecation boli were found in DBA. In both strains, hippocampal lesions enhanced locomotor activity in the open field while amygdaloid lesions increased the number of contacts with the novel object. No significant lesion × strain interaction was recorded for any of the behaviours analyzed in the open field of the novelty situation. Significant strain × day, lesion × day and strain × lesion × day interactions were found thus indicating that previously described strain or lesion main effects were more pronounced on a particular day of testing. Despite the behavioural differences shown by sham lesioned C57 and DBA mice, the effects of the lesions differ in intensity but generally go in the same direction whatever the strain considered. Thus, while a strain-dependent selective involvement of subcortical areas in associative spatial learning has been previously reported, this does not seem to be the case for non-associative forms of learning.

Original languageEnglish
Pages (from-to)155-164
Number of pages10
JournalBehavioural Processes
Volume27
Issue number3
DOIs
Publication statusPublished - 1992

Keywords

  • Amygdala
  • Hippocampus
  • Inbred mice
  • Lesion
  • Open field behaviour

ASJC Scopus subject areas

  • Animal Science and Zoology
  • Ecology, Evolution, Behavior and Systematics
  • Behavioral Neuroscience

Fingerprint Dive into the research topics of 'Modifications of open field and novelty behaviours by hippocampal and amygdaloid lesions in two inbred strains of mice: Lack of strain × lesion interactions'. Together they form a unique fingerprint.

Cite this