title: Learning in year-old female autoimmune BXSB mice.
abstract: BXSB/ MpJ-Yaa and NZB/BINJ mice have been used as animal models for both developmental learning disability and systemic autoimmune disease. Approximately 40-60% of these animals show ectopic clusters of neurons in Layer I of cortex similar to those found in postmortem analyses of human dyslexics, and all exhibit an autoimmune condition similar to systemic lupus erythematosus (SLE) in humans. The expression of immune disease in the BXSB strain, unlike in humans, is more severe in males than females. Most previous studies have examined the behavioral sequelae of neocortical ectopias at a relatively young age, when the BXSB females (unlike the male BXSB and female and male NZBs) are not yet showing high titers of autoantibodies associated with their lupus-like form of autoimmune disease. This study examined the behavior of BXSB females at an age subsequent to autoimmune disease onset. When contrasted with younger animals, year-old BXSB females showed good learning behavior, with no differences in Lashley maze learning and remarkably good performance in a visual discrimination learning task. These results are consistent with other data which indicate that many types of learning behavior are apparently unperturbed by systemic autoimmune disease. Results also showed significant interactions between a measure of lateral paw preference and the presence or absence of ectopias in Lashley maze learning. Animals without ectopias that exhibited a right lateral paw preference showed the greatest number of errors on a number of test measures. These findings support previous results indicating that behavioral effects associated with ectopias may vary based upon the behavioral laterality of affected animals.
authors.affiliation: Biobehavioral Sciences Graduate Degree Program, University of Connecticut, Storrs 06269, USA.
authors.forename: G W
authors.initials: GW
authors.lastname: Boehm
authors.forename: G F
authors.initials: GF
authors.lastname: Sherman
authors.forename: B J
authors.initials: BJ
authors.lastname: Hoplight
authors.forename: L A
authors.initials: LA
authors.lastname: Hyde
authors.forename: D M
authors.initials: DM
authors.lastname: Bradway
authors.forename: A M
authors.initials: AM
authors.lastname: Galaburda
authors.forename: S A
authors.initials: SA
authors.lastname: Ahmed
authors.forename: V H
authors.initials: VH
authors.lastname: Denenberg
mesh_terms: D000367:Age Factors; D000818:Animals; D017153:Antibodies, Anticardiolipin / Q000097:blood; D000974:Antibodies, Antinuclear / Q000097:blood; D001327:Autoimmune Diseases / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000002:abnormalities / Q000473:pathology*; D005260:Female; D007839:Functional Laterality; D007074:Immunoglobulin G / Q000097:blood; D007858:Learning / Q000502:physiology*; D008180:Lupus Erythematosus, Systemic / Q000503:physiopathology*; D051379:Mice; D008815:Mice, Inbred Strains; D019579:Neocortex / Q000473:pathology; D011597:Psychomotor Performance / Q000502:physiology; D012737:Sex Factors; D013223:Statistics as Topic
chemical_list: D017153:Antibodies, Anticardiolipin; D000974:Antibodies, Antinuclear; D007074:Immunoglobulin G