Fatherhood alters behavioural and neural responsiveness in a spatial task.

The hormones and experiences of pregnancy, parturition and lactation have been shown to dramatically remodel the female rat's hippocampus, potentially enhancing behaviours critical for meeting the increased demands of motherhood. Previous work in our laboratory has also suggested that pup exposure, apart from pregnancy and lactation, constitutes an important influence on ancillary maternal behaviour (e.g. foraging behaviour). In the present study, we press the parental model further by examining the effect of pup exposure on the hippocampus of males from a biparental mouse species, the California mice (Peromyscus californicus). Males were either Fathers (i.e. first-time fathers housed with a female from mating until 7 days after parturition), pup-exposed virgins (PEV; i.e. sexually naïve males briefly exposed to pups daily for 7 days) or Virgins (i.e. never exposed to females or pups). A dry-land maze (DLM), as used for assessing spatial learning, was employed to determine the foraging abilities of the males. The results indicated that, on the most challenging day of testing (i.e. acquisition day), California mouse Fathers demonstrated superior memory for the task compared to PEVs and Virgins. In addition to the behavioural data, significantly more fos-immunoreactivity was observed in the CA1, CA3 and dentate gyrus regions of the hippocampi of Fathers than PEVs or Virgins in response to the probe trial. Additionally, a trend for altered performance on the DLM was observed in the PEVs on the last day of testing, which was accompanied by the highest levels of nestin-immunoreactivity, an indicant of neuroplasticity, of the three groups. In summary, these data suggest that, in accordance with previous observations of maternal rats, the paternal brain is similarly influenced by parental experience, as demonstrated by accompanying modifications to relevant neurobiological and behavioural responses.

Immunologic detection and measurement of glycated apolipoprotein B with site specific monoclonal antibodies.

Nonenzymatic glycation of apolipoprotein B (apo B) is a post-secretory modification of low density lipoprotein (LDL) that affects its atherogenic potential and is implicated in the accelerated atherosclerosis associated with diabetes. To facilitate assessment of apo B glycation, we produced hybridomas secreting monoclonal antibodies specific for glycated apo B. SP 2/0 myeloma cells were fused with spleen cells from BALB/c mice immunized with purified apo B glycated non-reductively in vitro. Specificity of monoclonal antibodies secreted by the cloned cell line designated ES12 was demonstrated by immunoblotting and by direct ELISA, wherein the antibodies reacted with glycated epitopes residing in LDL but not in other plasma proteins, and did not react with nonglycated apo B or nonglycated LDL. Immunoblotting of human plasma with ES12 monoclonal antibody yielded an approx. 180,000 molecular weight component showing co-identity with apo B, indicating site specificity for glycated epitopes residing in apo B of the LDL complex and absence of reactivity with other nonenzymatically glycated plasma proteins. This reactivity of ES12 with the physiologic form of glycated apo B that occurs in vivo differs from properties of other antibodies raised against glycated lipoproteins, which recognized glycated residues only after reductive conversion to glucitol-lysine and which do not discriminate between different glycated proteins. In a competitive ELISA, mean concentration of glycated LDL, measured as apo B equivalents, in eight separate plasma samples was 19.7 +/- 1.9 micrograms/ml, representing 3.5 +/- 0.3% of total apo B. The ES12 monoclonal antibody allows specific determination of plasma glycated LDL concentrations, which may have diagnostic and pathogenetic importance.