Social Play Behavior in Adolescent Rats is Mediated by Functional Activity in Medial Prefrontal Cortex and Striatum

Social play behavior is a characteristic, vigorous form of social interaction in young mammals. It is highly rewarding and thought to be of major importance for social and cognitive development. The neural substrates of social play are incompletely understood, but there is evidence to support a role for the prefrontal cortex (PFC) and striatum in this behavior. Using pharmacological inactivation methods, ie, infusions of GABA receptor agonists (baclofen and muscimol; B&M) or the AMPA/kainate receptor antagonist 6,7-dinitroquinoxaline-2,3(1H,4H)-dione (DNQX), we investigated the involvement of several subregions of the medial PFC and striatum in social play. Inactivation of the prelimbic cortex, infralimbic cortex, and medial/ventral orbitofrontal cortex using B&M markedly reduced frequency and duration of social play behavior. Local administration of DNQX into the dorsomedial striatum increased the frequency and duration of social play, whereas infusion of B&M tended to have the same effect. Inactivation of the nucleus accumbens (NAcc) core using B&M increased duration but not frequency of social play, whereas B&M infusion into the NAcc shell did not influence social play behavior. Thus, functional integrity of the medial PFC is important for the expression of social play behavior. Glutamatergic inputs into the dorsomedial striatum exert an inhibitory influence on social play, and functional activity in the NAcc core acts to limit the length of playful interactions. These results highlight the importance of prefrontal and striatal circuits implicated in cognitive control, decision making, behavioral inhibition, and reward-associated processes in social play behavior.     

Abstracts from other journals

The aim of the present study was to clinically evaluate fissure sealants on the occlusal fissures and buccal pits of permanent first and second molars after 20 and 15 years, respectively. The population consisted of 72 children, each of whom had had their four first molars sealed between 1977 and 1980. At the annual examinations, all caries-free, newly erupted second molars were sealed. When sealant was applied to the second molars, the first molars were checked and sealant was reapplied to those that had deficient sealants. At the follow-up, when the subjects were 26–27 years of age, 27 in the original group had moved from the community. Thus, the present result is based on 45 subjects. One hundred and fifty-three sealed first molars and 161 sealed second molars were available for inspection. At the follow-up examination of the first molars 20 years after sealant had been applied, 65% showed complete retention, 22% partial retention without caries, and 1306 caries or restoration in the occlusal fissures or buccal pits. At the 15-year follow-up of the second molars, the corresponding figures were 65%, 30% and 5%, respectively. Of the restored or carious molars, significantly more were found in the mandible than in the maxilla ( P  < 0.001). This longitudinal study showed that pit and fissure sealants, applied during childhood, have a long-lasting, caries-preventive effect.     

Direct demonstration that autologous bone marrow transplantation for solid tumors can return a multiplicity of tumorigenic cells

Patients with solid tumors are increasingly being treated by autologous bone marrow transplantation (BMT). Although response rates appear to be increased, disease recurrence is the commonest cause of treatment failure. Whether relapse is entirely due to residual disease in the patient or arises also from infiltrating malignant cells contained in the autologous marrow transplant has not been resolved. If the latter explanation is correct, then purging would be required as part of the transplantation procedure. We used retrovirally mediated transfer of the neomycin-resistance gene to mark BM harvested from eight patients with neuroblastoma in clinical remission. The marked marrow cells were subsequently reinfused as part of an autologous BMT. At relapse, we sought the marker gene in malignant cell populations. Three patients have relapsed, and in each the marker gene was detected by phenotypic and genetic analyses of resurgent malignant cells at medullary and extramedullary sites. Analysis of neuroblast DNA for discrete marker gene integration sites suggested that at least 200 malignant cells, each capable of tumor formation, were introduced with the autologous marrow transplant and contributed to relapse. Thus, autologous BMTs administered to patients with this solid tumor may contain a multiplicity of malignant cells that subsequently contribute to relapse. The marker-gene technique we describe should permit evaluation of the mechanisms of relapse and the efficacy of purging in patients receiving autologous marrow transplantation for other solid tumors that infiltrate the marrow.