Estrogen acts on maternal circuitry to establish maternal behaviour in otherwise non-maternal rats. The precise mechanisms by which estrogen primes maternal circuitry are unknown; however, the medial preoptic area (MPOA) stimulates maternal behaviour whilst the medial amygdala (MeA) inhibits it. This thesis aimed to address the link between estrogen sensitivity, astroglia and maternal behaviour. Maternal care influences maternal behaviour of female offspring. One mechanism underlying this influence is differential estrogen sensitivity within the MPOA. Estrogen receptor alpha (ERalpha) expression was examined in offspring of High and Low licking/grooming (LG) dams within the MPOA. Enhanced expression ERalpha was limited to the medial preoptic nucleus in offspring of High LG dams and the anteroventral periventricular nucleus in Low LG dams. Adult nulliparous offspring of High and Low LG dams were assessed for maternal responsiveness using the pup sensitization paradigm. Offspring of Highs showed maternal behaviour significantly earlier than offspring of Lows. Brains of pup-exposed and pup-naive High and Low offspring were analyzed for astroglial markers glial fibrillary acidic protein (GFAP) and glutamine synthetase. Pup-naive animals showed more GFAP positive cells within the posteroventral MeA, with no differences within the MPOA and no effect of maternal care. Glutamine synthetase, a glial-derived enzyme necessary for glutamate production, showed greater expression within the MeA of High LG pup-naive animals; with no maternal care differences observed in pup-experienced animals. Thus, long-lasting changes within maternal circuitry established in early life are reflected in regionally specific enhanced estrogen sensitivity and latency to display maternal behaviour, but the effects are less clear with respect to astroglia.

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Pup directed maternal licking and grooming (LG) increases with corticosterone (CORT) supplimentation (Rees et al 2004). Increases in LG lead to an attenuation of the adult offspring's HPA response to stress (Liu et aI1997). Similarly, Neonatal increases in glucocorticoids lead, in adulthood, to the same attenuation of the HPA stress response (Catalani et aI1993). We hypothesize that dams exhibiting increased LG will have increased circulating CORT, and this increase will be reflected in their offspring. This thesis characterizes the HPA hormone profile adrenocorticotropic hormone (ACTH), CORT & Corticosterone Binding Globulin (CBG) in High LG (H) and Low LG (L) litters, 5 days postpartum (P4). Furthermore pup plasma CORT levels are determined at (P) 3,4,6,10 & 14. Finally P10 Hand L LG ACTH, CORT & CBG will be assessed after stress. RESULTS: H compared to L LG dams have significantly increased plasma CORT (p=0.03). At P4, H LG offspring have significantly increased plasma CORT (p=0.03) and significantly decreased plasma ACTH (p=0.04) as compared to L LG offspring. Plasma CBG levels are significantly lower in H compared to L LG offspring (p=0.01) at the same age. Across the Stress Hyporesponsive Period (SHRP) H LG offspring had significantly increased plasma CORT (p= 0.00) compared to L LG offspring at P3. Challenged with a stressor at P10, H LG offspring have an exaggerated plasma CORT response (p=0.00). This data suggests increases in plasma CORT in the dams leads to increased CORT in the high offspring, contributing perhaps to a more mature stress response at P10. / Key word abbreviation: (1) CORT - CORTicosterone, (2) ACTH - AdrenoCorticoTropin releasing Hormone, (3) CBG - Corticosteroid Binding Globulin, (4) SHRP - Stress Hypo-Responsive Period, (5) P - Post-natal day, (6) HPA - Hypothalamic-Pituitary-Adrenal, (7) LG - Licking/Grooming, (8) ADX/OVX - ADrenalectomized/OVarectomized.

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