Neurosciences
Program

Whitlow, Victoria (2009).  Effects of Neonatal Exposure to Antipsychotic Medication on Neuronal Expression of Glucocorticoid Receptor in the Rat Hippocampus and Medial and Orbital Prefrontal Cortices.  Mentor: Dr. Aileen Bailey. 

Abstract 

Antipsychotic medication is capable of crossing the placental barrier and is also secreted in breast milk (Miyazaki et al., 1986).  Pregnant women and new mothers with schizophrenia using antipsychotic medication must therefore make the decision whether to continue treating their illness or risk abnormal neuronal development of their child.  Perinatal exposure to antipsychotic medication could disrupt neuronal development and the proper organization of neuronal pathways, such as the connections of the Hypothalamic-Pituitary-Adrenal (HPA) axis and associated brain structures.  The HPA axis is involved in the adaptive stress response.  Activation of the HPA axis ultimately results in synthesis and secretion of glucocorticoid hormone by the adrenal cortex.  Circulating glucocorticoids bind with glucocorticoid receptors (GR) in the brain and induce changes that inhibit HPA axis activity and allow for the reestablishment of homeostasis.  However, abnormal neural organization of the HPA axis and associated structures could result in manifestation of neuropathology later in life.  In this study, rat neonates were either exposed to daily haloperidol (8 mg/kg) or vehicle injections or were given no injections and handled only.  Following in situ hybridization protocol, hippocampal subfields and two regions of the prefrontal cortex were analyzed for neuronal expression of GR in brain sections obtained once subjects reached adulthood.  Significance was found only in the CA1 of the hippocampus between rats having received vehicle injections and rats that were handled only.  Explanation of these unexpected results as well as possible sources or error and future directions of study are discussed.