Microtubule-associated protein MAP2 expression in olfactory bulb in schizophrenia Lise Rioux * , Delta Ruscheinsky, Steven Edward Arnold Center for Neurobiology and Behavior, Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA Received 13 October 2003; received in revised form 26 March 2004; accepted 22 May 2004 Abstract Previous studies have described alterations in presynaptic and postsynaptic elements in various parts of the CNS in schizophrenia, which may, at least in part, be due to abnormalities in neurodevelopmental processes. The olfactory bulb (OB) is a unique CNS area for examining synaptic development and plasticity in schizophrenia because it undergoes continuous reinnervation throughout life. Moreover, olfactory deficits and reduced OB volume have been observed in schizophrenia. We investigated the expression in the OB of the microtubule-associated protein MAP2, which has been shown to be abnormally expressed in the hippocampal region in schizophrenia. In both developing and mature neurons, MAP2 is an important structural component of dendrites and participates in the modification of synaptic organization. We used immunocytochemistry with phosphoepitope-specific and phosphorylation-state-independent antibodies to examine MAP2 expression in the glomerular layer of the OB in elderly subjects with chronic schizophrenia and controls. Phosphorylation-independent MAP2 expression was significantly reduced in schizophrenia, while phosphorylated MAP2 expression did not differ between groups. These results are consistent with faulty OB innervation in schizophrenia. D 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: AP18; Glomerulus; Dendrite; Plasticity 1. Introduction Psychophysical studies have documented deficits in odor detection, identification, and memory in schizo- phrenia (Moberg et al., 1999). Clinical neurobiological studies have shown that the olfactory bulb (OB) is smaller and that olfactory evoked response potentials are abnormal in schizophrenia (Moberg et al., 1999; Turetsky et al., 2000). Additionally, postmortem stud- ies have described cellular and molecular abnormali- ties in the olfactory epithelium (Arnold et al., 2001). Given the mounting evidence for abnormal neuro- development in schizophrenia, the OB provides a valuable window into the cellular and molecular pro- cesses of axon guidance, synaptogenesis and synaptic plasticity that may go awry in schizophrenia (Arnold and Rioux, 2001). Its value as a model system lies on the fact that the OB undergoes continuous reinnerva- tion throughout life as olfactory receptor neurons (ORNs) in the neuroepithelium of the nose turn over and send new axons to synapse with the glomeruli of 0165-1781/$ - see front matter D 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.psychres.2004.05.022 * Corresponding author. Present address: Laboratory for Bio- Imaging and Anatomical Informatics, Department of Neurobiology and Anatomy, Drexel University College of Medicine, 2900 Queen Lane, Philadelphia, PA 19129-1096, USA. Tel.: +1-215-991-8410; fax: +1-215-843-9367. E-mail address: lrioux@earthlink.net (L. Rioux). www.elsevier.com/locate/psychres Psychiatry Research 128 (2004) 1 – 7