The hippocampus has been a focus of increasing interest in the schizophrenia research community since the 1980s (Heckers and Konradi, 2002). A large literature has convincingly shown that hippocampal volume is smaller in schizophrenia patients (for review/meta-analysis, see Steen et al., 2006), as well as in their first-degree relatives (Boos et al., 2007). This is complemented by functional neuroimaging studies, which suggest that hippocampal activity is increased at baseline, but decreased during task performance (numerous studies, see PubMed results). A recent study reports that increased blood volume in the CA1 subfield of the hippocampus may predict the at-risk, or prodromal, stage of psychotic disorders (Schobel et al., 2009; see SRF related news story).
A much-discussed synthesis of hippocampal pathology in schizophrenia, which grew out of a 2007 Society for Neuroscience symposium, also gives the hippocampus a central role (Lisman et al., 2008; see also SRF related related meeting report). One hypothesis in this suite of models is that decreased hippocampal GABA signaling in schizophrenia disinhibits the outputs from the structure, leading to an overactive dopamine system (Lodge et al., 2009; see SRF related meeting report and slidecast by A.A. Grace), while another posits that the hippocampal GABA deficiency can be traced to faulty input from the basolateral amygdala (Berretta et al., 2009; see SRF related news story).
This discussion was exploratory, so we rely on our readers' comments to bring up the findings you find most compelling from your own and others’ research.