Mark D. Stipetic

Natural killer cell activity in schizophrenia and schizoaffective disorder : a pilot study

Natural killer cell activity was prospectively studied in 15 patients with chronic schizophrenia and in seven patients with schizoaffective disorder, depressed type. These patients were compared to individually matched normal controls. No mean differences in natural killer cell activity between the patient groups and their controls were observed.

The BE (2)-M17 neuroblastoma cell line synthesizes and secretes corticotropin-releasing factor

The BE (2)-M17 human neuroblastoma has previously been shown to express corticotropin-releasing factor (CRF) mRNA following retinoic acid treatment. It is demonstrated in this report that both cell extracts and cell incubation medium of retinoic acid-treated BE (2)-M17 cells were shown to contain CRF-like immunoreactivity (CRF-LI) by RIA. CRF-LI secretion and content were also dose-dependently increased by forskolin. In addition, cell extracts were applied to a C18 Vydac column and peak CRF-LI from the collected fractions was shown to coincide in time of elution with peak immunoreactivity seen with oxidized synthetic CRF standard. Thus, in containing the CRF peptide, the BE (2)-M17 cells are useful models for further study of CRF cellular and genetic regulation.

Corticotropin-releasing factor is secreted in the BE(2)-C neuroblastoma cell and is responsive to forskolin

The BE(2)-C human neuroblastoma has been shown to express corticotropin-releasing factor (CRF) messenger RNA. In this study, BE(2)-C cells were treated 5 days with 5 microM retinoic acid. Cell extracts were also applied onto a C18 Vydac column and fractions were assayed for CRF-like immunoreactivity (CRF-LI) which coincided in time of elution with oxidized or non-oxidized CRF synthetic CRF standard. With forskolin treatment, secretion media and cell extract CRF-LI increased in a concentration-dependent fashion. Thus, this cell line synthesizes and secretes CRF and is a good model for studying CRF regulation.

An Association between Increased Concentrations of Cerebrospinal Fluid Dopamine Sulfate and Higher Negative Symptom Scores in Patients with Schizophrenia and Schizoaffective Disorder

There has been much speculation as to the role of dopamine in the etiology and/or manifestation of positive and negative symptoms. Traditionally, cerebrospinal fluid (CSP) concentrations of homovanillic acid (HVA) has been used as an index of central dopaminergic activity. Relea~l dopamine is metabolized to HVA, by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) (Cooper et al 1991). A review of the CSF HVA literature, however, reveals no consistent correlations between HVA and schizophrenic symptomatoiogy (reviewed by Pickax et al ! 9907. Yet there is sufficient data to suggest that dopamine activity is abnormal in schizophrenia (Davis et al 19917. Therefore the evaluation of other putative measures of dopamine release or metabolism seems warranted. Released dopamine is also converted to dopamine sulfate (DASO47 by the enzyme phenolsulphotransferase (PST7 (Jenner and Rose, 1973). in the brain, it appears that the sulfoconjugation of dopamine occurs primarily outside of dopaminergic neurons (Tyce et al 1988). Therefore CSF DASO~ concentrations may reflect an important alternate route of dopamine metabolism. Assessment of PST-dependent DASO4 independently, or in re-