PubMed Health⌕ Search

Biomedical subjects

J A Frederick

Publications and source records attributed to J A Frederick.

7 recordsLinked to original sources

Effects of clozapine and haloperidol on 5-HT6 receptor mRNA levels in rat brain.

The high affinity of 5-HT6 receptors for atypical antipsychotic drugs, and their localization in limbic and cortical regions of the brain, suggest that they might play a role in the pathophysiology of schizophrenia. To determine if this receptor is regulated by antipsychotics, rats were injected with clozapine (20 mg/kg/day), haloperidol (2 mg/kg/day), or vehicle daily for 2 weeks, and 5-HT6 receptor mRNA levels were measured by in situ hybridization. Clozapine but not haloperidol significantly decreased 5-HT6 expression in all subfields of the hippocampus. No drug effects were observed in cortical or forebrain structures. These results suggest that downregulation of this receptor in the hippocampus might be a characteristic of atypical antipsychotic drugs, although this hypothesis will require testing with other atypical antipsychotics.

Animals↗

Effects of 20-min audio-visual stimulation (AVS) at dominant alpha frequency and twice dominant alpha frequency on the cortical EEG.

The effects of audio-visual stimulation at the dominant alpha frequency and twice dominant alpha frequency on the EEG were investigated. An eyes-closed baseline EEG determined each subject's dominant alpha frequency. Subjects were stimulated at their dominant alpha frequency and at twice dominant alpha frequency for 20 min on two occasions. A 30-min post-session eyes-closed EEG was recorded after each session. Power data were analyzed for 19 locations in six bandpasses using repeated-measures ANOVAs and appropriate post-hoc tests. Alpha stimulation significantly increased power over baseline levels in the delta 1, delta 2, theta, beta 1 and beta 2, with significant effects remaining 30 min later in beta 1. Twice alpha stimulation significantly increased theta, beta 1 and beta 2 power over baseline levels, with significant effects remaining 30 min later in theta, alpha, beta 1 and beta 2.

Acoustic Stimulation↗

Instruments for assessment of auditory hallucinations.

The study of individual symptoms of schizophrenia, such as auditory hallucinations, can contribute to effective treatment strategies. We review existing instruments for the assessment of characteristics and dimensions of auditory hallucinations in schizophrenia and other psychiatric disorders and describe their psychometric properties and implications for their use in clinical research and practice. In addition, three widely used global measurement scales for symptoms of schizophrenia, each of which contain questions that pertain to hallucinations, are included.

Hallucinations↗

Nitric oxide may upregulate in vivo hepatic protein synthesis during endotoxemia.

Nitric oxide (NO) has been implicated as a mediator of hemodynamic and metabolic changes associated with endotoxemia and inflammation. In vitro studies suggest that NO inhibits hepatocyte protein synthesis but the role of NO in the regulation of hepatic protein synthesis in vivo is not known. In this study, rats were given endotoxin or saline after pretreatment with the NO synthase inhibitor NG-nitro-L-arginine or solvent, and plasma levels of nitrite (NO2), nitrate (NO3), and aspartate aminotransferase and hepatic protein synthesis rate in vivo were measured after 4 and 10 hours. The NG-nitro-L-arginine effectively blocked the increase in serum NO2/NO3 seen in endotoxemia and also inhibited the increase in hepatic protein synthesis in endotoxemic rats. The aspartate aminotransferase levels were elevated in endotoxemic rats pretreated with NG-nitro-L-arginine. Results support previous reports of a protective effect of NO on the liver in endotoxemia and suggest that NO may upregulate hepatic protein synthesis in vivo. Further study is needed to clarify the reason for the apparent difference between the effect of NO on hepatic protein synthesis in vivo and in vitro.

Amino Acid Oxidoreductases↗

Effect of sepsis or cytokine administration on release of gut peptides.

The effect of sepsis on plasma levels of various gut peptides was studied in rats. Sepsis was induced by cecal ligation and puncture (CLP); control animals underwent sham operation. Sixteen hours after CLP or sham operation, portal and systemic blood was drawn, and plasma levels of gastrin, vasoactive intestinal peptide (VIP), secretin, peptide YY (PYY), gastrin-releasing peptide (GRP), and substance P were determined by radioimmunoassay. Plasma levels of gastrin, VIP, PYY, and secretin were elevated in septic rats compared with nonseptic animals, with the highest levels noted in portal blood. There was no effect of sepsis on GRP or substance P levels. In other experiments, human recombinant interleukin 1 alpha (IL-1 alpha) or recombinant tumor necrosis factor alpha (TNF alpha) was injected intraperitoneally (300 micrograms/kg body weight in 3 divided doses over 16 hours). There was no change in plasma levels of gut peptides after IL-1 alpha injection. TNF alpha induced elevation of PYY levels in portal plasma with no change in other gut peptide levels. The results suggest that sepsis stimulates release of certain gut peptides and that TNF, but not IL-1, may be partly responsible for this response. The mechanism of the release of gut peptides and its significance in the pathophysiologic changes induced by sepsis remain to be determined.

Animals↗

Is the metabolic response to sepsis in skeletal muscle different in infants and adults? An experimental study in rats.

In this study we compared the effect of sepsis on muscle protein metabolism in infant (3 to 4 weeks) and adult (3 to 4 months) rats. Sepsis was induced by cecal ligation and puncture (CLP). Control animals underwent sham operation. Sixteen hours after CLP or sham operation, metabolic studies were performed in incubated intact extensor digitorum longus muscles from infant rats or in strips of the same muscle from adult rats. Protein synthesis rate was determined as incorporation of 3H-phenylalanine into protein; total and myofibrillar protein breakdown rates were determined as release of tyrosine and 3-methylhistidine, respectively. Mortality rate following CLP was similar in both age groups. Basal protein synthesis rate was 3 times higher, total protein breakdown rate was 50% higher, and myofibrillar protein breakdown rate was 3 times higher in infant than in adult animals. However, the relative changes in protein turnover rates induced by sepsis were similar in infant and adult rats: protein synthesis rate decreased by approximately 30%, total protein breakdown increased by 40% to 50%, and myofibrillar protein breakdown increased severalfold. The data suggest that despite prominent differences in basal protein turnover rates between infant and adult rats, the effect of sepsis on muscle protein metabolism is not age dependent.

Adenosine Triphosphate↗