Published in:
01-03-2013 | Original Paper
Alteration in plasma corticosterone levels following long term oral administration of lead produces depression like symptoms in rats
Authors:
Saida Haider, Sadia Saleem, Saiqa Tabassum, Saima Khaliq, Saima Shamim, Zehra Batool, Tahira Parveen, Qurat-ul-ain Inam, Darakhshan J. Haleem
Published in:
Metabolic Brain Disease
|
Issue 1/2013
Login to get access
Abstract
Lead toxicity is known to induce a broad range of physiological, biochemical and behavioral dysfunctions that may result in adverse effects on several organs, including the central nervous system. Long-term exposure to low levels of lead (Pb2+) has been shown to produce behavioral deficits in rodents and humans by affecting hypothalamic-pituitary-adrenal (HPA) axis. These deficits are thought to be associated with altered brain monoamine neurotransmission and due to changes in glucocorticoids levels. This study was designed to investigate the effects of Pb2+exposure on growth rate, locomotor activity, anxiety, depression, plasma corticosterone and brain serotonin (5-HT) levels in rats. Rats were exposed to lead in drinking water (500 ppm; lead acetate) for 5 weeks. The assessment of depression was done using the forced swimming test (FST). Estimation of brain 5-HT was determined by high-performance liquid chromatography with electrochemical detection. Plasma corticosterone was determined by spectroflourimetric method. The present study showed that long term exposure to Pb2+ significantly decreased the food intake followed by the decrease in growth rate in Pb2+exposed rats as compared to control group. No significant changes in open field activity were observed following Pb2+exposure while significant increase in anxiogenic effect was observed. Increased plasma corticosterone and decreased 5-HT levels were exhibited by Pb2+exposed rats as compared to controls. A significant increase in depressive like symptoms was exhibited by Pb2+exposed rats as compared to control rats. The results are discussed in the context of Pb2+ inducing a stress-like response in rats leading to changes in plasma corticosterone and brain 5-HT levels via altering tryptophan pyrrolase activity.