Effects of developmental stress and lead (Pb) on corticosterone after chronic and acute stress, brain monoamines, and blood Pb levels in rats

Abstract

Despite restrictions, exposure to lead (Pb) continues. Moreover, exposure varies and is often higher in lower socioeconomic status (SES) families and remains a significant risk to cognitive development. Stress is another risk factor. Lower SES may be a proxy for stress in humans. When stress and Pb co-occur, risk may be increased. A few previous experiments have combined Pb with intermittent or acute stress but not with chronic stress. To determine if chronic developmental stress affects outcome in combination with Pb, we tested such effects on growth, organ weight, brain monoamines, and response to an acute stressor. Sprague Dawley rats were gavaged with Pb acetate (1 or 10 mg/kg) or vehicle every other day from postnatal day (P)4-29 and reared in standard or barren cages. Subsets were analyzed at different ages (P11, 19, 29). Chronic stress did not alter blood Pb levels but altered HPA axis response during early development whereas Pb did not. Pb treatment and rearing each altered organ to body weight ratios, most notably of thymus weights. Both Pb and rearing resulted in age-and region-dependent changes in serotonin and norepinephrine levels and in dopamine and serotonin turnover. The model introduced here may be useful for investigating the interaction of Pb and chronic developmental stress.

Developmental manganese neurotoxicity in rats: Cognitive deficits in allocentric and egocentric learning and memory

“…Gavage solutions were given in a volume of 3 mL/kg of VEH every other day from P4-28. Gavage was used to avoid maternal exposure and its effects on maternal-pup behavior (Graham et al, 2011). This exposure regimen produces increased serum and brain Mn (Amos-Kroohs et al, 2015) but does not increase corticosterone above that of untreated littermates (Graham et al, 2011).…”

Effects of Neonatal Methamphetamine and Stress on Brain Monoamines and Corticosterone in Preweanling Rats

“…Standard-caged housing was as described above. For barren-caged housing, the woodchip bedding and stainless steel hut were replaced with a single paper towel, as described in Gilles et al (1996), with modification (Graham et al 2011). Cages and paper towels were changed each day.…”

“…Tissue concentrations of DA, DOPAC, homovanillic acid (HVA), norepinephrine (NE), 5-HT, and 5-hydroxyindoleacetic acid (5-HIAA) in the neostriatum, hippocampus, and prefrontal cortex were quantified via high performance liquid chromatography with electrochemical detection (as described in Graham et al 2011). Frozen samples (−80 °C) were weighed, thawed, and sonicated in proper volumes of 0.1 N perchloric acid (Fisher Scientific, Pittsburgh, PA) and centrifuged at 4 °C for 14 min (13,000 RCF).…”

“…Because early life stress and MA exposure induce changes in the stress response, neurochemistry, and behavior of the exposed animals (Vorhees et al 2009; Graham et al 2011), we examined the combined effect of chronic developmental stress and MA exposure on stress responses and neurochemistry. Monoamines and their metabolites were determined in the neostriatum, hippocampus, and prefrontal cortex at two ages (P15 and P20).…”

CURCUMIN ATTENUATES LEAD (Pb)–INDUCED NEUROBEHAVIORL AND NEUROBIOCHEMICAL DYSFUNCTION: A REVIEW

“…The level of oxidative stress markers such as protein carbonyl and lipid peroxidation observed in LA treated rats were increased, whereas the activity of enzymatic antioxidants, non-enzymatic antioxidants and neurotoxicity biomarker were strongly depleted. Developmental stress induced by the accumulation of lead was studied previously [25][26][27][28][29][30]. Liu et al (2013) evaluated the impact of puerarin and its protective effect on mice lead-induced cognitive impairment by modifying the enzyme activities, including, nitric oxide synthase, monoamine oxidase, and acetyl cholinesterase [25].…”