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Abstract

Long-term exposure to a low level of lead is associated with learning deficits. Several types of learning have been correlated to hippocampal protein kinase C (PKC) activation. This study was designed to determine if there is a correlation between the effects of lead on hippocampal PKC activation and those on learning performance. Rats were exposed to 0.2% (w/v) lead acetate at different developmental stages including a maternally exposed group, a postweaning exposed group, and a continuously exposed group. The continuously lead exposed rats tended to avoid less frequently and not respond more frequently in two-way active avoidance training than did controls. This training process was associated with translocation of hippocampal PKC activity from cytosol to membrane. Two-way analysis of variance of data indicates that there is a significant training and lead treatment interaction in the ratio of membrane to cytosolic PKC activity (F3,32 = 3.013; p = 0.044). The interaction is attributable to the absence of the training-induced PKC translocation in the continuously lead exposed rats. In addition, no significant changes were observed in learning performance and training-induced hippocampal PKC activation after maternal and postweaning lead exposure. Continuous and longer duration of lead exposure appears to affect the learning performance and hippocampal PKC activation. These data suggest that a change in the activation of hippocampal PKC may be involved in the lead-induced deficit in learning.

Influence of clozapine on neurodevelopmental protein expression and behavioral patterns in animal model of psychiatric disorder induced by low-level of lead

“…Additionally, a few behavioral patterns in open field test were reversed by clozapine treatment (Table 2). These results are consistent with previous studies showing that lead exposure may cause hyperactivity and deficits in learning and memory both in experimental animals and humans [31333435]. In PPI test, lead exposure failed to significantly affect the startle amplitude in a no-PPI trial in a previous study, but not startle amplitude at 120 dB [36].…”

Evaluation of passive avoidance learning and spatial memory in rats exposed to low levels of lead during specific periods of early brain development

“…Pregnant females were individually housed in maternity cages. The administration of lead (Pb) to the animals was performed according to the previously published protocol which had produced a blood lead levels 25-35 μg/dl in adult rats maintained on lead [19,20]. This dosage was selected as the blood lead levels 25-35 μg/dl seen in segments of population leaving in the area of environmental lead contamination throughout the world (Toscano and Guilarte, 2005) [21].…”

Using mouse models of autism spectrum disorders to study the neurotoxicology of gene–environment interactions

“…Lead-induced brain damage preferentially occurs in the prefrontal cortex, the cerebellum and hippocampus; all areas important for cognitive function, motor skill, and memory processes. Experiments in non-human primates and rodent models have consistently shown neurodevelopmental deficits due to lead exposure, including impairments in higher-order learning (Rice 1990), memory, and attention (Chen, Ma et al 1997; Salinas and Huff 2002). …”