Imidacloprid Induces Neurobehavioral Deficits and Increases Expression of Glial Fibrillary Acidic Protein in the Motor Cortex and Hippocampus in Offspring Rats Following in Utero Exposure

The potential for neurotoxicity following in utero exposure to imidacloprid is not known. Timed pregnant Sprague-Dawley rats (300–350 g) on d 9 of gestation were treated with a single intraperitoneal injection (ip) of imidacloprid (337 mg/kg, 0.75 × LD50, in corn oil). Control rats were treated with corn oil. On postnatal day (PND) 30, all male and female offspring were evaluated for (a) acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activity, (b) ligand binding for nicotinic acetylcholine receptors (nAChR) and muscarinic acetylcholine receptors (m2 mAChR), (c) sensorimotor performance (inclined plane, beam-walking, and forepaw grip), and (d) pathological alterations in the brain (using cresyl violet and glial fibrillary acidic protein [GFAP] immunostaining). The offspring of treated mothers exhibited significant sensorimotor impairments at PND 30 during behavioral assessments. These changes were associated with increased AChE activity in the midbrain, cortex and brainstem (125–145% increase) and in plasma (125% increase). Ligand binding densities for [3H]cytosine for α4β2 type nAchR did not show any significant change, whereas [3H]AFDX 384, a ligand for m2mAChR, was significantly increased in the cortex of offspring (120–155% increase) of imidacloprid-treated mothers. Histopathological evaluation using cresyl violet staining did not show any alteration in surviving neurons in various brain regions. On the other hand, there was a rise in GFAP immunostaining in motor cortex layer III, CA1, CA3, and the dentate gyrus subfield of the hippocampus of offspring of imidacloprid-treated mothers. The results indicate that gestational exposure to a single large, nonlethal, dose of imidacloprid produces significant neurobehavioral deficits and an increased expression of GFAP in several brain regions of the offspring on PND 30, corresponding to a human early adolescent age. These changes may have long-term adverse health effects in the offspring.

Source:
DOI:10.1080/15287390701613140
Mohamed B. Abou-Donia, Larry B. Goldstein, Sarah Bullman, T. Tu, Wasi A. Khan, Ankelika M. Dechkovskaia & Ali A. Abdel-Rahman
Journal of Toxicology and Environmental Health, Part A: Current Issues
Volume 71, Issue 2, 2008
pages 119-130
article attached
Information on GFAP:
http://en.wikipedia.org/wiki/Glial_fibrillary_acidic_protein
Information on the Anatomy of the Hippocampus:
http://en.wikipedia.org/wiki/Hippocampus_anatomy