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ToxSci Advance Access published online on December 1, 2004
Toxicological Sciences, doi:10.1093/toxsci/kfi046
Toxicological Sciences © Society of Toxicology 2004; all rights reserved
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Received September 21, 2004
Accepted November 3, 2004

Neurotoxicology

Dietary Exposure to Aroclor 1254 Alters Central and Peripheral Vasopressin Release in Response to Dehydration in the Rat

Cary G. Coburn 1*, Elizabeth R. Gillard 2, and Margarita C. Currás-Collazo 3

1 Environmental Toxicology Program, University of California, Riverside
2 Department of Cell Biology & Neuroscience, University of California, Riverside
3 Department of Cell Biology & Neuroscience, University of California, Riverside; Environmental Toxicology Program, University of California, Riverside

* To whom correspondence should be addressed.
Cary G. Coburn, E-mail: Cgcoburn{at}aol.com


  Abstract

Central vasopressin (VP) release from magnocellular neuroendocrine cells (MNCs) in the supraoptic nucleus (SON) occurs from their somata and dendrites within the SON several hours after acute dehydration, and is an important autoregulatory mechanism influencing the systemic release of VP from MNC terminals in the posterior pituitary. To begin to explore the impact of polychlorinated biphenyls (PCBs) on brain mechanisms of body fluid regulation, both central and systemic VP release in response to acute dehydration were assessed in adult male rats fed the commercial PCB mixture Aroclor 1254 (30 mg/kg/day) for 15 days. Water intake and body weight were recorded daily, and on day 15 rats were dehydrated by intraperitoneal injection of 3.5 M saline (controls received physiological saline) and sacrificed 4-6 hrs later. Intranuclear VP release was measured in SON tissue punches in vitro, and systemic VP release was measured in the same rats. SON prepared from dehydrated PCB-naive rats released significantly more VP than did SON from control rats (4.9 ± 0.8 vs. 2.7 ± 0.4 pg/ml/µg). In contrast, while Aroclor 1254 exposure had no effect on baseline water intake, weight gain, or plasma osmolality responses to dehydration in PCB-fed rats, the SON failed to respond with increased VP release during dehydration. Consistent with previous studies showing an inhibitory effect of central VP on plasma VP output, dehydrated PCB-fed rats had an exaggerated 863% increase in plasma VP over basal levels, compared to a 241% increase in PCB-naïve rats, suggesting that the MNC system is subtly disrupted.

Keywords: osmoregulation; magnocellular neuroendocrine cells; polychlorinated biphenyls; somatodendritic release; supraoptic nucleus.
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