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Neonatal exposure to methylmercury produces changes in patterns of tissue growth and function, in part, due to alterations in adrenergic neuronal input. To explore the mechanisms by which these changes come about, newborn rats were exposed to methylmercury (1 or 2.5 mg/kg per day) throughout the preweaning stage and the ontogeny of adrenergic receptor binding sites evaluated in liver, kidney, heart and lung, using [3H]prazosin (alpha 1-receptors), [3H]rauwolscine (alpha 2-receptors) and [125I]pindolol (beta-receptors). In the kidney, methylmercury caused decreases in beta- and alpha 1-receptor binding and increases in alpha 2-binding; previous work has shown that beta-receptor-mediated responses are generally enhanced in methylmercury-exposed pups, and the down-regulation of beta-receptor binding thus probably represents a compensatory action secondary to alterations in post-receptor coupling mechanisms. The effects of methylmercury on hepatic adrenergic receptors were different from those seen in the kidney, with substantial elevations in beta- and alpha 1-receptor binding apparent in the preweaning stage; this agrees also with the differences in effects of the mercurial on trophic reactivity and growth in the 2 tissues. Despite the fact that methylmercury causes activation of neonatal cardiac sympathetic nerves, beta-receptor binding sites in the heart were unaffected by methylmercury exposure; the failure to down-regulate cardiac postsynaptic receptors in the face of increased nerve activity again represents an anomaly of synaptic regulatory function. These results indicate that methylmercury alters adrenergic responsiveness, in part, through actions on the development of receptor binding sites, and further, that the organ-specificity and receptor subtype-selectivity are consistent with subsequent effects of the organomercurial on adrenergic participation in target organ growth; however, changes in receptor binding alone do not account for all of the effects of methylmercury on synaptic activity or trophic responses.
T A Slotkin, and
R J Kavlock, and
T Cowdery, and
L Orband, and
M Bartolome, and
W L Whitmore, and
J Bartolome
August 2003,
European journal of pharmacology,
T A Slotkin, and
R J Kavlock, and
T Cowdery, and
L Orband, and
M Bartolome, and
W L Whitmore, and
J Bartolome
October 1991,
Molecular pharmacology,
T A Slotkin, and
R J Kavlock, and
T Cowdery, and
L Orband, and
M Bartolome, and
W L Whitmore, and
J Bartolome
January 1989,
The Journal of neuroscience : the official journal of the Society for Neuroscience,
T A Slotkin, and
R J Kavlock, and
T Cowdery, and
L Orband, and
M Bartolome, and
W L Whitmore, and
J Bartolome
May 1980,
Neuropharmacology,
T A Slotkin, and
R J Kavlock, and
T Cowdery, and
L Orband, and
M Bartolome, and
W L Whitmore, and
J Bartolome
January 1990,
Acta neuropathologica,
T A Slotkin, and
R J Kavlock, and
T Cowdery, and
L Orband, and
M Bartolome, and
W L Whitmore, and
J Bartolome
January 1987,
Brain research bulletin,
T A Slotkin, and
R J Kavlock, and
T Cowdery, and
L Orband, and
M Bartolome, and
W L Whitmore, and
J Bartolome
January 1984,
Neurotoxicology,
T A Slotkin, and
R J Kavlock, and
T Cowdery, and
L Orband, and
M Bartolome, and
W L Whitmore, and
J Bartolome
March 1984,
European journal of pharmacology,
T A Slotkin, and
R J Kavlock, and
T Cowdery, and
L Orband, and
M Bartolome, and
W L Whitmore, and
J Bartolome
December 1984,
Research communications in chemical pathology and pharmacology,
T A Slotkin, and
R J Kavlock, and
T Cowdery, and
L Orband, and
M Bartolome, and
W L Whitmore, and
J Bartolome
January 1983,
Advances in biochemical psychopharmacology,
