title: Effects of the noradrenergic neurotoxin DSP-4 on luteinizing hormone levels, catecholamine concentrations, alpha 2-adrenergic receptor binding, and aromatase activity in the brain of the Japanese quail.
abstract: Previous investigations have established that DSP-4 reliably enhances the activating effects of testosterone on copulatory behavior in adult male quail. In the present study, we wanted to clarify the neurochemical changes that parallel these behavioral effects and to determine whether DSP-4 also affects non-behavioral steroid-dependent sexually dimorphic reproductive processes. We first showed using the Palkovits microdissection technique combined with assay by high-performance liquid chromatography (HPLC) that DSP-4 specifically depletes norepinephrine in several nuclei of the brain such as the medial preoptic nucleus, the ventromedial nucleus of the hypothalamus or the intercollicular nucleus but leaves intact the noradrenergic innervation in other areas such as the infundibulum or nucleus accumbens. Other amines such as dopamine and serotonin were not affected by the drug. Surprisingly DSP-4 did not decrease the binding of tritiated p-aminoclonidine in any of the brain areas which were studied by quantitative autoradiography. This suggests that most of the alpha 2-adrenergic receptors are located at the postsynaptic level but alternative interpretations are discussed. Testosterone treatment of castrated birds specifically reduced the density of alpha 2-adrenergic receptors in the dorsal infundibulum and in the medial mammillary nucleus. The possible relations of this receptor change to the control of luteinizing hormone (LH) secretion are discussed. Finally it was shown that DSP-4 treatment decreases plasma LH levels (which reveals the stimulatory effect of norepinephrine on LH secretion) but increases the testosterone-induced aromatase activity in the preoptic area. This latter effect could be one of the mechanisms by which DSP-4 potentiates copulatory behavior in testosterone-treated quail.
authors.affiliation: Laboratory of General and Comparative Biochemistry, University of Liège, Belgium.
authors.forename: J
authors.initials: J
authors.lastname: Balthazart
authors.forename: G F
authors.initials: GF
authors.lastname: Ball
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000378:metabolism; D000818:Animals; D001141:Aromatase / Q000378:metabolism*; D001596:Benzylamines / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002395:Catecholamines / Q000378:metabolism*; D003000:Clonidine / Q000031:analogs & derivatives / Q000378:metabolism; D003370:Coturnix / Q000378:metabolism*; D007986:Luteinizing Hormone / Q000097:blood*; D008297:Male; D009498:Neurotoxins / Q000494:pharmacology; D011784:Quail / Q000378:metabolism*; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D013739:Testosterone / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D001596:Benzylamines; D002395:Catecholamines; D009498:Neurotoxins; D011942:Receptors, Adrenergic, alpha; D013739:Testosterone; C016986:apraclonidine; D007986:Luteinizing Hormone; D001141:Aromatase; D003000:Clonidine; C012102:DSP 4