Abstract
In Heteropneustes fossilis, contents and turnovers of hypothalamic catecholamines (CA) and activities of dopamine-β-hydroxylase (DBH) and phenylethanolamine-N-methyltransferase (PNMT) showed significant seasonal variations with significantly high day values. The seasonal pattern of dopamine (DA) on one hand and that of noradrenaline (NA) and adrenaline (A) on the other hand showed an inverse relationship, the former decreasing and the latter increasing during the progress of gonadal recrudescence. The DBH and PNMT levels were low in the resting phase and increased to the peak in the prespawning (DBH) and spawning (PNMT) phases. Maintenance of the fish under long photoperiods (16L:8D) and high temperature (28 ± 2°) stimulated the NA and A, and DBH and PNMT activities, and suppressed the DA mechanism, the changes being maximal in the raised temperature groups. In the resting phase (December), ovariectomy (OVX) or estradiol-17β, (E 2) replacement in 4-week ovariectomized fish did not produce any significant effects on the CA and enzyme activities. On the contrary, in the prespawning phase (May), OVX produced differential and biphasic responses on CA and the enzymes. The contents and turnovers of both NA and A increased significantly at 2-5 weeks and decreased in the sixth week. However, the reverse was true for DA. The DBH and PNMT activities (assayed only 3, 4, and 6 weeks after OVX) were elevated significantly in the third and fourth weeks but decreased in the sixth week. Plasma levels of gonadotropin (GTH) increased significantly at all durations of OVX in a bimodal pattern while the E 2 levels decreased consistently. Supplementation with a low dose (0.1 μg/g BW) or E 2 restored the NA and A and enzyme activities while the higher doses (0.5, 1.0, and 5.0 μg/g BW) depleted them. The reverse was true for DA. The low dose of E 2 restored the GTH level while the higher ones inhibited it significantly. These results indicate that both environmental photoperiod and temperature and E 2-negative feedback act on the CA to modulate GTH secretion.
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