Abstract
Electron microscope studies revealedthat 6-hydroxydopamine (6-HODA) destroyed the aminergic (type ‘B’) neurosecretory axons entering the rostral pars distalis of the teleost Tilapia mossambica. 6-HODA had no effect upon plasma sodium or pituitary prolactin levels in seawater (SW) fish, although it prevented the fall in plasma sodium levels normally associated with transfer to fresh water (FW). Furthermore, the prolactin cells of 6-HODA-treated fish transferred to FW were activated as judged by ultrastructural and physiological criteria. These observations lead us to suggest that neurosecretory axons of hypothalamic origin and plasma osmolality interact to regulate teleost prolactin cells. On the other hand, 6-HODA evoked no obvious ultrastructural changes in the ACTH cells and no significant alterations in plasma cortisol concentrations. Thus, it would appear that type ‘B’ axons do not provide the major control of ACTH secretion in Tilapia.