By Nira Ben-Jonathan (auth.), Nelson D. Horseman (eds.)
It is an real privilege to have the ability to gather and edit a brand new quantity on "Prolactin," the 1st in different a long time to be dedicated to this interesting hormone in all its elements. the most obvious scientific reason for realizing prolactin (PRL) is the widespread prevalence of prolactinomas, the commonest form of pituitary tumor. thankfully, clinical administration of prolactinomas might be in keeping with our below status of the body structure of hypothalamic keep watch over of the lactotroph. Armed with this data, cures for proiactinomas are hugely profitable and good tolerated. Be explanation for the old and sensible significance of information concerning the hypothala mus-Iactotroph axis, the 1st chapters of this quantity are devoted to reviewing the body structure, improvement, and mobile biology of lactotroph law. Chapters concentrating on prolactinomas and similar scientific matters persist with those. PRL is the first hormone that's chargeable for "parental care" in lots of verte brate species. This reproductive procedure isn't really specified to mammals, however it has devel oped via evolution to be the imperative distinguishing characteristic of the mammalian lifestyles cycle. one of the mammals, mice became the best learn species in recent times. this is often traced to the improvement of quite a lot of tools for manipulating mouse genetics, and thereby influencing improvement, body structure and behaviour. Mice additionally supply a profound representation of the physiological demanding situations confronted in maternity. woman mice suffer a post-partum estrous, and sometimes are either pregnant and lactating simultaneously.
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Dwarf mice treated with PRL beginning at 21d or 30d had TIDA populations comparable to those of untreated dwarfs, approximately 50% of the normal population. These findings are summarized in Table 2-2. That PRL treatment beginning at 21d was not effective in maintaining the TIDA neurons suggests that the phenomena responsible for the loss of cells or phenotype (TH and DA production) are already operating at 21d of age. Table 2-2. Timing and specificity ofPRL replacement effects in Ames dwarf (df/dt) mice Treatment oPRL beg.
Role of Prolactin in Developmental Differentiation of Hypothalamic Dopaminergic Neurons 39 by lifelong PRL deficiency. Although CA fluorescence and TH immunoreactivity are reduced markedly in A12, cell number in -/- mice is comparable to that in +/- littermates. Interpretation must invoke, therefore, the currently popular "necessary and sufficient" trial ofPRL effect. While replacement studies in panhypopituitary dwarf mice show that PRL (alone, among PRL, GH and TSH deficiencies) is sufficient to maintain TIDA neuron differentiation, PRL evidently is not necessary (or specific) in this effect.
Neuroendocrinology 1990; 52:70-4. Phelps CJ, Carlson SW, Vaccarella MY. Hypothalamic dopaminergic neurons in prolactin-deficient Ames dwarf mice: localization and quantification of deficit by tyrosine hydroxylase immunocytochemistry. J Neuroendocrinol1994; 6: 145-52. Phelps C1. Isolated deficiency of tyrosine hydroxylase immunoreactivity in tuberoinfundibular neurons in pituitary prolactin-deficient Snell dwarf mice. Brain Res 1987; 416:354-8. Phelps CJ, Romero MA, Ma1camp C, Joseph SR. TIDA neuron number in developing Snell dwarf mice.