Hypothalamic extracts from frogs (Rana pipiens) were found to contain a significant quantity of immunoreactive LHRH (3.27 +/- 0.63 ng/hypothalamus) (mean +/- SE) measured by radioimmunoassay. In additional radioimmunoassay studies of gross brain LHRH distribution in R. pipiens and R. catesbeiana, 16% of the total frog brain LHRH was located within the telencephalon-septum-optic chiasm regions while the remainder was distributed within the infundibular hypothalamic-pituitary complex. Immunohistochemical studies using the peroxidase-anti-peroxidase (PAP) unlabeled antibody enzyme technique demonstrated the presence of LHRH selectively within some neuronal perikarya located primarily in the median septal nucleus. Fibers containing immunoreactive LHRH were seen in the vicinity of these neuronal cell bodies and in the medial and lateral septal nuclei. In addition, LHRH-containing fibers extended to the median eminence and posterior pituitary, transversing a course beneath the preoptic recess or through the medial forebrain bundle, and then through the lateral infundibular hypothalamus to enter the median eminence bilaterally. LHRH within the median eminence was located in both the inner subependymal and outer glandular zones. On the basis of earlier physiological studies, it is proposed that this LHRH-peptidergic septo-infundibular pathway is involved in control of cyclic gonadotropin activity in the frog.

Animals↗

PubMed1976

Prolactin-releasing factor (PRF) in porcine hypothalamic extract distinct from TRH.

Extracts of porcine hypothalamic fragments (HF) bring about the release of prolactin when injected into estrogen-progesterone pretreated male rats. To determine the extent to which this prolactin-releasing activity (PRA) is attributable to thyrotropin-releasing hormone (TRH) and/or vasopressin (VP), (both hormones capable of releasing prolactin in this preparation), PRA was assayed following destruction of TRH and VP by incubation in rat serum, and after separation on Sephadex G-25 columns. Acetic acid (2N) extracts of HF contain 22 to 27 ng TRH and 650 to 1000 ng of VP per HF as determined by immunoassay. Incubation for 1 h in fresh rat serum degraded 91 to 99% of both TRH and VP. PRA fell after incubation, but was still detectable, indicating residual activity that resisted degradation. Prolactin release responses to HF extracts and to TRH were log-dose dependent, but had different activity slopes. The minimal detected dose of TRH which released prolactin was 10 ng, while minimal effective doses of serum inactivated HF extract contained only 0.6 ng of TRH. Maximum effects with serum-inactivated HF extract were achieved with 2 HF equivalents containing 2.6 ng of TRH. More than 400 ng of TRH were required to give an equivalent PRA response. Sephadex G-25 chromatography of hypothalamic extracts using 2.0 N acetic acid separated a fraction which after treatment with serum to inactivate most TRH present caused marked prolactin release and contained only 0.7 ng of TRH and 0.3 ng of VP per dose. Evidence for a PIF was the demonstration that retarded fractions from the column significantly decreased plasma prolactin levels. The finding of PRA in hypothalamic extracts separate from both TRH and VP is evidence for the existence of a distinct prolactin-releasing factor.

Animals↗

PubMed1976

Inherited hypothyroidism.

Familial hypothyroidism results from both thyroidal and extrathyroidal dysfunction. Specific intrathyroidal abnormalities in thyroid hormone synthesis causing goitrous hypothyroidism are iodide trap defect, organification defect, "coupling" defect, iodoprotein defect, and dehalogenase defect. The diagnostic studies for each are outlined utilizing radioiodine(131I) studies. Other causes of cretinism include failure of the thyroid gland to respond to TSH and lack of pituitary TSH (or hypothalamic TRH). The syndrome of peripheral resistance to thyroid hormone is discussed. The diagnosis of inherited hypothyrodism rests on an adequate family history and measurement of both T4 and TSH levels which can be determined in cord blood or peripheral blood from the infant. The importance of early treatment of hypothyroidism in the neonatal period to prevent brain damage is emphasized. The rec:nt discovery of the importance of reverse T3 (RT3) in fetal thyroid metabolism is described, and the possibility of amniocentesis as an aid in prenatal diagnosis is considered. The place of intrauterine administration of thyroid hormone to the fetus at risk from hypothyroidism is uncertain at this time and requires carefully controlled studies and long-term follow-up.

Biological Transport↗

PubMed1975

Editorial: "Hyper-thyroiditis" - a diagnostic pitfall.

Explore the source record for details and available documents.

Diagnosis, Differential↗

PubMed1975

Thyrotoxicosis due to "silent" thyroiditis.

3 patients (2 male, 1 female) presented with symptoms of thyrotoxicosis associated with elevated blood-levels of thyroid hormone and a markedly depressed thyroidal uptake of 131-I. The male patients (aged 59 and 47) each had a cardiac arrhythmia, but did not have any thyroid pain or swelling. The female with a goitre had no discomfort in the neck. Thyrotoxicosis factitia was excluded by history. The subsequent course of their disease was typical of subacute thyroiditis. The elevated thyroid-hormone levels spontaneously fell to normal over a few weeks. In 1 patient, however, chemical hypothyroidism developed. These patients could have been diagnosed as having hyperthyroidism, rather than subacute thyroiditis, since thyroid pain--and swelling in 2 of the cases--was absent. The correct diagnosis was suspected only after finding a thyroidal uptake of 131-I near zero. The thyroidal uptake of 131-I is still important as a routine diagnostic aid in thyroid disease.

Adult↗

PubMed1975