Irving I. Geschwind

The action of prolactin on the sex accessory glands of the male rat.

Summary Prolactin synergizes with testosterone to increase the wet weight of the dorsolateral prostate of the rat and the functional activity of this gland, as indicated by an increase in zinc content. Prolactin, in the absence of testicular androgens, increased the uptake of zinc by the dorsolateral prostate.

Dynamics of Luteinizing Hormone (LH) Secretion in the Cycling Ewe A Radioimmunoassay Study

Summary Three out of four cycling ewes followed for two full cycles showed a marked increase in radioimmunoassayable circulating LH levels shortly after the onset of estrus; although samples were taken every 8 hr, only one sample showed the increase in each cycle. The same four ewes were used to determine the half-life and distribution volume of exogenous ovine LH; an average half-life of 28 min and an uncorrected distribution volume of 9.14% of body weight were found. The results have been interpreted as indicating that almost all the LH was released from the pituitary in a surge lasting not more than 3 hr, and that the normal cycling ewe pituitary synthesizes approximately 0.5 mg of NIH-LH-S1 equivalent per day.

Studies on prolactin inhibition of thyroxine-induced metamorphosis in Rana catesbeiana tadpoles☆

Abstract Simultaneously administered prolactin partially prevents the induction by thyroxine of β-glucuronidase in tadpole tail, but does not affect the increases in hepatic ornithine transcarbamylase and tyrosine aminotransferase activities resulting from exposure to thyroxine. Prolactin also decreases the concentration of water-soluble protein of the tail below the levels found in tadpoles in thyroxine or control groups. The decrease in water-soluble protein appears to be mainly due to an increased water content of the tails of tadpoles treated with prolactin.

Evidence that serotonin may be a melanocyte stimulating hormone releasing factor in the lizard, Anolis carolinensis

Abstract Various substances were tested for an effect on MSH release from the pituitary of the lizard, Anolis carolinensis . On the basis of the following findings it is believed that serotonin may be an MSH releasing factor in this animal. 1. (1) Serotonin creatinine sulphate in the incubation medium stimulated MSH release from hemipituitaries at all stages of the incubation. At 2.6 × 10 −8 M serotonin, a stimulatory effect could just be detected, while at 7.8 × 10 −8 M , total MSH released was increased twofold and at 2.6 × 10 −7 M , more than threefold. 5-Methoxytryptamine at 2.6 × 10 −7 M doubled MSH release, but at the same concentration 5-hydroxytryptophan had no stimulatory effect. The effect of 2.6 × 10 −7 M serotonin was reduced by imidazole (10 m M ), suggesting that serotonin acts to stimulate MSH release through the adenyl cyclase-cyclic AMP mechanism. 2. (2) Subcutaneous injections of serotonin creatinine sulphate darkened green Anolis . Injected doses ranging from 3 to 10 μg/g caused skin darkening, beginning after 2 min and lasting for about 15 min. Since it lacked a direct darkening effect in vitro on melanocytes of Anolis skin, injected serotonin was believed to be acting directly on the pars intermedia of the pituitary. 3. (3) The precursor of serotonin, 5-hydroxytryptophan, had no direct action on melanocytes nor on the release of MSH from the pituitary in vitro , but injections of 14–200 μg/g caused darkening of lizards, beginning after a short delay of about 12 min and lasting for up to 48 hr with the larger doses. Tryptophan injections did not cause lizards to darken. Melatonin injections (20–100 μg/g) reversed 5-hydroxytryptophan-induced darkening, an effect which lasted for about 30 min with the larger doses of melatonin. Melatonin, by itself, in vitro , had no clear effect on MSH release from the pituitary but the stimulatory effect of 2.6 × 10 −7 M serotonin was reduced significantly by the presence of equimolar melatonin. Injected synthetic mammalian MRF (H.cysH. tyr. ile. gln. asn. OH) did not cause darkening of lizards and MIF-I (H-pro, leu. gly. NH 2 ) did not cause paling of 5-hydroxytryptophan-darkened lizards. MIF-I and MRF at 1 μg/ml had no effect on MSH release in vitro .

Hypothalamic control of gonadotropin release in amphibia: evidence from studies of gonadotropin release in vitro and in vivo.

Homogenates of frog (Rana pipiens) hypothalami stimulated in vitro release of bioassayable LH-like gonadotropin from frog hemipituitaries. In the first of two experiments gonadotropin release was significantly increased 3.7 times by 3.6 hypothalami/ml. In the second experiment 3.6 hypothalami/ml doubled the rate of gonadotropin release, but this increase was not statistically significant. A homogenate of frog neural and intermediate lobes did not increase the rate of gonadotropin release. Frog hypothalamic extract alone had no effect in the bioassay. Synthetic GnRH (Abbott), tested in vitro at 10 and 100 ng/ml each in two experiments, increased the release of gonadotropin between 2.6 and 10 times. Synthetic TRH did not stimulate in vitro release of gonadotropin. One microgram of GnRH injected into the dorsal lymph sac of PMS-pretreated Xenopus laevis caused ovulation in two out of four toads, while 1 μg of GnRH injected three times daily for 4 days into Xenopus with initially regressed ovaries had initiated vitellogenesis in one of two toads when the ovaries were examined after 8 days. In the absence of Ca2+ in the incubation medium, no stimulatory action of hypothalamic extract or GnRH on gonadotropin release was observed, and in this respect the action of releasing factors on frog gonadotropin release is similar to that on LH release in mammals. High potassium ion levels (5 times normal) stimulated in vitro release of gonadotropin 5.8 times over controls, another observation similar to experimence with mammals. It is concluded that the frog hypothalamus contains a factor capable of causing in vitro release of LH-like gonadotropin from the frog pituitary and that this factor may be similar in nature and mechanism of action to mammalian GnRH, which in frogs is active in vivo and in vitro.

Production of glucagon antibodies and their role in metabolism and immunoassay of glucagon.

Summary The antibody content of sera from rabbits treated intermittently with free glucagon or glucagon conjugated with ovalbumin was measured at intervals during a 2-year period. Circulating nonprecipitating antibody, capable of binding glucagon-I131, was detectable within one month, and was still detectable after 4 to 5 month periods during which no antigen was administered. Glucagon-I131 injected into an immunized rabbit was rapidly bound to antibody, remained chromatographically intact and was only slowly cleared from the circulation. Glucagon-I131 could be dissociated from its antibody at acid pH. The preferential salt precipitation technic used for immunochemical assay of insulin proved applicable to measurement of minute amounts of glucagon. The authors are indebted to Dr. Otto K. Behrens, Eli Lilly & Co. for supplies of recrystallized glucagon and for tests of antibody inhibition of glucagon activity in cats. We wish to acknowledge the technical assistance of Miss Angela Lee.

The characteristics of melanocyte stimulating hormone release from incubated pituitaries of the lizard, Anolis carolinensis

A procedure for studying melanocyte stimulating hormone (MSH) release from incubated hemipituitaries of the lizard, Anolis carolinensis, is described. Hemipituitaries incubated in vitro at 30° for 5 hr, released bioassayable MSH into the incubation medium; an initial phase of rapid release lasted .5-1 hr, followed by a lower rate of release during the remainder of the incubation. There was no evidence that MSH released from hemipituitaries and accumulated in the media influenced subsequent MSH release during the incubations. Release of MSH was dependent on the presence of Ca2+ in the medium. Increase of medium K+ to 56 mM did not alter the rate of MSH release at any stage of the incubation. The explanted lizard pars intermedia responded to low temperature in an unusual way. Tissue incubated at 15° released MSH at a lower rate than at 30°, but tissue incubated at 1–2° released MSH at a rate indistinguishable from that of tissue at 30°. MSH release at 1–2° was prevented by omitting Ca2+ from the medium, suggesting that MSH release in the cold was not the result of cell damage. When tissue was incubated at 1–2° during the first half-hour of incubation and allowed to rewarm to 30° there was no detectable increase in the rate of MSH release; when the same tissue was recooled to 1–2° during the fourth hour and rewarmed during the fifth, a greatly increased release of MSH resulted, indicating that during the initial period of release, but not at later times, the tissue was resistant to the effect of cooling on hormone release. Theophylline (8 mM) significantly increased MSH release at all stages of the incubation except during the first half-hour, suggesting that MSH release may be stimulated by raised intracellular cyclic AMP levels. Imidazole (10 mM), a cyclic AMP phosphodiesterase stimulator, significantly reduced MSH release by 82% during the first half-hour of incubation and again at 1–3 hr by 44%, but had no significant effect on MSH release at other times. These results may indicate that “basal” release at the earliest stage is linked to the adenyl cyclase-cyclic AMP mechanism, but it is not certain that MSH release is tightly linked to cyclic AMP production at later stages of the incubation.

Influence of prolactin on thyroxine-induced changes in hepatic and tail enzymes and nitrogen metabolism in Rana catesbeiana tadpoles.

Summary Thyroxine administered either alone or in conjunction with prolactin caused a decrease in hepatic protein concentration and an increase in hepatic glutamic dehydrogenase activity and specific activity in Rana catesbeiana tadpoles. Hepatic lactic dehydrogenase activity is decreased after thyroxine treatment, while prolactin alone caused an increase in the activity and specific activity of this enzyme, Tail lactic dehydrogenase activity, on the other hand, increased following thyroxine treatment. Thyroxine-treated animals were shown to have increased urea excretion which is prevented when prolactin is simultaneously administered, confirming the findings of Medda and Frieden (5). On the other hand, the pattern of ammonia excretion is identical in tadpoles treated with thyroxine or prolactin plus thyroxine. The possibility of a prolactin-thyroxine antagonism in mammals was examined in rats. It was found that prolactin, in the dose administered, had no antagonistic action on thyroxine-induced precocious eye opening.

Growth hormone activity in the lungfish pituitary

Abstract In contrast to results previously obtained with extracts of the pituitaries of five different species of teleosts and with extracts of the elasmobranch Squalus acanthias , reported below, extracts of the pituitary of the lungfish Protopterus aethiopicus showed definite evidence of growth hormone activity in the tibia test assay in the hypophysectomized rat.

Investigation of the cross-reaction of rat prolactin with antisera to ovine prolactin.

Abstract Although a number of investigators have employed antisera to ovine prolactin to localize the prolactin-containing cells of rat pituitaries by the fluorescent-antibody method, a cross-reaction between antisera to ovine prolactin and rat prolactin cannot be demonstrated using Ouchterlony or biological neutralization methods. However, a very small partial cross-reaction has been detected using a highly sensitive radioimmunotechnique. The significance of these results is discussed.