The organization of the pancreatic islets of Zonotrichia leucophrys gambelii is generally similar to that of other avian species. There are dark islets, mixed islets, light islets, and occasionally isolated islet cells. The density of islet tissue is greatest in the splenic lohe. Dark islets, which include A- and D-cells, are of varying size. Light islets consist of a pericapillary layer of B-cells with a peripheral layer of D- and sometimes A-cells. Mixed islets contain varying amounts of light and dark elements.

The concentration differences of more than 40 amino acids and related compounds in the amniotic fluid, allantoic fluid, and plasma of the chicken embryo are maintained by specific barriers. Since the amniotic and allantoic membranes are not innervated, we proposed that these barriers are controlled by hormones. Specific effects of insulin and prolactin on the amino compounds in the three fluids confirmed this hypothesis and raised the question of the possible role of growth factors. Application of insulin-like growth factor-I (IGF-I) to the chorioallantoic membrane of day 13 chicken embryos caused the following concentration changes in 41 amino compounds measured 1 and 2 h later: (1) in the amniotic fluid, an increase of 40 compounds, regardless of the presence or absence of a concomitant stress effect on these compounds; only NH3 was not affected; (2) in the allantoic fluid, a decrease of reduced glutathione (GSH) and anserine, and an increase of NH3; (3) in the plasma, a decrease of 24 compounds. Within the same time frame, stress caused in the amniotic fluid a drop of the concentration of 29, and an increase of 5, amino compounds; IGF-I reversed the stress effect on all 29 compounds the concentrations of which had dropped and enhanced the stress-induced increase of the other 5 compounds. In the allantoic fluid, stress induced an increase of GSH; IGF-I reversed this effect. In the plasma, stress caused an increase of 9 compounds; IGF-I counteracted the increase in 7 cases. These findings indicate new and unexpected roles of IGF-I in the prenatal regulation of amino compounds.

The impact of three different magnesium diets (70, 1,000 and 9,000 ppm) on total, ionized and bound magnesium as well as ionized calcium in serum and total calcium and magnesium in femoral bone, skeletal muscle, heart and liver of male Sprague-Dawley rats was investigated. The percentage of ionized serum magnesium was unproportionally high in rats fed a low magnesium (70 ppm) diet. Femoral magnesium was correlated with ionized and total serum magnesium. In contrast, there was generally no correlation between total serum magnesium and the magnesium fractions in skeletal muscle, heart and liver. In rats fed the magnesium deficient diet, total cardiac concentration of magnesium was even significantly increased along with total calcium content, while there were no effects on total muscle and liver magnesium. Within the single groups, ionized serum calcium was never proportional to dietary magnesium, but in all three magnesium diet groups together, it was inversely correlated with dietary magnesium. Moreover, ionized serum calcium was inversely correlated with both ionized and total serum magnesium. In all 3 groups together, the concentrations of total calcium and magnesium in heart and skeletal muscle were correlated, within the single groups correlation existed only in the 1000 ppm group. Magnesium influx via calcium channels during low magnesium intake has been seen in non cardiac tissues [35,36], but nothing similar is known about non selective channels for divalent cations in the heart [33]. Thus, magnesium uptake by cardiac cells along with calcium seems to be possible, especially at low intracellular magnesium concentrations, but is still poorly investigated. We suggest that the calcium-antagonistic effect of magnesium is related to the turnover rate of magnesium rather than to its tissue concentrations.

So far, more than 40 free amino acids and related compounds have been identified in plasma, amniotic fluid, and/or allantoic fluid of the 13-day chicken embryo. Concentration differences, and greatly varying behavior of these compounds under experimental conditions, revealed the presence of specific barriers among the three fluids. We tested the hypotheses that (1) the absence of an innervation of amnion and allantois indicates a hormonal control of their barriers, and (2) changes in the concentrations of certain amino compounds in the three fluids indicate anabolic or catabolic actions of hormones. Insulin, prolactin, and stress caused complex changes of the concentrations of amino compounds in all three fluids within 30 min. Some of these changes indicated breakdown of embryonic tissues, while others must have been due to transfer of amino compounds among the three fluid compartments. However, there was no significant effect on the glucose concentration in any of the three compartments under any of the experimental conditions. This is the first demonstration of hormonal effects on the amino compounds in the extraembryonic fluids of nonmammalian amniotes.

Plasma, allantoic and amniotic fluid of the 13-day chicken embryo contain numerous free amino acids and related compounds. Of these, 40 were investigated using an HPLC-fluorometric technique. The concentration differences of the amino compounds between the fluid compartments are maintained by three bidirectional barriers, i.e. a blood/allantoic barrier, a blood/amnion barrier and an allantois/amnion barrier. Intraallantoic injection of 4.5 μmol/egg of asparagine (ASN), aspartic acid (ASP), valine (VAL) or serine (SER) revealed a strong allantois/blood barrier for these compounds. In contrast, there was equilibration between allantoic and amniotic fluid for ASN, ASP and SER, and an upward trend of the VAL concentration in the amniotic fluid, due to an `overspill' from the allantois. The injections also affected endogenous amino compounds in all three fluid compartments. Asparagine had the most varied effects, including a strong drop of ten plasma amino acids. After all four types of injection, a number of endogenous amino compounds equilibrated between allantois and the normally hyporegulated amnion. Since allantois and amnion are non-innervated, the selective changes of the barriers and the drop of plasma amino acids must be mediated by so far unidentified humoral messengers.

The innervated chromaffin cells of the eel (Anguilla rostrata) release norepinephrine (NE) and epinephrine (E), while a component of the macrovascular wall releases dopamine (DA). The release of the three catecholamines is governed by complex controls which include adrenergic, nicotinergic, muscarinergic, and opioid mechanisms. To gain insight into the interactions between neural and autocrine factors in stimulated catecholamine release, we investigated the effect of adrenergic (phentolamine and propranolol) and muscarinergic (atropine) receptor antagonists, and of autocrine opioids (met-enkephalin, codeine, and morphine) on electrostimulated catecholamine secretionin situ.The hind brain (close to the root of nerve IX) of anesthetized eels was stimulated at four different time points, and segments of the posterior cardinal vein or the caudal vein were perfused with a saline solution, with or without test substances. Electrostimulation (30 s) four times within a total study duration of 14 min increased the release of DA, NE, and E into the perfusate of the cardinal vein. The vessel contains the innervated adrenomedullary equivalent. In the noninnervated caudal vein electrical stimulation had no impact on total DA release, while there was a slight decrease of NE release and a slight increase of E release. In the cardinal vein, both the alpha-adrenergic receptor antagonist phentolamine and the beta-adrenergic receptor antagonist propranolol strongly reduced the effect of electrostimulation on catecholamine release. Met-enkephalin reduced the release of all three catecholamines to a similar degree; its impact on NE release was especially strong. Codeine reduced the catecholamine release moderately, while morphine had no effect. Atropine reduced the release of all three catecholamines in a pattern similar to that of met-enkephalin. The findings on the posterior cardinal vein indicate that neurally stimulated NE and E release (1) involves autocrine/paracrine adrenergic mechanisms, (2) involves a muscarinergic mechanism, and possibly also endogenous codeine and morphine; and (3) is antagonized by met-enkephalin. The findings on the caudal vein are further evidence that macrovascular DA release is not under direct neural control.

The perifused posterior cardinal vein of the American eel (Anguilla rostrata) releases spontaneously dopamine (DA), norepinephrine (NE), and epinephrine (E). NE and E are secreted by innervated chromaffin cells, while DA is most likely released from a component of the vascular wall. Stimulation with acetylcholine strongly enhances the release of DA and E, and to a lesser degree the release of NE. Nicotine stimulates the release of all three catecholamines. Muscarine reduces the basal release of NE. Muscarine does not prevent nicotinic stimulation of NE and E release, but abolishes the nicotine effect on DA release. The muscarinic antagonist atropine stimulates the release of NE, but not of DA and E. The beta-adrenergic receptor antagonist propranolol suppresses the acetylcholine-stimulated release of NE and E, and reduces the DA response. From these findings, it appears that (1) nicotinic receptors regulate NE and E secretion from the chromaffin cells, (2) muscarinic receptors inhibit basal NE release, and (3) acetylcholine-stimulated release of NE and E requires the interaction with adrenergic receptors. On the other hand, DA release involves both nicotinic and adrenergic receptors, while the reduction of nicotine-stimulated (but not basal) DA release involves muscarinic receptors.

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The day 13–14 chicken embryo is a useful model for studies on prenatal stress responses. Free dopamine, norepinephrine and epinephrine in its plasma, amniotic and allantoic fluid respond to a variety of stresses. The allantoic fluid also contains conjugated catecholamines and conjugated steroids. However, a blood/allantois barrier excludes free thyroid hormones and free steroids, and insulin. On the other hand, the allantoic fluid contains at least 40 amino acids (including six excitatory amino acids) and related compounds. Most, possibly all, components of the allantoic fluid are regulated at specific blood/allantois and amnion/allantois barriers, and they respond to ethanol stress and metabolite loading differentially. The avian allantois is a depot for important metabolites and messenger substances which seems to be controlled by as yet unidentified hormones