Effect of polyamine depletion on cone photoreceptors of the developing rabbit retina.

Purpose: To measure the concentrations of polyamines, determine their cellular and subcellular localization, and analyze effects of their depletion in developing rabbit retina.

Methods: Isolated retinas at different developmental stages were analyzed for polyamine content by high-performance liquid chromatography (HPLC). An antibody against polyamines was used to localize endogenous stores in both freshly harvested retinas and neonatal retinal explants.

Insulin-like growth factor-I receptor antagonism results in increased cytotoxicity of breast cancer cells to doxorubicin and taxol.

Therapeutic strategies for patients with advanced-stage adenocarcinoma of the breast frequently include the use of cytotoxic chemotherapy. Insulin-like growth factor I (IGF-I) receptor, a key factor in cell-cycle regulation, is frequently overexpressed in high-grade breast cancers. IGF-I receptor overexpression in these tumors may provide a target for novel molecular therapy against this disease.

Subclavian artery injuries.

Thirty-two consecutive patients with subclavian artery injuries were evaluated to assess the mechanism of injury, types of repair, and results. In this series, most wounds were from firearms. Although the mortality was high (19%), most patients had the vessel repaired successfully.

Antihypertensives and the risk of serious hypoglycemia in older persons using insulin or sulfonylureas.

Context: Beta-Blockers and angiotensin-converting enzyme (ACE) inhibitors are effective antihypertensive agents for patients with diabetes mellitus. However, beta-blockers attenuate some components of the autonomic response to hypoglycemia and could increase the risk of hypoglycemia. ACE inhibitors may increase insulin sensitivity and predispose users to hypoglycemia.

Central stimulation of oxytocin release in the lactating rat by N-methyl-D-aspartate: requirement for coactivation through non-NMDA glutamate receptors or the glycine coagonist site.

Excitatory amino acid (EAA) neurotransmitters participate in the regulation of secretion of several neuropeptides, including oxytocin (OT), via actions at different receptors. In earlier studies, release of OT could be achieved reliably by injection into the supraoptic nucleus (SON) of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate receptor agonists, but not by treatment with N-methyl-D-aspartate (NMDA) alone. This prompted further examination of the possible role of NMDA receptors in OT release following central coapplication of NMDA and AMPA-site agonists, or of NMDA and agonists active at the glycine coagonist site.

Role of multiple voltage-sensitive calcium channels in depolarization-induced release of neuropeptide y and luteinizing hormone-releasing hormone from rat median eminence-arcuate nucleus.

The objective of the present studies was to identify the subtypes of voltage-sensitive Ca(2+) channels (VSCC) that regulate the basal and depolarization-induced release of neuropeptide Y (NPY) and LH-releasing hormone (LHRH) from rat hypothalamus. Tissues containing median eminence-arcuate nucleus (ME-ARC) were dissected from male rats and incubated in vitro in the presence and absence of agents selectively affecting N- or L-type VSCC. KCl depolarization-induced release of NPY, but not basal release, was abolished by Ca(2+)-free/EGTA medium and was significantly reduced by cobalt.

Stimulation of oxytocin release in the lactating rat by a central interaction of alpha 1-adrenergic and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid-sensitive excitatory amino acid mechanisms.

These studies tested for a facilitatory interaction between noradrenergic and excitatory amino acid mechanisms controlling oxytocin (OT) release in the lactating rat. Lactating females were cannulated in the supraoptic nucleus of the hypothalamus (SON) or into the third ventricle and treated with the alpha 1-agonist phenylephrine (PHE) or the glutamate receptor agonist alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), either alone or together. Treatment with PHE increased plasma OT dose dependently after microinjection into the SON area; strong stimulation also occurred after third ventricle injection of the drug.

Stimulation of oxytocin release in the lactating rat by central excitatory amino acid mechanisms: evidence for specific involvement of R,S-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid-sensitive glutamate receptors.

To examine whether an excitatory amino acid (EAA) neurotransmitter may influence the secretion of oxytocin (OT), agonists and antagonists selective for three major groups of EAA receptors were microinjected into the area of right supraoptic nucleus (SON) of conscious unrestrained lactating rats. An increase in plasma OT concentration was induced by the EAA receptor agonist R,S-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and kainic acid, but not by agonists at other EAA receptors, such as N-methyl-D-aspartic acid (NMDA) or the metabotropic agonist (1S,3R)-1-amino-cyclopentane-1,3-dicarboxylic acid. Increasing AMPA doses between 0.

Low-osmolar contrast media in the 1990s. Guidelines for urography in a cost-sensitive environment.

Objectives: The author reviews the clinical, ethical, medicolegal, and economic consequences of the routine versus limited use of low-osmolar contrast media for patients undergoing urographic and other radiologic studies.

Methods: A comprehensive review of the literature since the introduction of low-osmolar contrast media was conducted, focussing on medical decision making and the economic impact of those decisions on radiologic studies requiring the administration of water-soluble contrast agents.

Results: Compared with high-osmolar ionic contrast media, routine use of low-osmolar agents for intravascular injection during diagnostic imaging results in fewer idiosyncratic reactions in patients and potentially less renal injury in a subgroup of critically ill patients.

Neurochemical regulation of hypothalamic oxytocin messenger ribonucleic acid levels during early lactation in rats.

The objective of the present studies was to investigate whether the stimulatory influence of the suckling offspring on the level of hypothalamic oxytocin (OT) messenger RNA (mRNA) in early lactation in rats is mediated by activation of the central noradrenergic and/or oxytocinergic systems, both of which have been strongly implicated in suckling-induced OT release. Experiments tested whether the effect of litter separation immediately postpartum to reduce hypothalamic OT mRNA could be mimicked by pharmacological disruption of either noradrenergic or oxytocinergic signals. Bilateral microinjections of the catecholamine neurotoxin 6-hydroxydopamine into either the supraoptic nucleus (SON) or paraventricular nucleus/anterior commissural nucleus regions significantly reduced the concentrations of norepinephrine in these areas, but did not alter the relative levels of OT mRNA in these regions, suggesting that the stimulatory inputs provided by the suckling offspring are not transmitted through the noradrenergic system.

Central stimulation of oxytocin release in the lactating rat: interaction of neuropeptide Y with alpha-1-adrenergic mechanisms.

The possible cooperation of neuropeptide Y (NPY) and alpha-1-adrenergic mechanisms in the release of oxytocin (OT) in conscious, nonsuckled lactating rats was examined following microinjections of NPY and its analogs and/or alpha-adrenergic drugs into the supraoptic nucleus (SON) or anterior paraventricular nucleus/anterior commissural nucleus (PVN/ACN). The alpha-1-adrenergic agonist phenylephrine dose dependently increased plasma OT after injection into the SON or the PVN/ACN, and this was prevented by treatment with the specific alpha-alpha-1-adrenergic receptor antagonist prazosin, but not by the alpha-2 antagonist rauwolscine. The alpha-2-adrenergic agonist clonidine did not increase plasma OT.

Activation of central D-1 dopamine receptors stimulates oxytocin release in the lactating rat: evidence for involvement of the hypothalamic paraventricular and supraoptic nuclei.

The stimulatory effect of dopamine (DA) on the release of oxytocin (OT) in lactating rats is exerted at the D-1 DA receptor subtype. Because the neural loci mediating this effect have not been identified, the objective of the present studies was to test whether OT release in the lactating rat would be elevated after central administration of a D-1 DA receptor agonist into the third ventricle (3V) or directly into either the rostral paraventricular/anterior commissural nucleus area (PVN/ACN), the central paraventricular nucleus area, or the supraoptic nucleus (SON), all of which contain OT neurosecretory cells. Lactating rats were implanted with a stainless steel cannula directed into one of the above areas or into the arcuate-ventromedial region of the medial basal hypothalamus (MBH), or sites dorsal to the PVN/ACN or SON, which served as anatomical controls.

Afferent stimulation regulates oxytocin messenger ribonucleic Acid during early lactation in rats.

The physiological factors that regulate the levels of oxytocin (OT) mRNA in the rat hypothalamo-neurohypophyseal system during lactation are unknown. The major objective of the present studies was to test whether afferent stimuli provided by the offspring influence the level of OT mRNA in the magnocellular nuclei of the hypothalamus, i.e.

Relationship of calbindin D-28k and cholinergic neurons in the nucleus basalis of Meynert of the monkey and the rat.

Double-labeling immunocytochemistry reactions were carried out in the monkey and the rat nucleus basalis of Meynert (NBM) to determine the extent of overlap between cholinergic neurons and neurons immunoreactive for calbindin-D-28k (CaBP), a Vitamin D-dependent calcium binding protein. The results indicate that most, but not all, NBM cholinergic neurons in the monkey are immunoreactive for CaBP. On the other hand, none of the rat NBM cholinergic neurons are immunoreactive for CaBP.

Prolactin stimulates the release of oxytocin in lactating rats: evidence for a physiological role via an action at the neural lobe.

The present studies were designed to investigate whether prolactin (PRL) influences the secretion of oxytocin (OT) in lactating rats, and to test whether the previously reported inhibitory and stimulatory effects of dopamine-2 (D-2) agonists and antagonists, respectively, on OT release might be secondary to their respective inhibitory and stimulatory effects on the release of PRL. Intravenous administration of either rat (r) or ovine (o) PRL to lactating, nonsuckled rats increased basal plasma concentrations of OT. rGH was ineffective, but administration of oGH did produce some stimulation of OT release.

Neuropeptide Y modulates the binding of a gonadotropin-releasing hormone (GnRH) analog to anterior pituitary GnRH receptor sites.

Neuropeptide Y (NPY) increases LH secretion in part by enhancing the release of LH in response to GnRH. The present studies examined whether NPY influences the binding of GnRH to its receptors and also assessed whether specific binding sites for NPY exist in rat anterior pituitary membranes. In concentrations from 66-200 nM, NPY dose-dependently enhanced the binding of a 125I-labeled GnRH agonist, [D-Ala6, des-Gly10]GnRH ethylamide (GnRHa; 30 pM) to anterior pituitary membranes of chronically ovariectomized rats; higher concentrations of NPY were ineffective.

Calcitonin inhibits thyrotropin-releasing hormone-induced increases in cytosolic Ca2+ in isolated rat anterior pituitary cells.

Calcitonin (CT) and related peptides, such as CT gene-related peptide and salmon CT (sCT)-like peptide, are present in the rat nervous system and the pituitary gland, and sCT markedly inhibits basal and TRH-stimulated PRL release from anterior pituitary (AP) cells. Because TRH-induced PRL release is known to involve increases in cytosolic free Ca2+ derived from both extracellular and intracellular sources, the objective of the present study was to test whether sCT interferes with this effect. Secretogogue-induced elevations of cytosolic free Ca2+ ([Ca2+]i) in acutely dispersed AP cells were monitored using the fluorescent Ca2+ indicator Indo-1 AM and flow cytometry.