We have produced and characterized a new high titer, highly specific antiserum for luteinizing hormone-releasing hormone (LHRH), and demonstrated its usefulness for radioimmunoassay (RIA) and immunocytochemistry. The antiserum can be used at a final dilution of 1:500,000 to 1:600,000 for RIAs with a sensitivity of 0.2 pg/tube. Both the amino and carboxy terminal ends of the LHRH molecule are required for antibody recognition, and the antigenic determinant appears to be part of a three-dimensional structure of LHRH. Fragments of LHRH and other brain peptides are not recognized by the antiserum. Using immunocytochemical techniques, we have localized LHRH-containing neurons in the medial basal hypothalamus of the rhesus monkey, guinea pig, and rat. Staining of LHRH fibers and cell bodies was eliminated by preabsorbtion of the immune serum with synthetic LHRH. This antiserum should be useful in studies that require quantification of very low amounts of LHRH and in studies that require correlation between immunocytochemical localization and tissue content or secretion of LHRH.

Animals↗

PubMedDate not supplied

Rapid effects of estrogen to modulate G protein-coupled receptors via activation of protein kinase A and protein kinase C pathways.

17Beta-estradiol (E2) rapidly (<20 min) attenuates the ability of mu-opioids to hyperpolarize guinea pig hypothalamic neurons. We have used intracellular recordings from female guinea pig hypothalamic slices to characterize the receptor and intracellular pathway(s) mediating E2's rapid effects. E2 acts stereospecifically with physiologically relevant concentration-dependence (EC50 = 8 nM) to cause a fourfold reduction in the potency of the mu-opioid agonist (D-Ala2-N-Me-Phe4-Gly5-ol)-enkephalin and the GABA(B) agonist baclofen to activate an inwardly rectifying K+ conductance in hypothalamic neurons. Both the nonsteroidal estrogen diethylstilbestrol and the anti-estrogen ICI 164,384 blocked E2 actions to uncouple mu-opioid receptors. Using a pharmacological Schild analysis, we found that ICI 164,384 competed for this E2 receptor with a Ke of approximately 0.3 nM. The protein synthesis inhibitor cycloheximide did not block the estrogenic uncoupling of the mu-opioid receptor from its K+ channel, implying a rapid, nongenomic mechanism of E2 action. The effects of E2 were mimicked by the bath application of the protein kinase A (PKA) activators, forskolin and Sp-cAMP, and the protein kinase C (PKC) activator phorbol-12,13-dibutyrate. Furthermore, the selective PKA antagonists Rp-cAMP and KT5720, which have different chemical structures and modes of action, both blocked the effects of E2. In addition, the actions of E2 were blocked by the selective PKC inhibitor Calphostin C. Therefore, it appears that E2 can activate both PKA and PKC to cause a heterologous desensitization of both mu-opioid and GABA(B) receptors, which has the potential to alter synaptic transmission in many regions of the CNS.

Animals↗

PubMedDate not supplied

Rapid actions of plasma membrane estrogen receptors.

Functional evidence for the existence of plasma membrane estrogen receptors in a variety of cell types continues to accumulate. Many of these functions originate from rapid signaling events, transduced in response to 17beta-estradiol (E(2)). It has been convincingly shown that E(2) activates phosphoinositol 3-kinase and protein kinase B/AKT, and stimulates ERK and p38 MAP kinases. In part, this stems from G-protein activation and the resulting calcium flux. As a result, the link between E(2) action at the cell membrane and discrete biological actions in the cell has been strengthened. There is now convincing in vitro evidence that E(2) can modulate the functions of neural and vascular cells via non-genomic actions. Thus, the actions of discrete pools of E(2) receptors are likely to contribute to the overall effects of the sex steroids.

Animals↗

PubMedDate not supplied

Fluorine 18-labeled fluorodeoxyglucose myocardial scintigraphy with Anger gamma cameras for assessing myocardial viability.

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Fluorodeoxyglucose F18↗

PubMedDate not supplied

Efficacy of oral rehydration solutions in a rat model of secretory diarrhea.

Controversy continues regarding the ideal composition of glucose/electrolyte solutions used for oral rehydration of infants and children with acute diarrhea. We have used cholera toxin-treated rat small intestine as a model of secretory diarrhea to assess the efficacy of oral rehydration solutions by intestinal perfusion. All solutions tested reversed net water secretion but a hypotonic bicarbonate-free solution was more effective than other solutions, including the World Health Organization oral rehydration solution (p less than 0.003). Net sodium secretion persisted with all solutions tested but there was a significant linear relationship between sodium concentration of the solution perfused and net sodium transport (r = 0.75, p less than 0.05). Cholera toxin treatment alone and in combination with perfusion of oral rehydration solutions significantly reduced plasma sodium concentration and osmolality (p less than 0.05), the effects being most marked with low sodium solutions. Although direct parallelism between observations in this animal model of secretory diarrhea and human diarrheal disease has not been established as yet, the model may be useful in assessing clinical efficacy of new oral rehydration solutions and in systematic analysis of the relative benefits of their individual components.

Animals↗

PubMedDate not supplied

Stages of bone marrow transplantation: a psychiatric perspective.

Patients undergoing bone marrow transplantation were closely followed by a psychiatric service functioning as part of a multidisciplinary team. A somewhat predictable pattern of psychological reactions to the stress of various stages of the procedure appeared to emerge. Approaches to patient evaluation, typical patient responses, and suggestions for working with these patients and their families are described.

Adaptation, Psychological↗