Biomedical subjects

Cordian Beyer

Publications and source records attributed to Cordian Beyer.

21 records · Page 2Linked to original sources

PubMed2002

Sry does not fully sex-reverse female into male behavior towards pups.

Investigations in mice suggest that the Y-chromosomal genes affect certain behaviors. Here, we studied whether a part of the Y chromosome, the Sxr locus, has an effect on induction of motivation for parental care (pup retrieval) or of parental aggression towards pups (infanticide). XX females, XX males with the Sxr locus on the X chromosome, and XY males of the C57BL/6J strain were tested. The induced pup retrieval or infanticide behaviors were genotype-dependent. XX mice always retrieved pups and never were infanticidal. On the first test, significantly more XY males (38%) than XX males (17%) were infanticidal. When the same animals were tested for a second time, all except one of the XX males retrieved pups. Overall, motivation for parental care was highest in XX females, followed by XX males, and lowest in XY mice. On the other hand, the incidence of infanticide was highest in XY males, lower in XX males, and absent in XX females. We conclude that the Sxr locus of the Y chromosome, when operating in a XX background, partially erases but does not fully defeminize motivation for pup retrieval. Further, it induces infanticide to a level higher than that of XX females but significantly lower than that of normal males (XY). Hence, we suggest that genes outside the sex-determining region of the Y chromosome and/or genes on autosomes are necessary for manifestation of full male-type parental behavior.

Animals↗

PubMed2002

Activation of neuronal N-methyl-D-aspartate receptor channels by lipid emulsions.

UNLABELLED: Lipid emulsions are widely used as carriers for hypnotics such as propofol, etomidate, and diazepam. It is assumed that the emulsions alone exert no effect on cellular functions nor influence the pharmacokinetics, pharmacodynamics, or anesthetic and analgetic potency of the hypnotics they carry. To elucidate possible interactions between lipid emulsions and cell membranes, in particular membrane-bound proteins, we investigated the effects of commercially available lipid emulsions on the cell membranes of cultured cortical neurons from the mouse by using the whole-cell configuration of the patch-clamp technique. Of nine lipid emulsions tested, three, i.e., Intralipid, Structolipid, and, to a much lesser extent, Abbolipid, activated membrane currents in the neuronal cells in a dilution-dependent manner. The emulsion-induced currents were not affected by picrotoxin or bicuculline but were inhibited by DL-AP5 and ketamine. The voltage dependence of the currents was influenced by the presence of Mg(2+) in a way that is typical for currents conducted by N-methyl-D-aspartate receptor channels. We conclude that Intralipid, Structolipid, and Abbolipid activate N-methyl-D-aspartate receptor channels in cortical neurons. IMPLICATIONS: Lipid emulsions are widely used as carriers for hypnotics such as propofol, etomidate, or diazepam. We tested nine commercially available lipid emulsions and demonstrate that three of them--Intralipid, Structolipid, and Abbolipid--activate NMDA receptor channels in the membranes of cortical neuronal cells.

2-Amino-5-phosphonovalerate↗

PubMed2002

Estradiol stimulates GDNF expression in developing hypothalamic neurons.

Estrogens stimulate the differentiation of neurons and neural networks in the CNS. The concordance of the cellular responses of estrogens and growth factors suggests that both factors may interact on the cellular level to ensure their developmental role. We have put forward this hypothesis and analyzed the effect of estrogens on the expression of glial cell line-derived neutrotrophic factor (GDNF) in developing hypothalamic cells. Using Western blotting and competitive RTPCR, we have demonstrated that 17beta-estradiol (E2) increases the expression of GDNF in hypothalamic cell cultures. E2-induced GDNF expression was seen in neurons but not astrocytes. GDNF induction by E2 appeared to be transmitted through nonclassical estrogen action, since the application of the nuclear estrogen receptor antagonists ICI 182, 780 did not abolish this effect. Only inhibitors of intracellular Ca(2+) and cAMP/protein kinase A signaling were effective in preventing E2 effects. We conclude that E2 is capable of influencing GDNF expression in the developing hypothalamus. Thus, it is conceivable that developmental E2 effects in the hypothalamus are partially mediated through the regulation of other important developmental signals such as growth factors.

Animals↗