Acute hypoxia differentially affects the NMDA receptor NR1, NR2A and NR2B subunit mRNA levels in the developing chick optic tectum: stage-dependent plasticity in the 2B-2A ratio.

It is known that the NMDA-R NR1 subunit is needed for the receptor activity and that under hypoxia the evolution toward apoptosis or neuronal survival depends on the balance NR2A/NR2B subunits. This paper analyzes the effect of acute hypoxia on the above mentioned subunits mRNAs during development. The mean percentage of NR1+ neurons displayed the higher plasticity during development while the NR2A+ neurons the higher stability.

Hypoxia-induced apoptotic cell death is prevented by oestradiol via oestrogen receptors in the developing central nervous system.

The neuroprotective effects of oestrogens have been demonstrated against a variety of insults, including excitotoxicity, oxidative stress and cerebral ischemia under certain conditions. However, the molecular mechanisms underlying oestrogen neuroprotection are still unclear. We aimed to determine whether 17beta-oestradiol (E(2)) administration post-hypoxia (p-hx) was neuroprotective and whether these actions were mediated through oestrogen receptors (ER).

Acute hypoxia differentially affects the gamma-aminobutyric acid type A receptor alpha(1), alpha(2), beta(2), and gamma(2) subunit mRNA levels in the developing chick optic tectum: stage-dependent sensitivity.

This investigation analyzes the effect of an acute hypoxic treatment on the level of four (alpha(1), alpha(2), beta(2), and gamma(2)) subunit mRNAs of the GABA(A) receptor in layer "i" of the developing chick optic tectum. Our results show that 1 hr of normobaric acute hypoxia significantly changes the subunit mRNA levels. Different subunit mRNAs display different sensitivity to hypoxia: alpha(1), beta(2), and gamma(2) mRNAs are highly sensitive, whereas alpha(2) mRNA is almost not affected.

Hypoxia-induced cell death and activation of pro- and anti-apoptotic proteins in developing chick optic lobe.

Exposure of the CNS to hypoxia is associated with cell death. Our aim was to establish a temporal correlation between cellular and molecular alterations induced by an acute hypoxia evaluated at different post-hypoxia (p-h) times and at two stages of chick optic lobe development: embryonic days (ED) 12 and 18. TUNEL assays at ED12 disclosed a significant increase (300%) in pyknotic cells at 6 h p-h, while at ED18 no morphological changes were observed in hypoxic versus controls.

Modulatory action of zinc on GABA(A) receptor complex during avian CNS development.

In the present work, we studied the effect of zinc on GABA(A) receptor complex at three developmental stages of chick optic lobe (embryonic day 14, post-hatching day 1, and adulthood), in order to investigate the role of this cation in central nervous system (CNS) functional maturation. It was demonstrated that zinc exerts an inhibitory modulation of both GABA binding and GABA-gated chloride flux in a concentration-dependent manner with maximal effects at 100 microM zinc concentration. Maximal inhibition was higher at the embryonic stage and declined thereafter, disclosing minimal values at the adult stage.

Biosynthesis of progesterone derived neurosteroids by developing avian CNS: in vitro effects on the GABAA receptor complex.

It has been demonstrated in different vertebrate species that the GABAA receptor complex is modulated by certain steroids. Theses results prompted work on the synthesis of these neurosteroids in the Central Nervous System. However, there are scarcely any studies analyzing their production or their modulatory effects on this receptor during development.

Neurosteroid modulation of GABA binding sites in developing avian central nervous system.

Our aim was to examine the effect of the potent neurosteroid 3 alpha-hydroxy-5 alpha-pregnan-20-one (3 alpha, 5 alpha-P) on [3H]-GABA binding to its receptor sites in the chick optic lobe. Binding was performed on synaptic membranes isolated at different stages of development and two different membrane preparation procedures were applied to expose high and low affinity GABA binding sites. The addition of 3 alpha, 5 alpha-P was shown to increase [3H]-GABA binding in an age- and concentration-dependent manner.

Ontogeny of two different benzodiazepine binding sites in the chick optic lobe.

The developmental time-course of type I and type II benzodiazepine receptors in the chick optic lobe was determined using a triazolopyridazine, CL 218872. At embryonic day 13 most of the binding sites corresponded to type II (98.23%), while type I represented only a minor proportion (1.

Presence of endogenous inhibitors of benzodiazepine binding in developing chick optic lobe.

An endogenous inhibitor of benzodiazepine receptor binding was removed from synaptic membranes of developing chick optic lobe by an exhaustive buffer washing procedure. This treatment increased [3.H]flunitrazepam binding at all stages of development, although this effect was greater at early stages (embryonic day 14-16).

Effect of diazepam on the low affinity GABA binding sites at different developmental stages of the chick optic lobe.

The developmental profile of GABA receptor sites was studied under experimental conditions where the low affinity binding site is mainly measured. The in vitro effects of nanomolar concentrations of diazepam upon low affinity GABA binding sites during development were also examined. The addition of 50 nM diazepam enhanced specific [(3)H]GABA binding at all stages of development, this stimulation being greater at early stages (10th-14th embryonic day).