Population Structure of Humpback Whales from Their Breeding Grounds in the South Atlantic and Indian Oceans

Although humpback whales are among the best-studied of the large whales, population boundaries in the Southern Hemisphere (SH) have remained largely untested. We assess population structure of SH humpback whales using 1,527 samples collected from whales at fourteen sampling sites within the Southwestern and Southeastern Atlantic, the Southwestern Indian Ocean, and Northern Indian Ocean (Breeding Stocks A, B, C and X, respectively). Evaluation of mtDNA population structure and migration rates was carried out under different statistical frameworks. Using all genetic evidence, the results suggest significant degrees of population structure between all ocean basins, with the Southwestern and Northern Indian Ocean most differentiated from each other. Effective migration rates were highest between the Southeastern Atlantic and the Southwestern Indian Ocean, followed by rates within the Southeastern Atlantic, and the lowest between the Southwestern and Northern Indian Ocean. At finer scales, very low gene flow was detected between the two neighbouring sub-regions in the Southeastern Atlantic, compared to high gene flow for whales within the Southwestern Indian Ocean. Our genetic results support the current management designations proposed by the International Whaling Commission of Breeding Stocks A, B, C, and X as four strongly structured populations. The population structure patterns found in this study are likely to have been influenced by a combination of long-term maternally directed fidelity of migratory destinations, along with other ecological and oceanographic features in the region

Time-dependent changes in rat brain neuroactive steroid concentrations and GABAA receptor function after acute stress

The time courses of changes in rat brain neuroactive steroid concentrations and gamma-aminobutyric acid type A (GABAA) receptor function elicited by acute stress were investigated in animals exposed to CO2 for 1 min, a treatment known to induce stress in rats and panic attacks in humans. Inhalation of CO2 induced increases in cerebral cortical steroid concentrations, the time dependence of which varied with the steroid examined. Thus, progesterone and deoxycorticosterone showed maximal increases (10- and 4-fold, respectively) 10 min after CO2 inhalation and had returned to basal values by 30 and 60 min, respectively. In contrast, pregnenolone and 3alpha-hydroxy-5alpha-pregnan-20-one (allopregnanolone) concentrations showed maximal increases (+174 and + 200%, respectively) at 30 min, were still higher than control at 60 min and returned to control values 120 min after stress. Inhalation of CO2 also resulted in increases in plasma steroid concentrations, most of which peaked at 30 min and had returned to control values by 60 min. A parallel analysis of the stress-induced changes in GABAA receptor function, assessed either biochemically by t-[35S]butylbicyclophosphorothionate ([35S]TBPS) binding to cerebral cortical membranes or behaviorally by the punished responding score in Vogel's test, showed that the effects of CO2 inhalation on both parameters were maximal (+51 and -40%, respectively) after 10 min; the behavioral reaction returned to normal after 60 min, whereas [35S]TBPS binding had returned to control values 120 min after stress. The results show that: (a) the maximal increase in the brain concentrations of allopregnanolone, a potent and efficacious positive modulator of GABAA receptors, occurred at a time (30 min) when both conflict behavior and [35S]TBPS binding begun to decrease, and (b) both allopregnanolone concentrations and [35S]TBPS binding had returned to control values 120 min after CO2 inhalation. The data are thus consistent with a physiological role of neuroactive steroids in restoring GABAergic tone after stress

Isoniazid-induced inhibition of GABAergic transmission enhances neurosteroid content in the rat brain

Isoniazid (375 mg/kg, s.c.), a drug that decreases GABAA receptor-mediated transmission, elicited a time-dependent increase of neuroactive steroid (pregnenolone, progesterone and allotetrahydrodeoxycorticosterone) concentrations in rat brain and plasma. This treatment also time-dependently increased the plasma concentration of corticosterone. Brain and plasma neuroactive steroid levels peaked between 40 and 120 min after isoniazid administration, respectively, and returned to control values by 5 hr. Acute foot shock stress mimicked the effect of isoniazid by increasing in a time-dependent manner the same neuroactive steroids both in brain and plasma. Abecarnil (0.3 mg/kg, i.p.), a beta-carboline derivative with anxiolytic properties, antagonized the effect of both isoniazid and foot shock on brain and plasma neuroactive steroids and on plasma corticosterone level. These data indicate that an inhibition of central GABAergic transmission enhances the concentrations of THDOC and its precursors pregnenolone and progesterone in the rat brain and plasma as well as the plasma levels of corticosterone. This finding suggests that GABA exerts a tonic inhibitory action on the mechanisms involved in the regulation of the synthesis and release of these neuroactive steroids in the central nervous system and plasma

Dexamethasone therapy in preterm infants with developing bronchopulmonary dysplasia: Effect on pulmonary surfactant disaturated phosphatidylcholine kinetics

The role of corticosteroid in severe bronchopulmonary dyplasia (BPD) is still debated. Scanty data are available on the corticosteroids effect on surfactant metabolism. Our objective was to compare surfactant kinetics in preterm infants with developing BPD, before and after dexamethasone (DEXA) treatment. Twenty-eight studies were performed in 14 preterm infants (birth weight 786 +/- 192 g, gestational age 26 +/- 1 wk) on high ventilatory setting, before (age 22 +/- 11 d) and after (age 33 +/- 11 d) DEXA. C-labeled dipalmitoyl-phosphatidylcholine (DPPC) was administered endotrachelly to trace pulmonary surfactant. Surfactant disaturated-phosphatidylcholine (DSPC) kinetics and pools were calculated from DSPC C-enrichment curves of serial tracheal aspirates and bi-compartmental analysis. Total protein and myeloperoxidase (MPO) activity in tracheal aspirates were also measured and expressed per ml of Epithelial Lining Fluid (ELF). After DEXA, DSPC alveolar pool increased significantly from 8.2 +/- 7.6 to 10.6 +/- 11.3 mg/kg (p = 0.039), total proteins and MPO were reduced from 8.8 +/- 8.6 to 3.1 +/- 2.1 mg/ml ELF (p = 0.046) and from 1822 +/- 1224 to 1261 +/- 987 mU/mlELF (p = 0.028) respectively. In conclusion, DEXA treatment in mechanically ventilated preterm infants with severe respiratory failure and at high risk of developing BPD, significantly reduced inflammatory markers and increased alveolar surfactant DSPC pool