The Spatial Clustering of Low Luminosity AGN

We present the first multi-parameter analysis of the narrow line AGN clustering properties. Estimates of the two-point correlation function (CF) based on SDSS DR2 data reveal that Seyferts are clearly less clustered than normal galaxies, while the clustering amplitude (r_0) of LINERs is consistent with that of the parent galaxy population. The similarities in the host properties (color and concentration index) of Seyferts and LINERs suggest that the difference in their r_0 is not driven by the morphology-density relation. We find that the luminosity of [O I] emission shows the strongest influence on AGN clustering, with low L([O I]) sources having the highest r_0. This trend is much stronger than the previously detected dependence on L([O III]), which we confirm. There is a strong correspondence between the clustering patterns of objects of given spectral type and their physical properties. LINERs, which exhibit high r_0, show the lowest luminosities and obscuration levels, and relatively low gas densities (n_e), suggesting that these objects harbor black holes that are relatively massive yet weakly active or inefficient in their accretion, probably due to the insufficiency of their fuel supply. Seyferts, which have low r_0, are luminous and show large n_e, suggesting that their black holes are less massive but accrete quickly and efficiently enough to clearly dominate the ionization. The low r_0 of the H II galaxies can be understood as a consequence of both the morphology-density and star formation rate-density relations, however, their spectral properties suggest that their centers hide amidst large amounts of obscuring material black holes of generally low mass whose activity remains relatively feeble. Our own Milky Way may be a typical such case.[abridged]Comment: 27 pages, color figures, some are severely degraded in resolution, emulateapj. See http://www.physics.drexel.edu/~constant/work/agnclustering.ps for high resolution version. Accepted to Ap

The Seyfert Population in the Local Universe

The magnitude-limited catalog of the Southern Sky Redshift Survey (SSRS2), is used to characterize the properties of galaxies hosting Active Galactic Nuclei. Using emission-line ratios, we identify a total of 162 (3%) Seyfert galaxies out of the parent sample with 5399 galaxies. The sample contains 121 Seyfert 2 galaxies and 41 Seyfert 1. The SSRS2 Seyfert galaxies are predominantly in spirals of types Sb and earlier, or in galaxies with perturbed appearance as the result of strong interactions or mergers. Seyfert galaxies in this sample are twice as common in barred hosts than the non-Seyferts. By assigning galaxies to groups using a percolation algorithm we find that the Seyfert galaxies in the SSRS2 are more likely to be found in binary systems, when compared to galaxies in the SSRS2 parent sample. However, there is no statistically significant difference between the Seyfert and SSRS2 parent sample when systems with more than 2 galaxies are considered. The analysis of the present sample suggests that there is a stronger correlation between the presence of the AGN phenomenon with internal properties of galaxies (morphology, presence of bar, luminosity) than with environmental effects (local galaxy density, group velocity dispersion, nearest neighbor distance).Comment: 35 pages, 13 figures, Accepted to be publised in Astronomical Journa

Calcium release from presynaptic internal stores is required for ethanol to increase spontaneous gammaaminobutyric acid release onto cerebellum Purkinje neurons

ABSTRACT Recent data have demonstrated that ethanol increases ␥-aminobutyric acid (GABA) release in many brain regions, but little is known about the mechanism responsible for this action. Consistent with previous results, ethanol increased miniature inhibitory postsynaptic current (mIPSC) frequency at the interneuron-Purkinje cell synapse in the slice and in mechanically dissociated neurons. These data suggest that ethanol is increasing spontaneous GABA release at this synapse. It is generally accepted that ethanol increases levels of intracellular calcium and that changes in intracellular calcium can alter neurotransmitter release. Therefore, we examined the contribution of calcium-dependent pathways to the effect of ethanol on spontaneous GABA release at the interneuron-Purkinje cell synapse. Ethanol continued to increase mIPSC frequency in a nominally calcium-free extracellular solution and in the presence of a voltage-dependent calcium channel inhibitor, cadmium chloride. These data suggest that influx of extracellular calcium does not play a critical role in the mechanism of ethanol-enhanced spontaneous GABA release. However, a sarco/ endoplasmic-reticulum calcium ATPase pump inhibitor (thapsigargin), an inositol 1,4,5-trisphosphate receptor antagonist (2-aminoethoxydiphenylborate) and a ryanodine receptor antagonist (ryanodine) significantly reduced the ability of ethanol to increase mIPSC frequency. In addition, ethanol was still able to increase mIPSC frequency in the presence of intracellular 1,2-bis(2-aminophenoxy)ethane-N,N,NЈ,NЈ-tetraacetic acid (BAPTA) and a cannabinoid receptor antagonist N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM-251); thus, retrograde messengers are not involved in ethanol-enhanced spontaneous GABA release. Overall, these data suggest that calcium release from presynaptic internal stores plays a vital role in the mechanism of ethanol-enhanced spontaneous GABA release at the interneuronPurkinje cell synapse

Ethanol-enhanced GABA release: A focus on G protein-coupled receptors

While research on the actions of ethanol at the GABAergic synapse has focused on postsynaptic mechanisms, recent data have demonstrated that ethanol also facilitates GABA release from presynaptic terminals in many, but not all, brain regions. The ability of ethanol to increase GABA release can be regulated by different G protein-coupled receptors (GPCRs), such as the cannabinoid-1 receptor, corticotropin-releasing factor 1 receptor, GABAB receptor, and the 5-hydroxytryptamine 2C receptor. The intracellular messengers linked to these GPCRs, including the calcium that is released from internal stores, also play a role in ethanol-enhanced GABA release. Hypotheses are proposed to explain how ethanol interacts with the GPCR pathways to increase GABA release and how this interaction contributes to the brain region specificity of ethanol-enhanced GABA release. Defining the mechanism of ethanol-facilitated GABA release will further our understanding of the GABAergic profile of ethanol and increase our knowledge of how GABAergic neurotransmission may contribute to the intoxicating effects of alcohol and to alcohol dependence

Small scale systems of galaxies I. Photometric and spectroscopic properties of members

This paper is the first of a series addressed to the investigation of galaxy formation/evolution in small scale systems of galaxies (SSSGs) which are located in low density cosmic environments. Our algorithm for SSSG selection includes galaxy systems of 2 or more galaxies lying within 1000 km/s and a 200 h_{100}^{-1} kpc radius volume. We present the analysis of the photometric and spectroscopic properties of 19 member galaxies belonging to a sample of 11 SSSGs. In the $\mu_e - r_e$ plane, early-type members may be considered "ordinary", not "bright" galaxies in the definition given by Capaccioli et al.(1992) with a significant fraction of galaxies having a disk or disky isophotes. We do not detect fine structure and signatures of recent interaction events in the early-type galaxy population, a picture also confirmed by the spectroscopy. At odd, there are several spiral members with open arm configurations as expected in interacting systems. At the same time, emission lines in the spectra of spiral members fall in the HII regions regime defined with diagnostic diagrams (Veilleux & Osterbrock 1987). None of the objects displays unambiguous indication of nuclear activity, although fourspiral nuclei could be ascribed to the class of Seyferts. The star formation rate seems enhanced over the average expected in spiral galaxies only for poorer SSSGs in particular pairs (<50 solar masses per year) but without being in the range of starburst systems.Comment: 24 pages, including 6 figures and 6 tables. Accepted for publication in A

Brain Regional Differences in the Effect of Ethanol on GABA Release from Presynaptic Terminals

Whereas ethanol has behavioral actions consistent with increased GABAergic function, attempts to demonstrate a direct enhancement of GABA-gated currents by ethanol have produced mixed results. Recent work has suggested that a part of the GABAergic profile of ethanol may result from enhanced GABA release from presynaptic terminals. The present study examines the effect of ethanol on GABA release in several brain regions to assess the regional nature of ethanol-induced GABA release. Whole-cell voltage clamp recording of spontaneous inhibitory postsynaptic currents (sIPSCs) from mechanically dissociated neurons and miniature inhibitory postsynaptic currents (mIPSCs) and paired-pulse ratio (PPR) from a slice preparation were used to quantify GABA release. Ethanol produced a concentration-dependent increase in the frequency of sIPSCs recorded from mechanically dissociated cerebellar Purkinje neurons and mIPSCs from substantia nigra neurons without having an effect on sIPSCs recorded from lateral septal or cerebrocortical neurons. This regional difference in the effect of ethanol on GABA release was confirmed with PPR recording from brain slices. These data indicate that ethanol can act on presynaptic terminals to increase GABA release in some brain regions while having little or no effect on GABA release in others. This regional difference is consistent with earlier in vivo studies in which ethanol affected neural activity and sensitivity to GABA in some, but not all, brain sites

The PLC/IP3R/PKC pathway is required for ethanol-enhanced GABA release

Research on the actions of ethanol at the GABAergic synapse has traditionally focused on postsynaptic mechanisms, but recent data demonstrate that ethanol also increases both evoked and spontaneous GABA release in many brain regions. Using whole-cell voltage-clamp recordings, we previously showed that ethanol increases spontaneous GABA release at the rat interneuron-Purkinje cell synapse. This presynaptic ethanol effect is dependent on calcium release from internal stores, possibly through activation of inositol 1,4,5-trisphosphate receptors (IP3Rs). After confirming that ethanol targets vesicular GABA release, in the present study we used electron microscopic immunohistochemistry to demonstrate that IP3Rs are located in presynaptic terminals of cerebellar interneurons. Activation of IP3Rs requires binding of IP3, generated through activation of phospholipase C (PLC). We find that the PLC antagonist edelfosine prevents ethanol from increasing spontaneous GABA release. Diacylglycerol generated by PLC and calcium released by activation of the IP3R activate protein kinase C (PKC). Ethanol-enhanced GABA release was blocked by two PKC antagonists, chelerythrine and calphostin C. When a membrane impermeable PKC antagonist, PKC (19-36), was delivered intracellularly to the postsynaptic neuron, ethanol continued to increase spontaneous GABA release. Overall, these results suggest that activation of the PLC/IP3R/PKC pathway is necessary for ethanol to increase spontaneous GABA release from presynaptic terminals onto Purkinje cells

Red Blood Cell and Endothelial eNOS Independently Regulate Circulating Nitric Oxide Metabolites and Blood Pressure

Background: Current paradigms suggest that nitric oxide (NO) produced by endothelial cells (ECs) through endothelial nitric oxide synthase (eNOS) in the vessel wall is the primary regulator of blood flow and blood pressure. However, red blood cells (RBCs) also carry a catalytically active eNOS, but its role is controversial and remains undefined. This study aimed to elucidate the functional significance of RBC eNOS compared with EC eNOS for vascular hemodynamics and nitric oxide metabolism. Methods: We generated tissue-specific loss- and gain-of-function models for eNOS by using cell-specific Cre-induced gene inactivation or reactivation. We created 2 founder lines carrying a floxed eNOS (eNOSflox/flox) for Cre-inducible knockout (KO), and gene construct with an inactivated floxed/inverted exon (eNOSinv/inv) for a Cre-inducible knock-in (KI), which respectively allow targeted deletion or reactivation of eNOS in erythroid cells (RBC eNOS KO or RBC eNOS KI mice) or in ECs (EC eNOS KO or EC eNOS KI mice). Vascular function, hemodynamics, and nitric oxide metabolism were compared ex vivo and in vivo. Results: The EC eNOS KOs exhibited significantly impaired aortic dilatory responses to acetylcholine, loss of flow-mediated dilation, and increased systolic and diastolic blood pressure. RBC eNOS KO mice showed no alterations in acetylcholine-mediated dilation or flow-mediated dilation but were hypertensive. Treatment with the nitric oxide synthase inhibitor Nγ-nitro-l-arginine methyl ester further increased blood pressure in RBC eNOS KOs, demonstrating that eNOS in both ECs and RBCs contributes to blood pressure regulation. Although both EC eNOS KOs and RBC eNOS KOs had lower plasma nitrite and nitrate concentrations, the levels of bound NO in RBCs were lower in RBC eNOS KOs than in EC eNOS KOs. Reactivation of eNOS in ECs or RBCs rescues the hypertensive phenotype of the eNOSinv/invmice, whereas the levels of bound NO were restored only in RBC eNOS KI mice. Conclusions: These data reveal that eNOS in ECs and RBCs contribute independently to blood pressure homeostasis

Endothelial NOS (NOS3) impairs myocardial function in developing sepsis

Endothelial nitric oxide synthase (NOS)3-derived nitric oxide (NO) modulates inotropic response and diastolic interval for optimal cardiac performance under non-inflammatory conditions. In sepsis, excessive NO production plays a key role in severe hypotension and myocardial dysfunction. We aimed to determine the role of NOS3 on myocardial performance, NO production, and time course of sepsis development. NOS3(−/−) and C57BL/6 wildtype mice were rendered septic by cecum ligation and puncture (CLP). Cardiac function was analyzed by serial echocardiography, in vivo pressure and isolated heart measurements. Cardiac output (CO) increased to 160 % of baseline at 10 h after sepsis induction followed by a decline to 63 % of baseline after 18 h in wildtype mice. CO was unaltered in septic NOS3(−/−) mice. Despite the hyperdynamic state, cardiac function and mean arterial pressure were impaired in septic wildtype as early as 6 h post CLP. At 12 h, cardiac function in septic wildtype was refractory to catecholamines in vivo and respective isolated hearts showed impaired pressure development and limited coronary flow reserve. Hemodynamics remained stable in NOS3(−/−) mice leading to significant survival benefit. Unselective NOS inhibition in septic NOS3(−/−) mice diminished this survival benefit. Plasma NO(x)- and local myocardial NO(x)- and NO levels (via NO spin trapping) demonstrated enhanced NO(x)- and bioactive NO levels in septic wildtype as compared to NOS3(−/−) mice. Significant contribution by inducible NOS (NOS2) during this early phase of sepsis was excluded. Our data suggest that NOS3 relevantly contributes to bioactive NO pool in developing sepsis resulting in impaired cardiac contractility. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00395-013-0330-8) contains supplementary material, which is available to authorized users