Quasinormal modes of Unruh's Acoustic Black Hole

We have studied the sound perturbation of Unruh's acoustic geometry and we present an exact expression for the quasinormal modes of this geometry. We are obtain that the quasinormal frequencies are pure-imaginary, that give a purely damped modes.Comment: 5 Page

Quasinormal Modes and Stability Criterion of Dilatonic Black Hole in 1+1 and 4+1 Dimensions

We study the stability of black holes that are solutions of the dilaton gravity derived from string-theoretical models in two and five dimensions against to scalar field perturbations, using the Quasinormal Modes (QNMs) approach. In order to find the QNMs corresponding to a black hole geometry, we consider perturbations described by a massive scalar field non-minimally coupled to gravity. We find that the QNM's frequencies turn out to be pure imaginary leading to purely damped modes, that is in agreement with the literature of dilatonic black holes. Our result exhibits the unstable behavior of the considered geometry against the scalar perturbations. We consider both the minimal coupling case, i.e., for which the coupling parameter $\zeta$ vanishes, and the case $\zeta={1/4}$.Comment: sevarl changes, some reference was added, 10 pages, 4 figure

Quasinormal modes and Stability Analysis for 4-dimensional Lifshitz Black Hole

We study the Lifshitz black hole in 4-dimensions with dynamical exponent z=2 and we calculate analytically the quasinormal modes of scalar perturbations. These quasinormal modes allows to study the stability of the Lifshitz black hole and we have obtained that Lifshitz black hole is stable.Comment: 7 pages, 2 figures. arXiv admin note: text overlap with arXiv:1205.058

Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries

Transient receptor potential canonical type 3 (TRPC3) channels are non-selective cation channels and regulate intracellular Ca2+ concentration. We examined the role of TRPC3 channels in agonist-, membrane depolarization (high K+)-, and mechanical (pressure)-induced vasoconstriction and vasorelaxation in mouse mesenteric arteries. Vasoconstriction and vasorelaxation of endothelial cells intact mesenteric arteries were measured in TRPC3 wild-type (WT) and knockout (KO) mice. Calcium concentration ([Ca2+]) was measured in isolated arteries from TRPC3 WT and KO mice as well as in the mouse endothelial cell line bEnd.3. Nitric oxide (NO) production and nitrate/nitrite concentrations were also measured in TRPC3 WT and KO mice. Phenylephrine-induced vasoconstriction was reduced in TRPC3 KO mice when compared to that of WT mice, but neither high K+- nor pressure-induced vasoconstriction was altered in TRPC3 KO mice. Acetylcholine-induced vasorelaxation was inhibited in TRPC3 KO mice and by the selective TRPC3 blocker pyrazole-3. Acetylcholine blocked the phenylephrine-induced increase in Ca2+ ratio and then relaxation in TRPC3 WT mice but had little effect on those outcomes in KO mice. Acetylcholine evoked a Ca2+ increase in endothelial cells, which was inhibited by pyrazole-3. Acetylcholine induced increased NO release in TRPC3 WT mice, but not in KO mice. Acetylcholine also increased the nitrate/nitrite concentration in TRPC3 WT mice, but not in KO mice. The present study directly demonstrated that the TRPC3 channel is involved in agonist-induced vasoconstriction and plays important role in NO-mediated vasorelaxation of intact mesenteric arteries.Fil: Yeon, Soo-In. Yonsei University College of Medicine; Corea del SurFil: Kim, Joo Young. Yonsei University College Of Medicine; . Yonsei University College of Medicine; Corea del SurFil: Yeon, Dong-Soo. Kwandong University College of Medicine; Corea del SurFil: Abramowitz, Joel. National Institute of Environmental Health Sciences; Estados UnidosFil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institute of Environmental Health Sciences; Estados UnidosFil: Muallem, Shmuel. National Institutes of Health; Estados UnidosFil: Lee, Young-Ho. Yonsei University College of Medicine; Corea del Su

Activation of endothelial transient receptor potential C3 channel is required for small conductance calcium-activated potassium channel activation and sustained endothelial hyperpolarization and vasodilation of cerebral artery

BACKGROUND: Transient receptor potential C3 (TRPC3) has been demonstrated to be involved in the regulation of vascular tone through endothelial cell (EC) hyperpolarization and endothelium-dependent hyperpolarization-mediated vasodilation. However, the mechanism by which TRPC3 regulates these processes remains unresolved. We tested the hypothesis that endothelial receptor stimulation triggers rapid TRPC3 trafficking to the plasma membrane, where it provides the source of Ca(2+) influx for small conductance calcium-activated K(+) (SKCa) channel activation and sustained EC hyperpolarization. METHODS AND RESULTS: Pressurized artery studies were performed with isolated mouse posterior cerebral artery. Treatment with a selective TRPC3 blocker (Pyr3) produced significant attenuation of endothelium-dependent hyperpolarization-mediated vasodilation and endothelial Ca(2+) response (EC-specific Ca(2+) biosensor) to intraluminal ATP. Pyr3 treatment also resulted in a reduced ATP-stimulated global Ca(2+) and Ca(2+) influx in primary cultures of cerebral endothelial cells. Patch-clamp studies with freshly isolated cerebral ECs demonstrated 2 components of EC hyperpolarization and K(+) current activation in response to ATP. The early phase was dependent on intermediate conductance calcium-activated K(+) channel activation, whereas the later sustained phase relied on SKC a channel activation. The SKC a channel-dependent phase was completely blocked with TRPC3 channel inhibition or in ECs of TRPC3 knockout mice and correlated with increased trafficking of TRPC3 (but not SKC a channel) to the plasma membrane. CONCLUSIONS: We propose that TRPC3 dynamically regulates SKC a channel activation through receptor-dependent trafficking to the plasma membrane, where it provides the source of Ca(2+) influx for sustained SKC a channel activation, EC hyperpolarization, and endothelium-dependent hyperpolarization-mediated vasodilation.Fil: Kochukov, Mikhail Y.. Baylor College of Medicine; Estados UnidosFil: Balasubramanian, Adithya. Baylor College of Medicine; Estados UnidosFil: Abramowitz, Joel. National Institute of Environmental Health Sciences Research; Estados UnidosFil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences Research; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Marrelli, Sean P.. Baylor College of Medicine; Estados Unido

Activation of endothelial transient receptor potential C3 channel is required for small conductance calcium-activated potassium channel activation and sustained endothelial hyperpolarization and vasodilation of cerebral artery

BACKGROUND: Transient receptor potential C3 (TRPC3) has been demonstrated to be involved in the regulation of vascular tone through endothelial cell (EC) hyperpolarization and endothelium-dependent hyperpolarization-mediated vasodilation. However, the mechanism by which TRPC3 regulates these processes remains unresolved. We tested the hypothesis that endothelial receptor stimulation triggers rapid TRPC3 trafficking to the plasma membrane, where it provides the source of Ca(2+) influx for small conductance calcium-activated K(+) (SKCa) channel activation and sustained EC hyperpolarization. METHODS AND RESULTS: Pressurized artery studies were performed with isolated mouse posterior cerebral artery. Treatment with a selective TRPC3 blocker (Pyr3) produced significant attenuation of endothelium-dependent hyperpolarization-mediated vasodilation and endothelial Ca(2+) response (EC-specific Ca(2+) biosensor) to intraluminal ATP. Pyr3 treatment also resulted in a reduced ATP-stimulated global Ca(2+) and Ca(2+) influx in primary cultures of cerebral endothelial cells. Patch-clamp studies with freshly isolated cerebral ECs demonstrated 2 components of EC hyperpolarization and K(+) current activation in response to ATP. The early phase was dependent on intermediate conductance calcium-activated K(+) channel activation, whereas the later sustained phase relied on SKC a channel activation. The SKC a channel-dependent phase was completely blocked with TRPC3 channel inhibition or in ECs of TRPC3 knockout mice and correlated with increased trafficking of TRPC3 (but not SKC a channel) to the plasma membrane. CONCLUSIONS: We propose that TRPC3 dynamically regulates SKC a channel activation through receptor-dependent trafficking to the plasma membrane, where it provides the source of Ca(2+) influx for sustained SKC a channel activation, EC hyperpolarization, and endothelium-dependent hyperpolarization-mediated vasodilation.Fil: Kochukov, Mikhail Y.. Baylor College of Medicine; Estados UnidosFil: Balasubramanian, Adithya. Baylor College of Medicine; Estados UnidosFil: Abramowitz, Joel. National Institute of Environmental Health Sciences Research; Estados UnidosFil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences Research; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Marrelli, Sean P.. Baylor College of Medicine; Estados Unido

Quasinormal modes, Superradiance and Area Spectrum for 2+1 Acoustic Black Holes

We present an exact expression for the quasinormal modes of acoustic disturbances in a rotating 2+1 dimensional sonic black hole (draining bathtub fluid flow) in the low frequency limit and evaluate the adiabatic invariant proposed by Kunstatter. We also compute,via Bohr-Sommerfeld quantization rule the equivalent area spectrum for this acoustic black hole, and we compute the superradiance phenomena for pure spinning 2+1 black holes.Comment: 10 pages, Final version, an appendix and some references was added, accepted by Phys. Lett.

The contribution of TRPC1, TRPC3, TRPC5 and TRPC6 to touch and hearing

Transient receptor potential channels have diverse roles in mechanosensation. Evidence is accumulating that members of the canonical subfamily of TRP channels (TRPC) are involved in touch and hearing. Characteristic features of TRP channels include their high structural homology and their propensity to form heteromeric complexes which suggests potential functional redundancy. We previously showed that TRPC3 and TRPC6 double knockout animals have deficits in light touch and hearing whilst single knockouts were apparently normal. We have extended these studies to analyse deficits in global quadruple TRPC1, 3, 5 and 6 null mutant mice. We examined both touch and hearing in behavioural and electrophysiological assays, and provide evidence that the quadruple knockout mice have larger deficits than the TRPC3 TRPC6 double knockouts. Mechano-electrical transducer currents of cochlear outer hair cells were however normal. This suggests that TRPC1, TRPC3, TRPC5 and TRPC6 channels contribute to cutaneous and auditory mechanosensation in a combinatorial manner, but have no direct role in cochlear mechanotransduction