Tryptophan hydroxylase is modulated by L-type calcium channels in the rat pineal gland

Calcium is an important second messenger in the rat pineal gland, as well as cAMP. They both contribute to melatonin synthesis mediated by the three main enzymes of the melatonin synthesis pathway: tryptophan hydroxylase, arylalkylamine N-acetyltransferase and hydroxyindole-O-methyltransferase. The cytosolic calcium is elevated in pinealocytes following alpha(1)-adrenergic stimulation, through IP3-and membrane calcium channels activation. Nifedipine, an L-type calcium channel blocker, reduces melatonin synthesis in rat pineal glands in vitro. With the purpose of investigating the mechanisms involved in melatonin synthesis regulation by the L-type calcium channel, we studied the effects of nifedipine on noradrenergic stimulated cultured rat pineal glands. Tryptophan hydroxylase, arylalkylamine N-acetyltransferase and hydroxyindole-O-methyltransferase activities were quantified by radiometric assays and 5-hydroxytryptophan, serotonin, N-acetylserotonin and melatonin contents were quantified by HPLC with electrochemical detection. The data showed that calcium influx blockaded by nifedipine caused a decrease in tryptophan hydroxylase activity, but did not change either arylalkylamine N-acetyltransferase or hydroxyindole-O-methyltransferase activities. Moreover, there was a reduction of 5-hydroxytryptophan, serotonin, N-acetylserotonin and melatonin intracellular content, as well as a reduction of scrotonin and melatonin secretion. Thus, it seems that the calcium influx through L-type high voltage-activated calcium channels is essential for the full activation of tryptophan hydroxylase leading to melatonin synthesis in the pineal gland. (c) 2007 Elsevier Inc. All rights reserved.

Progression of Diet-Induced Diabetes in C57BL6J Mice Involves Functional Dissociation of Ca(2+) Channels From Secretory Vesicles

OBJECTIVE The aim of the study was to elucidate the cellular mechanism underlying the suppression of glucose-induced insulin secretion in mice fed a high-fat diet (HFD) for 15 weeks. RESEARCH DESIGN AND METHODS-C57BL6J mice were fed a HFD or a normal diet (ND) for 3 or 15 weeks. Plasma insulin and glucose levels in vivo were assessed by intraperitoneal glucose tolerance test. Insulin secretion in vitro was studied using static incubations and a perfused pancreas preparation. Membrane currents, electrical activity, and exocytosis were examined by patch-clamp technique measurements. Intracellular calcium concentration ([Ca(2+)](i)) was measured by microfluorimetry. Total internal reflection fluorescence microscope (TIRFM) was used for optical imaging of exocytosis and submembrane depolarization-evoked [Ca(2+)](i). The functional data were complemented by analyses of histology and gene transcription. RESULTS After 15 weeks, but not 3 weeks, mice on HFD exhibited hyperglycemia and hypoinsulinemia. Pancreatic islet content and beta-cell area increased 2- and 1.5-fold, respectively. These changes correlated with a 20-50% reduction of glucose-induced insulin secretion (normalized to insulin content). The latter effect was not associated with impaired electrical activity or [Ca(2+)](i) signaling. Single-cell capacitance and TIRFM measurements of exocytosis revealed a selective suppression (>70%) of exocytosis elicited by short (50 ms) depolarization, whereas the responses to longer depolarizations were (500 ms) less affected. The loss of rapid exocytosis correlated with dispersion of Ca(2+) entry in HFD beta-cells. No changes in gene transcription of key exocytotic protein were observed. CONCLUSIONS HFD results in reduced insulin secretion by causing the functional dissociation of voltage-gated Ca(2+) entry from exocytosis. These observations suggest a novel explanation to the well-established link between obesity and diabetes. Diabetes 59:1192-1201, 2010

Expression and characterization of LTx2, a neurotoxin from Lasiodora sp effecting on calcium channels

Here, we described the expression and characterization of the recombinant toxin LTx2, which was previously isolated from the venomous cDNA library of a Brazilian spider, Lasiodora sp. (Mygalomorphae, Theraphosidae). The recombinant toxin found in the soluble and insoluble fractions was purified by reverse phase high-performance liquid chromatography (HPLC). Ca2+ imaging analysis revealed that the recombinant LTx2 acts on calcium channels of BC3H1 cells, blocking L-type calcium channels. (C) 2008 Elsevier Inc. All rights reserved.

Robustness of bipartite Gaussian entangled beams propagating in lossy channels

Subtle quantum properties offer exciting new prospects in optical communications. For example, quantum entanglement enables the secure exchange of cryptographic keys(1) and the distribution of quantum information by teleportation(2,3). Entangled bright beams of light are increasingly appealing for such tasks, because they enable the use of well-established classical communications techniques(4). However, quantum resources are fragile and are subject to decoherence by interaction with the environment. The unavoidable losses in the communication channel can lead to a complete destruction of entanglement(5-8), limiting the application of these states to quantum-communication protocols. We investigate the conditions under which this phenomenon takes place for the simplest case of two light beams, and analyse characteristics of states which are robust against losses. Our study sheds new light on the intriguing properties of quantum entanglement and how they may be harnessed for future applications.

From decoherence-free channels to decoherence-free and quasi-free subspaces within bosonic dissipative networks

We present a technique to build, within a dissipative bosonic network, decoherence-free channels (DFCs): a group of normal-mode oscillators with null effective damping rates. We verify that the states protected within the DFC define the well-known decoherence-free subspaces (DFSs) when mapped back into the natural network oscillators. Therefore, our technique to build protected normal-mode channels turns out to be an alternative way to build DFSs, which offers advantages over the conventional method. It enables the computation of all the network-protected states at once, as well as leading naturally to the concept of the decoherence quasi-free subspace (DQFS), inside which a superposition state is quasi-completely protected against decoherence. The concept of the DQFS, weaker than that of the DFS, may provide a more manageable mechanism to control decoherence. Finally, as an application of the DQFSs, we show how to build them for quasi-perfect state transfer in networks of coupled quantum dissipative oscillators.

Mitochondrial ATP-sensitive K(+) channels as redox signals to liver mitochondria in response to hypertriglyceridemia

We have recently demonstrated that hypertriglyceridemic (HTG) mice present both elevated body metabolic rates and mild mitochondrial uncoupling in the liver owing to stimulated activity of the ATP-sensitive potassium channel (mitoK(ATP)). Because lipid excess normally leads to cell redox imbalance, we examined the hepatic oxidative status in this model. Cell redox imbalance was evidenced by increased total levels of carbonylated proteins, malondialdehydes, and GSSG/GSH ratios in HTG livers compared to wild type. In addition, the activities of the extramitochondrial enzymes NADPH oxidase and xanthine oxidase were elevated in HTG livers. In contrast, Mn-superoxide dismutase activity and content, a mitochondrial matrix marker, were significantly decreased in HTG livers. isolated HTG liver mitochondria presented lower rates of H(2)O(2) production, which were reversed by mitoK(ATP) antagonists. In vivo antioxidant treatment with N-acetylcysteine decreased both mitoKATP activity and metabolic rates in HTG mice. These data indicate that high levels of triglycerides increase reactive oxygen generation by extramitochondrial enzymes that promote MitoK(ATP) activation. The mild uncoupling mediated by mitoK(ATP) increases metabolic rates and protects mitochondria against oxidative damage. Therefore, a biological role for mitoK(ATP) is a redox sensor is shown here for the first time in an in vivo model of systemic and cellular lipid excess, (C) 2009 Elsevier Inc. All rights reserved.

Joint space-time trellis decoding and channel estimation in correlated fading channels

This letter addresses the issue of joint space-time trellis decoding and channel estimation in time-varying fading channels that are spatially and temporally correlated. A recursive space-time receiver which incorporates per-survivor processing (PSP) and Kalman filtering into the Viterbi algorithm is proposed. This approach generalizes existing work to the correlated fading channel case. The channel time-evolution is modeled by a multichannel autoregressive process, and a bank of Kalman filters is used to track the channel variations. Computer simulation results show that a performance close to the maximum likelihood receiver with perfect channel state information (CSI) can be obtained. The effects of the spatial correlation on the performance of a receiver that assumes independent fading channels are examined.

MMSE precoder for unitary space–time codes in correlated time-varying channels

This letter addresses the problem of the design of a precoder for multiple transmit antenna communication systems with spatially and temporally correlated fading channels. By using the asymptotic (high signal-to-noise ratio) mean-square error of the channel estimates, the letter derives a precoder for unitary space-time codes that can exploit the spatiotemporal correlation in the time-varying fading channels. Simulation results illustrate that significant performance gains can be achieved by using the new precoder.

Blind equalization of non-irreducible and non-column-reduced channels driven by constant modulus signals

We address the blind equalization of finite-impulse-response (FIR), multiple-input multiple-output (MIMO) channels excited by constant modulus (CM) signals. It is known that the algorithms based on the constant modulus (CM) criterion can equalize an FIR MIMO channel that is irreducible and column-reduced. We show in this paper that the CM property of signals can be exploited to construct a zero-forcing equalizer for a non-irreducible and non-column-reduced channel. We also give a lower bound for the order of the equalizer. Simulation examples demonstrate the proposed result.

Precoder design for multi-antenna systems with temporally and spatially correlated fading channels

This paper addresses the problem of the design of a precoder for multiple transmit antenna communication systems with spatially and temporally correlated fading channels. Using the theories of matrix differential calculus, the paper derives a precoder for unitary space-time codes that can exploit the spatio-temporal correlation in the time-varying fading channels. The design criterion is based on minimizing the mean square error of the channel estimates. Computer simulation results show that a significant performance gain can be achieved by using the designed precoder.

Differential encoding technique for multi-antenna systems with correlated Rayleigh fading channels

Differential space-time modulation (DSTM) techniques developed for multi-antenna systems allow the receiver to detect the transmitted signal without the knowledge of the fading channels. It can be viewed as an extension of differential phase-shift keying (DPSK) in single antenna systems. In this paper, we derived the pairwise error probability upper bound of differential space-time coded systems with spatially correlated Rayleigh fading channels. Based on the performance analysis, we develop a novel DSTM scheme which can exploit the spatial correlation in the fading channels. It is found that by carefully designing the initial transmitted signal matrix, the performance of the differential space-time coded systems can be significantly improved.

Blind equalization of non-irreducible channels driven by MPSK signals

This paper deals with the problem of blind equalization of finite-impulse-response (FIR) and multiple-input multiple-output (MIMO) channels excited by M-ary phase shift keying (MPSK) signals. It is known that the algorithms based on the constant modulus (CM) criterion can equalize an FIR MIMO channel that is irreducible. The irreducible condition is restrictive since it requires that all source signals arrive at the receiving antennas simultaneously. In this paper, we show that the CM criterion can also be used to construct a zero-forcing equalizer for a channel that is non-irreducible. We also derive a lower bound for the order of the equalizer. The proposed result is validated by numerical simulations.

Blind identification of FIR MIMO channels by decorrelating subchannels

We study blind identification and equalization of finite impulse response (FIR) and multi-input and multi-output (MIMO) channels driven by colored signals. We first show a sufficient condition for an FIR MIMO channel to be identifiable up to a scaling and permutation using the second-order statistics of the channel output. This condition is that the channel matrix is irreducible (but not necessarily column-reduced), and the input signals are mutually uncorrelated and of distinct power spectra. We also show that this condition is necessary in the sense that no single part of the condition can be further weakened without another part being strengthened. While the above condition is a strong result that sets a fundamental limit of blind identification, there does not yet exist a working algorithm under that condition. In the second part of this paper, we show that a method called blind identification via decorrelating subchannels (BIDS) can uniquely identify an FIR MIMO channel if a) the channel matrix is nonsingular (almost everywhere) and column-wise coprime and b) the input signals are mutually uncorrelated and of sufficiently diverse power spectra. The BIDS method requires a weaker condition on the channel matrix than that required by most existing methods for the same problem.

An iterative equalization method for nonirreducible MIMO FIR channels

This paper deals with the equalization of a nonirreducible multiple-input multiple-output (MIMO) finite-impulse-response (FIR) channel provided that the estimate of the channel matrix is available. An iterative method is developed to perform the channel equalization. The effectiveness of the proposed equalization method is demonstrated by simulation examples.