Dynamics of electron transfer from high-potential cytochrome <Emphasis Type="Italic">c</Emphasis> to bacteriochlorophyll dimer in photosynthetic reaction centers as probed using laser-induced temperature jump

Laser-induced temperature jump experiments were used for testing the rates of thermoinduced conformational transitions of reaction center (RC) complexes in chromatophores of Chromatium minutissimum. The thermoinduced transition of the macromolecular RC complex to a state providing effective electron transport from the multiheme cytochrome c to the photoactive bacteriochlorophyll dimer within the temperature range 220–280 K accounts for tens of seconds with activation energy 0.166 eV/molecule. The rate of the thermoinduced transition in the cytochrome–RC complex was found to be three orders of magnitude slower than the rate of similar thermoinduced transition of the electron transfer reaction from the primary to secondary quinone acceptors studied in the preceding work (Chamorovsky et al. in Eur Biophys J 32:537–543, 2003). Parameters of thermoinduced activation of the electron transfer from the multiheme cytochrome c to the photoactive bacteriochlorophyll dimer are discussed in terms of cytochrome c docking onto the RC.     

Pituitary adenylate cyclase-activating polypeptide is up-regulated in cortical pyramidal cells after focal ischemia and protects neurons from mild hypoxic/ischemic damage

The protective effect of pituitary adenylate cyclase-activating polypeptide (PACAP) in stroke models is poorly understood. We studied patterns of PACAP, vasoactive intestinal peptide, and the PACAP-selective receptor PAC1 after middle cerebral artery occlusion and neuroprotection by PACAP in cortical cultures exposed to oxygen/glucose deprivation (OGD). Within hours, focal ischemia caused a massive, NMDA receptor (NMDAR)-dependent up-regulation of PACAP in cortical pyramidal cells. PACAP expression dropped below the control level after 2 days and was normalized after 4 days. Vasoactive intestinal peptide expression was regulated oppositely to that of PACAP. PAC1 mRNA showed ubiquitous expression in neurons and astrocytes with minor changes after ischemia. In cultured cortical neurons PACAP27 strongly activated Erk1/2 at low and p38 MAP kinase at higher nanomolar concentrations via PAC1. In astrocyte cultures, effects of PACAP27 on Erk1/2 and p38 were weak. During OGD, neurons showed severely reduced Erk1/2 activity and dephosphorylation of Erk1/2-regulated Ser112 of pro-apoptotic Bad. PACAP27 stimulation counteracted Erk1/2 inactivation and Bad dephosphorylation during short-term OGD but was ineffective after expanded OGD. Consistently, PACAP27 caused MEK-dependent neuroprotection during mild but not severe hypoxic/ischemic stress. While PACAP27 protected neurons at 1–5 nmol/L, full PAC1 activation by 100 nmol/L PACAP exaggerated hypoxic/ischemic damage. PACAP27 stimulation of astrocytes increased the production of Akt-activating factors and conferred ischemic tolerance to neurons. Thus, ischemia-induced PACAP may act via neuronal and astroglial PAC1. PACAP confers protection to ischemic neurons by maintaining Erk1/2 signaling via neuronal PAC1 and by increasing neuroprotective factor production via astroglial PAC1.     

Hearing Range of White-Tailed Deer as Determined by Auditory Brainstem Response

Abstract: Basic knowledge of white-tailed deer (Odocoileus virginianus) hearing can improve understanding of deer behavior and may assist in the development of effective deterrent strategies. Using auditory brainstem response testing, we determined that white-tailed deer hear within the range of frequencies we tested, between 0.25–30 kilohertz (kHz), with best sensitivity between 4–8 kHz. The upper limit of human hearing lies at about 20 kHz, whereas we demonstrated that white-tailed deer detected frequencies to at least 30 kHz. This difference suggests that research on the use of ultrasonic (frequencies >20 kHz) auditory deterrents is justified as a possible means of reducing deer—human conflicts.     

Halothane Increases Non-vesicular [<Superscript>3</Superscript>H]dopamine Release from Brain Cortical Slices

Experimental data suggest that halothane anesthesia is associated with significant changes in dopamine (DA) concentration in some brain regions but the mechanism of this effect is not well known. Rat brain cortical slices were labeled with [³H]DA to further characterize the effects of halothane on the release of this neurotransmitter from the central nervous system. Halothane induced an increase on the release of [³H]DA that was dependent on incubation time and anesthetic concentration (0.012, 0.024, 0.048, 0.072 and 0.096 mM). This effect was independent of extracellular or intracellular calcium. In addition, [³H]DA release evoked by halothane was not affected by TTX (blocker of voltage-dependent Na⁺ channels) or reserpine (a blocker of vesicular monoamine transporter). These data suggest that [³H]DA release induced by halothane is non-vesicular and would be mediated by the dopamine transporter (DAT) and norepinephrine transporter (NET). GBR 12909 and nomifensine, inhibitors of DAT, decreased the release of [³H]DA evoked by halothane. Nisoxetine, a blocker of NET, reduced the release of [³H]DA induced by halothane. In addition, GBR 12909, nisoxetine and, halothane decrease the uptake of [³H]DA into rat brain cortical slices. A decrease on halothane-induced release of [³H]DA was also observed when the brain cortical slices were incubated at low temperature and low extracellular sodium, which are known to interfere with the carrier-mediated release of the neurotransmitter. Ouabain, a Na⁺/K⁺ ATPase pump inhibitor, which induces DA release through reverse transport, decreased [³H]DA release induced by halothane. It is suggested that halothane increases [³H]DA release in brain cortical slices that is mediated by DAT and NET present in the plasma membrane.     

Electron and nuclear dynamics in many-electron atoms, molecules and chlorophyll-protein complexes: A review

It has been shown [V.A. Shuvalov, Quantum dynamics of electrons in many-electron atoms of biologically important compounds, Biochemistry (Mosc.) 68 (2003) 1333-1354; V.A. Shuvalov, Quantum dynamics of electrons in atoms of biologically important molecules, Uspekhi biologicheskoi khimii, (Pushchino) 44 (2004) 79-108] that the orbit angular momentum L of each electron in many-electron atoms is L = mVr = n? and similar to L for one-electron atom suggested by N. Bohr. It has been found that for an atom with N electrons the total electron energy equation E = −(Z^eff)²e⁴m/(2n²?²N) is more appropriate for energy calculation than standard quantum mechanical expressions. It means that the value of L of each electron is independent of the presence of other electrons in an atom and correlates well to the properties of virtual photons emitted by the nucleus and creating a trap for electrons. The energies for elements of the 1st up to the 5th rows and their ions (total amount 240) of Mendeleev' Periodical table were calculated consistent with the experimental data (deviations in average were 5 × 10^− 3). The obtained equations can be used for electron dynamics calculations in molecules. For H₂ and H₂⁺ the interference of electron-photon orbits between the atoms determines the distances between the nuclei which are in agreement with the experimental values. The formation of resonance electron-photon orbit in molecules with the conjugated bonds, including chlorophyll-like molecules, appears to form a resonance trap for an electron with E values close to experimental data. Two mechanisms were suggested for non-barrier primary charge separation in reaction centers (RCs) of photosynthetic bacteria and green plants by using the idea of electron-photon orbit interference between the two molecules. Both mechanisms are connected to formation of the exciplexes of chlorophyll-like molecules. The first one includes some nuclear motion before exciplex formation, the second one is related to the optical transition to a charge transfer state.     

Neuroprotection and free radical scavenging effects of <Emphasis Type="Italic">Osmanthus fragrans</Emphasis>

The ethanol extract of dried flowers Osmanthus fragrans (OFE) was assessed for free radical scavenging effects measured by the bleaching of the 1,1-diphenyl-2-picryl-hydrazyl (DPPH) radical, scavenging of the hydroxyl anion, investigation of the ferric reducing/antioxidant power (FRAP) and lipid-peroxidation inhibition in rat tissues. OFE contained a high amount of total flavonoid and polyphenol. OFE presented the effects in the metal reducing power, FRAP assay with IC₅₀ values of 0.23 μg/ml, and 7.74 μg/ml, respectively. OFE presented similar activities toward the DPPH and hydroxyl anion scavenging ability with IC₅₀ values of 10 μg/ml. OFE with IC₅₀ values between 46 and 97 μg/ml inhibited lipid peroxidation initiated by ferrous chloride in rat brain, liver, heart and kidney mitochodrias. Moreover, the neuroprotective activity of OFE was investigated under different insults (glutamate, arachidonic acid, and 6-hydroxydopamine) in Wistar rat primary cortical neurons. OFE with EC₅₀ values between 66 and 165 μg/ml attenuated the neurotoxicity on MTT and LDH assays. In addition, the AKT protein expression of excitotoxicity and oxidative stress was displayed by western blotting analysis. OFE could up-regulate the glutamate and 6-OHDA decreased AKT expression. This is the first demonstration of the neuroprotective, free radical scavenging and anti-oxidative effects of O. fragrans.     

Group I Metabotropic Glutamate Receptors: A Role in Neurodevelopmental Disorders?

Group I metabotropic glutamate receptors (mGlu1 and mGlu5) are coupled to polyphosphoinositide hydrolysis and are involved in activity-dependent forms of synaptic plasticity, both during development and in the adult life. Group I mGlu receptors can also regulate proliferation, differentiation, and survival of neural stem/progenitor cells, which further support their role in brain development. An exaggerated response to activation of mGlu5 receptors may underlie synaptic dysfunction in Fragile X syndrome, the most common inherited form of mental retardation. In addition, group I mGlu receptors are overexpressed in dysplastic neurons of focal cortical dysplasia and hemimegaloencephaly, which are disorders of cortical development associated with chronic epilepsy. Drugs that block the activity of group I mGlu receptors (in particular, mGlu5 receptors) are potentially helpful for the treatment of Fragile X syndrome and perhaps other neurodevelopmental disorders.     

Mechanisms of seizure propagation in a cortical model

We consider a mathematical model of mesoscopic human cortical ictal electrical activity. We compare the model results with ictal electrocortical data recorded from three human subjects and show how the two agree. We determine that, in the model system, seizures result from increased connectivity between excitatory and inhibitory cell populations, or from decreased connectivity within either excitatory or inhibitory cell populations. We compare the model results with the disinhibition and 4-AP models of epilepsy and suggest how the model may guide the development of new anticonvulsant therapies.