Perceptual coupling in rhythmic movement coordination: stable perception leads to stable action

Rhythmic movement coordination exhibits characteristic patterns of stability, specifically that movements at 0 degrees mean relative phase are maximally stable, 180 degrees is stable but less so than 0 degrees, and other coordinations are unstable without training. Recent research has demonstrated a role for perception in creating this pattern; perceptual variability judgments covary with movement variability results. This suggests that the movement results could be due in part to differential perceptual resolution of the target movement coordinations. The current study used a paradigm that enabled simultaneous access to both perception (between-trial) and movement (within-trial) stability measures. A visually specified 0 degrees target mean relative phase enabled participants to produce stable movements when the movements were at a non-0 degrees relationship to the target being tracked. Strong relationships were found between within-trial stability (the traditional movement measure) and between-trial stability (the traditional perceptual judgment measure), suggestive of a role for perception in producing coordination stability phenomena. The stabilization was incomplete, however, indicating that visual perception was not the sole determinant of movement stability. Rhythmic movement coordination is intrinsically a perception/action system.     

Novel Aromatic Polymer Electrolyte with Comb‐like Structure: Synthesis and Properties

Summary: A novel aromatic polymer electrolyte with pendant sulfodecyloxy groups was synthesized. The monomer 4 , bis[2‐(10′‐sulfodecyloxy)‐5‐chlorophenyl]sulfone, was synthesized from bis(2‐hydroxy‐5‐chlorophenyl)sulfide via bromoalkylation, oxidation, and sulfonation, and then polymerized via Ni‐catalyzed C C coupling polymerization to afford the title polymer electrolyte 6 . The polymer 6 was isolated as a brown powder with molecular weight of = 12 000. The high decomposition temperature of 6 (200 °C) was confirmed by TG/DTA‐MS measurement. Proton conductivity of 6 was measured using porous polyimide membrane as a supporting substrate. The pore‐filled membrane showed 1 × 10⁻⁵ S · cm⁻¹ of the proton conductivity at 80 °C and 90% RH.

Synthesis of aromatic polymer electrolyte having sulfodecyloxy groups via nickel‐catalyzed C C coupling polymerization.     

Gap-junction communication between subtypes of direction-selective ganglion cells in the developing retina

The On-Off direction-selective ganglion cells (DSGCs) in the rabbit retina comprise four distinct subtypes that respond preferentially to image motion in four orthogonal directions; each subtype forms a regular territorial array, which is overlapped by the other three arrays. In this study, ganglion cells in the developing retina were injected with Neurobiotin, a gap-junction-permeable tracer, and the DSGCs were identified by their characteristic type 1 bistratified (BiS1) morphology. The complex patterns of tracer coupling shown by the BiS1 ganglion cells changed systematically during the course of postnatal development. BiS1 cells appear to be coupled together around the time of birth, but, over the next 10 days, BiS1 cells decouple from each other, leading to the mature pattern in which only one subtype is coupled. At about postnatal day 5, before the ganglion cells become visually responsive, each of the BiS1 cells commonly showed tracer coupling both to a regular array of neighboring BiS1 cells, presumably destined to be DSGCs of the same subtype, and to a regular array of overlapping BiS1 cells, presumably destined to be DSGCs of a different subtype. The gap-junction intercellular communication between subtypes of DSGCs with different preferred directions may play an important role in the differentiation of their synaptic connectivity, with respect to either the inputs that DSGCs receive from retinal interneurons or the outputs that DSGCs make to geniculate neurons.     

The bimodal basis of the contractile response of the rabbit ear artery to norepinephrine and other agonists

Strips of rabbit ear artery exhibit biphasic contractile responses to l-norepinephrine (1-NE), histamine, and serotonin. Evidence is presented on the basis of an analysis of the response to 1-NE that the two phases of contraction are associated with different modes of excitation and can be influenced independently. The initial part of the response is phasic. The response after 4 sec agonist exposure is the same as that after 32 sec. It is probably associated with local radial propagation of excitation in that the initial excitatory period is short, the contraction is preceded by electrical change and is abolished upon tissue exposure to a solution in which all NaCl and KCl is replaced by potassium methylsulfate. In contrast the second contractile phase is related to the time of tissue exposure to the drug, is an equilibrium-like response and is not dependent upon cell membrane polarization. Since this phase is more affected by calcium depletion than the first, the sources of activator calcium for the two phases may be different: that for the first phase many originate predominantly from intracellular and that for the second from extracellular sources. These findings support the hypothesis that the biphasic contractile response of the vessel reflects two different modes of excitation of the muscle wall by the agonists: the first, a triggered, propagated event; the second, a slow, equilibrium-type, non-propagated response.     

A pentylenetetrazole-induced generalized seizure in early life enhances the efficacy of muscarinic receptor coupling to G-protein in hippocampus and neocortex of adult rat

We have previously shown that exposure to the anti-cholinesterase eserine provokes interictal-like discharges in the CA3 area of hippocampal slices from adult rats in which a generalized seizure has been induced by pentylenetetrazole (PTZ) when immature (at 20 days). Such increased responsiveness to acetylcholine (ACh) was not associated with any change in hippocampal acetylcholine or gamma-aminobutyric acid (GABA) content, GABAergic inhibition or density of ACh innervation, but was blocked by the muscarinic receptor antagonist atropine. We therefore turned to quantitative radioligand binding autoradiography, in situ hybridization and the [35S]GTPgammaS method to assess the properties of hippocampal and neocortical muscarinic receptors in adult rats having experienced a PTZ seizure at P20. The densities of M1 and M2 receptor binding sites, respectively labeled with [3H]pirenzepine and [3H]AFDX-384, as well as the amount of m1, m2 and m3 receptor mRNAs, did not differ from control in the hippocampus and neocortex of these rats. In contrast, in PTZ rats, both brain regions displayed a marked increase in [35S]GTPgammaS incorporation stimulated by ACh, bethanechol and particularly oxotremorine. This finding indicates that a generalized seizure in immature rat can entail a long-term and presumably permanent increase in the efficacy of G-protein coupling to muscarinic receptors in the hippocampus and neocortex of the adult. By analogy, such a mechanism could account for the susceptibility to epilepsy of human adults having suffered from prolonged convulsions in early life.     

Relaxant responses to calcium channel antagonists and potassium channel opener in human saphenous vein

1.-- As shown in a parallel study the magnitude of depolarization induced in human saphenous vein by raising external potassium ([K(+)](e)) falls markedly below the theoretical values predicted by the Goldman-Hodgkin-Katz equations. This anomaly prompted us to re-examine the relaxant actions of L-type (nifedipine) and T-type (mibefradil) Ca(2+) channel antagonists, and relaxant and electrophysiological effects of the K(+) channel opener, pinacidil, on saphenous veins contracted by the elevation of [K(+)](e). 2.-- Nifedipine produced concentration-dependent relaxations in tissues contracted at various high [K(+)](e). In tissues contracted with 20 mm [K(+)](e), the pIC(50) for nifedipine was significantly (8.20 +/- 0.05; n = 6; mean +/- SEM; P < 0.05) greater than in tissues contracted with > or =40 mm [K(+)](e). 3.-- Tissues contracted with 20 mm [K(+)](e) also relaxed in response to mibefradil (pIC(50) = 6.1 +/- 0.14) and pinacidil (pIC(50) = 6.45 +/- 0.08), the latter being almost completely reversed (93.4 +/- 9.9%) by addition of glibenclamide (10 microm). 4.-- The resting E(m) of smooth muscle cells of saphenous vein was -77.0 +/- 0.7 mV (n = 52), and 20 mm [K(+)](e) produced a modest but significant depolarization to -73.0 +/- 0.7 mV (n = 52). Incubation with pinacidil plus 20 mm [K(+)](e) resulted in a significant hyperpolarization of the E(m) to -82 +/- 0.6 mV (n = 52). 5.-- N(omega)-nitro-L-arginine methyl ester did not impede the relaxant responses of nifedipine, mibefradil or pinacidil. 6.-- In conclusion, the relaxant effects of nifedipine and pinacidil (i) occurred at an E(m) distinctly below the presumed threshold for the opening of the classic (Ca(V)1.3alpha(1)) L-type Ca(2+) channels, and (ii) did not depend on generation of nitric oxide.     

Isoproterenol does not enhance Ca-dependent Na/Ca exchange current in intact rabbit ventricular myocytes

Cardiac Na/Ca exchange (NCX, NCX1.1) is critical in cardiac myocyte Ca regulation, and its altered function contributes to inotropic state, systolic dysfunction in heart failure and arrhythmogenesis. Regulation of NCX is multifaceted, but protein kinase A (PKA) effects on NCX function are controversial. Here, we use three different and complementary approaches to compare NCX function +/-1 microM isoproterenol (ISO) in intact rabbit cardiac myocytes (in paired comparisons). First, in field-stimulated intact cells we inferred the cytosolic [Ca] ([Ca](i)) dependence of NCX function from the decay rate of caffeine-induced [Ca](i) transients. Second, we measured caffeine-induced [Ca](i) and inward I(NCX) simultaneously (perforated patch voltage clamp), to measure directly the [Ca](i) dependence of NCX rate. Third, using whole cell ruptured patch with [Ca](i) heavily buffered to 100 nM, [Na](i)=10 mM, and I(Ca), SR Ca release and Na/K pump all blocked, we recorded I(NCX) ramps at 37 degrees C. We find that NCX function is not altered by PKA activation under any of these three protocols, where intracellular conditions ranged from near-physiological to highly controlled. This does not rule out NCX modulation by PKA under all conditions, or in species other than rabbit. However, such effects are likely to be either minor (vs. other PKA actions on myocyte Ca handling) or indirect, such as secondary effects dependent on altered local [Ca](i) and [Na](i).     

神经刺激器耦合方式的探讨

本文介绍了部分植入式神经刺激器的体外脉冲发射装置与植入体内的感应接收器的耦合能量传递方式对诱导狗阴茎勃起的影响，并给出了实验结果。     

Bradykinin and inositol 1,4,5-trisphosphate-stimulated calcium release from intracellular stores in cultured bovine endothelial cells

The relative importance of intracellular and extracellular Ca²⁺ in the release of endothelium-derived relaxing factor (EDRF) and the mechanisms involved in the release of intracellular Ca²⁺ were investigated in cultured bovine endothelial cells. The release of EDRF by bradykinin, determined by bioassay, was dose-dependent showing an EC₅₀ of 4×10^–10 M. The bradykinin-induced EDRF release from endothelial cells was maintained in the presence of extracellular Ca²⁺. However, in the absence of external Ca²⁺, bradykinin-induced EDRF release was both attenuated and transient. In cells loaded to isotopic equilibrium with⁴⁵Ca, bradykinin increased the⁴⁵Ca efflux into both calcium-containing and calcium-free solutions, with an EC₅₀ for the increase in⁴⁵Ca efflux induced by bradykinin of 1.3×10^–9 M. The involvement of an intracellular Ca²⁺ store and the participation of a second messenger in its release were investigated in saponin-permeabilized endothelial cells. In saponin-permeabilized cells, ATP-sensitive calcium uptake was Ca²⁺,Mg²⁺-ATPase-dependent. The ATP-sensitive uptake of calcium at different free Ca²⁺ concentrations showed at least two compartments involved in the uptake of Ca²⁺. The⁴⁵Ca uptake into the compartment with the lowest affinity and highest capacity could be inhibited by sodium azide, suggesting that this uptake was into mitochondria. The majority of the⁴⁵Ca uptake into the azide-insensitive store could be released by inositol-1,4,5-trisphosphate (IP₃). The IP₃-induced release was not affected by apyrase or exogenous GTP. The EC₅₀ for the release of Ca²⁺ by IP₃ was 1.0 M and was unaffected by an inhibitor of IP₃ breakdown (2,3-diphosphoglyceric acid). The results suggest that the release of EDRF is dependent on extracellular Ca²⁺ influx and the release of intracellular Ca²⁺. The release of calcium from one of the high affinity intracellular Ca²⁺ stores is mediated by the intracellular second messenger, IP₃.