Limits on WWZ and WW\gamma couplings from p\bar{p}\to e\nu jj X events at \sqrt{s} = 1.8 TeV

We present limits on anomalous WWZ and WW-gamma couplings from a search for WW and WZ production in p-bar p collisions at sqrt(s)=1.8 TeV. We use p-bar p -> e-nu jjX events recorded with the D0 detector at the Fermilab Tevatron Collider during the 1992-1995 run. The data sample corresponds to an integrated luminosity of 96.0+-5.1 pb^(-1). Assuming identical WWZ and WW-gamma coupling parameters, the 95% CL limits on the CP-conserving couplings are -0.33<lambda<0.36 (Delta-kappa=0) and -0.43<Delta-kappa<0.59 (lambda=0), for a form factor scale Lambda = 2.0 TeV. Limits based on other assumptions are also presented.Comment: 11 pages, 2 figures, 2 table

Zgamma Production in pbarp Collisions at sqrt(s)=1.8 TeV and Limits on Anomalous ZZgamma and Zgammagamma Couplings

We present a study of Z +gamma + X production in p-bar p collisions at sqrt{S}=1.8 TeV from 97 (87) pb^{-1} of data collected in the eegamma (mumugamma) decay channel with the D0 detector at Fermilab. The event yield and kinematic characteristics are consistent with the Standard Model predictions. We obtain limits on anomalous ZZgamma and Zgammagamma couplings for form factor scales Lambda = 500 GeV and Lambda = 750 GeV. Combining this analysis with our previous results yields 95% CL limits |h{Z}_{30}| < 0.36, |h{Z}_{40}| < 0.05, |h{gamma}_{30}| < 0.37, and |h{gamma}_{40}| < 0.05 for a form factor scale Lambda=750 GeV.Comment: 17 Pages including 2 Figures. Submitted to PR

A Measurement of the W Boson Mass

We report a measurement of the W boson mass based on an integrated luminosity of 82 pb$^{-1}$ from \ppbar collisions at $\sqrt{s}=1.8$ TeV recorded in 1994--1995 by the \Dzero detector at the Fermilab Tevatron. We identify W bosons by their decays to $e\nu$ and extract the mass by fitting the transverse mass spectrum from 28,323 W boson candidates. A sample of 3,563 dielectron events, mostly due to Z to ee decays, constrains models of W boson production and the detector. We measure \mw=80.44\pm0.10(stat)\pm0.07(syst)~GeV. By combining this measurement with our result from the 1992--1993 data set, we obtain \mw=80.43\pm0.11 GeV.Comment: 11 pages, 5 figure

Frequency-specific hippocampal-prefrontal interactions during associative learning

Much of our knowledge of the world depends on learning associations (for example, face-name), for which the hippocampus (HPC) and prefrontal cortex (PFC) are critical. HPC-PFC interactions have rarely been studied in monkeys, whose cognitive and mnemonic abilities are akin to those of humans. We found functional differences and frequency-specific interactions between HPC and PFC of monkeys learning object pair associations, an animal model of human explicit memory. PFC spiking activity reflected learning in parallel with behavioral performance, whereas HPC neurons reflected feedback about whether trial-and-error guesses were correct or incorrect. Theta-band HPC-PFC synchrony was stronger after errors, was driven primarily by PFC to HPC directional influences and decreased with learning. In contrast, alpha/beta-band synchrony was stronger after correct trials, was driven more by HPC and increased with learning. Rapid object associative learning may occur in PFC, whereas HPC may guide neocortical plasticity by signaling success or failure via oscillatory synchrony in different frequency bands.National Institute of Mental Health (U.S.) (Conte Center Grant P50-MH094263-03)National Institute of Mental Health (U.S.) (Fellowship F32-MH081507)Picower Foundatio

Study of the ZZ\gamma and Z\gamma\gamma Couplings in Z(\nu\nu)\gamma Production

We have measured the ZZ-gamma and Z-gamma-gamma couplings by studying p-bar p -> (missing ET) gamma + X events at sqrt(s)=1.8 TeV with the D0 detector at the Fermilab Tevatron Collider. This first study of hadronic Z-gamma production in the neutrino decay channel gives the most stringent limits on anomalous couplings available. A fit to the transverse energy spectrum of the photon in the candidate event sample, based on a data set corresponding to an integrated luminosity of 13.1 pb^(-1), yields 95% CL limits on the anomalous CP-conserving ZZ-gamma couplings of |h^Z_(30)|<0.9, |h^Z_(40)|<0.21, for a form-factor scale Lambda = 500 GeV. Combining these results with our previous measurement using Z -> ee and mu-mu yields the limits:|h^Z_(30)|<0.8, |h^Z_(40)|<0.19 (Lambda = 500 GeV) and |h^Z_(30)|<0.4, |h^Z_(40)|<0.06 (Lambda = 750 GeV).Comment: 10 pages, 2 figures, 2 table

Limits on Anomalous WWγWW\gamma Couplings from ppˉ→Wγ+Xp\bar{p} \to W \gamma + X Events at s=1.8\sqrt{s}=1.8 TeV

We have measured the $WW\gamma$ gauge boson coupling parameters using $p\bar{p}\to \ell\nu\gamma+X$ ($\ell=e,\mu$) events at $\sqrt{s}=1.8$ TeV. The data, corresponding to an integrated luminosity of 89.1 pb^{-1}, were collected using the D0 detector at the Fermilab Tevatron Collider. The measured cross section times branching ratio for $p\bar{p} \to W\gamma+X$ with $p_T^\gamma$ > 10 GeV/c and $R_{\ell\gamma} > 0.7$ is ${11.8}^{+1.7}_{-1.6} \pm 2.0$ pb, in agreement with the Standard Model prediction. The one degree of freedom 95% confidence level limits on individual CP-conserving parameters are $-0.98<\Delta\kappa<1.01$ and $-0.33<\lambda<0.31$. Similar limits are set on the CP}violating coupling parameters.Comment: 10 pages, including two figures. Paper submitted to Phys. Rev. Let

Studies of Gauge Boson Pair Production and Trilinear Couplings

The gauge boson pair production processes Wg, WW, WZ, and Zg were studied using pbarp collisions corresponding to an integrated luminosity of ~14 pb-1 at a center-of-mass energy of sqrt(s) = 1.8 TeV. Analysis of Wg prod with subsequent W boson decay to lv (l=e,mu) is reported, including a fit to the pT spectrum of the photons which leads to limits on anomalous WWg couplings. A search for WW prod with subsequent decay to l-lbar-v-vbar (l=e,mu) is presented leading to an upper limit on the WW prod cross section and limits on anomalous WWg and WWZ couplings. A search for high pT W bosons in WW and WZ prod is described, where one W boson decays to an ev and the second W boson or the Z boson decays to two jets. A maximum likelihood fit to the pT spectrum of W bosons resulted in limits on anomalous WWg and WWZ couplings. A combined fit to the three data sets which provided the tightest limits on anomalous WWg and WWZ couplings is also described. Limits on anomalous ZZg and Zgg couplings are presented from an analysis of the photon ET spectrum in Zg events in the decay channels (ee, mu-mu, and v-vbar) of the Z boson.Comment: 77 Pages including 40 Figures. Submitted to PR

Search for the Trilepton Signature from the Associated Production of SUSY Chi_1^(+-) Chi_2^0 Gauginos

We report on a search for the trilepton signature from the associated production of supersymmetric gaugino pairs, Chi_1^(+-) Chi_2^0, within the context of minimal supersymmetric models that conserve R-parity. This search uses 95 pb^-1 of data taken with the \D0 detector at Fermilab's Tevatron collider at \sqrt{s} = 1.8 TeV. No evidence of a trilepton signature has been found, and a limit on the production cross section times branching fraction to trileptons as a function of Chi_1^(+-) mass is given.Comment: 16 pages, Latex (uses REVTeX V 3.0 style file), submitted to PR

Systemic NMDA antagonist CGP-37849 produces non-specific impairment in a working memory task: the effect does not resemble those of AP5 and of lesions of the hippocampus or fornix.

The N-methyl-D-aspartate (NMDA) receptor antagonist CGP-37849 (D,L-(E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid), administered i.p. (2.0 and 4.0 mg/kg), impaired rats' performance in a delayed matching-to-sample working memory task. This task is sensitive to hippocampal/fornix lesions or intracerebroventricular (i.c.v.) administration of another NMDA antagonist, AP5 (2-amino-5-phosphono-pentanoic acid) in a stimulus-specific manner: the highest impairment when simple stimuli are used repeatedly; moderate impairment when complex stimuli are used repeatedly; and no impairment when complex stimuli are used in a pseudo-trial-unique fashion. The effect of CGP-37849, unlike those of surgical lesions and of AP5, was not stimulus-specific and therefore cannot be solely attributed to blockade of NMDA-dependent long-term potentiation (LTP) in the hippocampus. We infer that systemic administration of NMDA antagonists may affect a broad range of anatomical structures thereby interfering with other neural mechanisms of memory and motor performance

Systemic NMDA receptor antagonist CGP-40116 does not impair memory acquisition but protects against NMDA neurotoxicity in rhesus monkeys.

A widely accepted hypothesis is that long-term potentiation (LTP) is a synaptic mechanism of memory. NMDA receptors are critically involved in induction but not maintenance of LTP; therefore, their blockade should impair memory acquisition but not retrieval. In Experiment 1, we investigated the effect of a systemic NMDA receptor antagonist, CGP-40116 [D-isomer of CGP-37849: (E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid (6 mg/kg, i.m.) 60 min before the testing session] on memory acquisition and retrieval by monkeys in the "object-in-place" visual memory task, an analog of human episodic memory. Only a small increase in error rate was produced (&lt; 3%), and this increase was observed in both retention and acquisition tests. This deficit is substantially smaller than the previously reported deficit after fornix transection in the same task, and is not specific to memory acquisition. In Experiment 2, we investigated the neuroprotective effect of CGP-40116. NMDA (68 nmol) was injected into the right hippocampus, then CGP-40116 (6 mg/kg) was given intramuscularly, and then NMDA was injected into the left hippocampus. The area of cell loss in CA1 and CA3 fields was smaller in both hemispheres compared with unprotected monkeys (without CGP-40116). Thus, CGP-40116 provides both retrograde and anterograde protection against NMDA neurotoxicity. These data (1) demonstrate that acquisition of episodic memories remains almost intact when an NMDA receptor antagonist is given in a dose sufficient to block NMDA receptors in the hippocampus, and (2) indirectly oppose the hypothesis that NMDA receptor-dependent LTP plays the key role in memory