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The first measurements of dielectron production at midrapidity (|ηc|<0.8) in proton-proton and proton-lead collisions at sNN−−−√ = 5.02 TeV at the LHC are presented. The dielectron cross section is measured with the ALICE detector as a function of the invariant mass mee and the pair transverse momentum pT,ee in the ranges mee < 3.5 GeV/c2 and pT,ee < 8.0 GeV/c2, in both collision systems. In proton-proton collisions, the charm and beauty cross sections are determined at midrapidity from a fit to the data with two different event generators. This complements the existing dielectron measurements performed at s√ = 7 and 13 TeV. The slope of the s√ dependence of the three measurements is described by FONLL calculations. The dielectron cross section measured in proton-lead collisions is in agreement, within the current precision, with the expected dielectron production without any nuclear matter effects for e+e− pairs from open heavy-flavor hadron decays. For the first time at LHC energies, the dielectron production in proton-lead and proton-proton collisions are directly compared at the same sNN−−−√ via the dielectron nuclear modification factor RpPb. The measurements are compared to model calculations including cold nuclear matter effects, or additional sources of dielectrons from thermal radiation.
The first measurements of dielectron production at midrapidity (|ηc|<0.8) in proton-proton and proton-lead collisions at sNN−−−√ = 5.02 TeV at the LHC are presented. The dielectron cross section is measured with the ALICE detector as a function of the invariant mass mT,ee and the pair transverse momentum pT,ee in the ranges mT,ee < 3.5 GeV/c2 and mT,ee < 8.0 GeV/c2, in both collision systems. In proton-proton collisions, the charm and beauty cross sections are determined at midrapidity from a fit to the data with two different event generators. This complements the existing dielectron measurements performed at s√ = 7 and 13 TeV. The slope of the s√ dependence of the three measurements is described by FONLL calculations. The dielectron cross section measured in proton-lead collisions is in agreement, within the current precision, with the expected dielectron production without any nuclear matter effects for e+e− pairs from open heavy-flavor hadron decays. For the first time at LHC energies, the dielectron production in proton-lead and proton-proton collisions are directly compared at the same sNN−−−√ via the dielectron nuclear modification factor RpPb. The measurements are compared to model calculations including cold nuclear matter effects, or additional sources of dielectrons from thermal radiation.
Recent studies suggest that synaptic lysophosphatidic acids (LPAs) augment glutamate-dependent cortical excitability and sensory information processing in mice and humans via presynaptic LPAR2 activation. Here, we studied the consequences of LPAR2 deletion or antagonism on various aspects of cognition using a set of behavioral and electrophysiological analyses. Hippocampal neuronal network activity was decreased in middle-aged LPAR2−/− mice, whereas hippocampal long-term potentiation (LTP) was increased suggesting cognitive advantages of LPAR2−/− mice. In line with the lower excitability, RNAseq studies revealed reduced transcription of neuronal activity markers in the dentate gyrus of the hippocampus in naïve LPAR2−/− mice, including ARC, FOS, FOSB, NR4A, NPAS4 and EGR2. LPAR2−/− mice behaved similarly to wild-type controls in maze tests of spatial or social learning and memory but showed faster and accurate responses in a 5-choice serial reaction touchscreen task requiring high attention and fast spatial discrimination. In IntelliCage learning experiments, LPAR2−/− were less active during daytime but normally active at night, and showed higher accuracy and attention to LED cues during active times. Overall, they maintained equal or superior licking success with fewer trials. Pharmacological block of the LPAR2 receptor recapitulated the LPAR2−/− phenotype, which was characterized by economic corner usage, stronger daytime resting behavior and higher proportions of correct trials. We conclude that LPAR2 stabilizes neuronal network excitability upon aging and allows for more efficient use of resting periods, better memory consolidation and better performance in tasks requiring high selective attention. Therapeutic LPAR2 antagonism may alleviate aging-associated cognitive dysfunctions.