Navegando por Autor "Petiz, Lyvia L."
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Artigo Chronic in vivo optogenetic stimulation modulates neuronal excitability, spine morphology, and Hebbian plasticity in the mouse hippocampus(2019-02-15) Moulin, Thiago C.; Petiz, Lyvia L.; Rayêe, Danielle; Winne, Jessica; Maia, Roberto G.; Cruz, Rafael V. Lima da; Amaral, Olavo B.; Leão, Richardson NavesProlonged increases in excitation can trigger cell‐wide homeostatic responses in neurons, altering membrane channels, promoting morphological changes, and ultimately reducing synaptic weights. However, how synaptic downscaling interacts with classical forms of Hebbian plasticity is still unclear. In this study, we investigated whether chronic optogenetic stimulation of hippocampus CA1 pyramidal neurons in freely moving mice could (a) cause morphological changes reminiscent of homeostatic scaling, (b) modulate synaptic currents that might compensate for chronic excitation, and (c) lead to alterations in Hebbian plasticity. After 24 hr of stimulation with 15‐ms blue light pulses every 90 s, dendritic spine density and area were reduced in the CA1 region of mice expressing channelrhodopsin‐2 (ChR2) when compared to controls. This protocol also reduced the amplitude of mEPSCs for both the AMPA and NMDA components in ex vivo slices obtained from ChR2‐expressing mice immediately after the end of stimulation. Finally, chronic stimulation impaired the induction of LTP and facilitated that of LTD in these slices. Our results indicate that neuronal responses to prolonged network excitation can modulate subsequent Hebbian plasticity in the hippocampus.Artigo Crosstalk between mitochondria, calcium channels and actin cytoskeleton modulates noradrenergic activity of locus coeruleus neurons(2019-03-03) Oliveira, Ramatis B. de; Petiz, Lyvia L.; Lim, Rebecca; Lipski, Janusz; Gravina, Fernanda S.; Brichta, Alan M.; Callister, Robert J.; Leão, Richardson Naves; van Helden, Dirk F.Locus coeruleus (LC) is the name of a group of large sized neurons located at the brain stem, which provide the main source of noradrenaline to the central nervous system, virtually, innervating the whole brain. All noradrenergic signalling provided by this nucleus is dependent on an intrinsic pacemaker process. Our study aims to understand how noradrenergic neurons finely tune their pacemaker processes and regulate their activities. Here we present that mitochondrial perturbation in the LC from mice, inhibits spontaneous firing by a hyperpolarizing response that involves Ca2+ entry via L‐type Ca2+ channels and the actin cytoskeleton. We found that pharmacological perturbation of mitochondria from LC neurons using the protonophore carbonyl cyanide m‐chlorophenylhydrazone (CCCP), induced a dominant hyperpolarizing response when electrophysiological approaches were performed. Surprisingly, the CCCP‐induced hyperpolarizing response was dependent on L‐type Ca2+ channel‐mediated Ca2+ entry, as it was inhibited by: removal of extracellular Ca2+; addition of Cd2+; nifedipine or nicardipine; but not by intracellular dialysis with the Ca2+ chelator BAPTA, the latter indicating that the response was not due to a global change in [Ca2+]c but does not exclude action at intracellular microdomains. Further to this, incubation of slices with cytochalasin D, an agent that depolymerises the actin cytoskeleton, inhibited the hyperpolarizing response indicating an involvement of the actin cytoskeleton. The data are consistent with the hypothesis that there is crosstalk between mitochondria and L‐type Ca2+ channels leading to modulation of noradrenergic neuronal activity mediated by the actin cytoskeleton.