8 research outputs found
Cell-specific synaptic plasticity induced by network oscillations
Gamma rhythms are known to contribute to the process of memory encoding.
However, little is known about the underlying mechanisms at the molecular,
cellular and network levels. Using local field potential recording in awake
behaving mice and concomitant field potential and whole-cell recordings in
slice preparations we found that gamma rhythms lead to activity-dependent
modification of hippocampal networks, including alterations in sharp wave-
ripple complexes. Network plasticity, expressed as long-lasting increases in
sharp wave-associated synaptic currents, exhibits enhanced excitatory synaptic
strength in pyramidal cells that is induced postsynaptically and depends on
metabotropic glutamate receptor-5 activation. In sharp contrast, alteration of
inhibitory synaptic strength is independent of postsynaptic activation and
less pronounced. Further, we found a cell type-specific, directionally biased
synaptic plasticity of two major types of GABAergic cells, parvalbumin- and
cholecystokinin-expressing interneurons. Thus, we propose that gamma frequency
oscillations represent a network state that introduces long-lasting synaptic
plasticity in a cell-specific manner
Sevoflurane Effects on Neuronal Energy Metabolism Correlate with Activity States While Mitochondrial Function Remains Intact
During general anesthesia, alterations in neuronal metabolism may induce neurotoxicity and/or neuroprotection depending on the dose and type of the applied anesthetic. In this study, we investigate the effects of clinically relevant concentrations of sevoflurane (2% and 4%, i.e., 1 and 2 MAC) on different activity states in hippocampal slices of young Wistar rats. We combine electrophysiological recordings, partial tissue oxygen (ptiO2) measurements, and flavin adenine dinucleotide (FAD) imaging with computational modeling. Sevoflurane minimally decreased the cerebral metabolic rate of oxygen (CMRO2) while decreasing synaptic transmission in naive slices. During pharmacologically induced gamma oscillations, sevoflurane impaired network activity, thereby decreasing CMRO2. During stimulus-induced neuronal activation, sevoflurane decreased CMRO2 and excitability while basal metabolism remained constant. In this line, stimulus-induced FAD transients decreased without changes in basal mitochondrial redox state. Integration of experimental data and computer modeling revealed no evidence for a direct effect of sevoflurane on key enzymes of the citric acid cycle or oxidative phosphorylation. Clinically relevant concentrations of sevoflurane generated a decent decrease in energy metabolism, which was proportional to the present neuronal activity. Mitochondrial function remained intact under sevoflurane, suggesting a better metabolic profile than isoflurane or propofol