Hippocampal Deletion of BDNF Gene Attenuates Gamma Oscillations in Area CA1 by Up-Regulating 5-HT3 Receptor

Background: Pyramidal neurons in the hippocampal area CA3 express high levels of BDNF, but how this BDNF contributes to oscillatory properties of hippocampus is unknown. Methodology/Principal Findings: Here we examined carbachol-induced gamma oscillations in hippocampal slices lacking BDNF gene in the area CA3. The power of oscillations was reduced in the hippocampal area CA1, which coincided with increases in the expression and activity of 5-HT3 receptor. Pharmacological block of this receptor partially restored power of gamma oscillations in slices from KO mice, but had no effect in slices from WT mice. Conclusion/Significance: These data suggest that BDNF facilitates gamma oscillations in the hippocampus by attenuating signaling through 5-HT3 receptor. Thus, BDNF modulates hippocampal oscillations through serotonergic system

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

ITBS-induced LTP-like plasticity parallels oscillatory activity changes in the primary sensory and motor areas of macaque monkeys

Recently, neuromodulation techniques based on the use of repetitive transcranial magnetic stimulation (rTMS) have been/nproposed as a non-invasive and efficient method to induce in vivo long-term potentiation (LTP)-like aftereffects. However,/nthe exact impact of rTMS-induced perturbations on the dynamics of neuronal population activity is not well understood./nHere, in two monkeys, we examine changes in the oscillatory activity of the sensorimotor cortex following an intermittent/ntheta burst stimulation (iTBS) protocol. We first probed iTBS modulatory effects by testing the iTBS-induced facilitation of/nsomatosensory evoked potentials (SEP). Then, we examined the frequency information of the electrocorticographic signal,/nobtained using a custom-made miniaturised multi-electrode array for electrocorticography, after real or sham iTBS. We/nobserved that iTBS induced facilitation of SEPs and influenced spectral components of the signal, in both animals. The latter/neffect was more prominent on the h band (4–8 Hz) and the high c band (55–90 Hz), de-potentiated and potentiated/nrespectively. We additionally found that the multi-electrode array uniformity of b (13–26 Hz) and high c bands were also/nafflicted by iTBS. Our study suggests that enhanced cortical excitability promoted by iTBS parallels a dynamic reorganisation/nof the interested neural network. The effect in the c band suggests a transient local modulation, possibly at the level of/nsynaptic strength in interneurons. The effect in the h band suggests the disruption of temporal coordination on larger/nspatial scales