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The hippocampal theta rhythm is frequently viewed as a clocking mechanism that coordinates the spiking activity of neurons across the hippocampus to form coherent neural assemblies. Phase precession is a form of temporal coding evidencing this mechanism and is degraded following systemic pharmacological disruption of cholinergic signaling. However, whether neural assemblies are commensurately degraded, as would be predicted from a clocking mechanism hypothesis, remains unknown. To address this, we recorded the spiking activity of hippocampal place cells as rats completed laps on a circle track for chocolate drink before versus during the influence of a systemic muscarinic acetylcholine receptor antagonist. We compared the integrity of hippocampal ensembles using three approaches. The first approach used cross-correlogram (CCG) analyses to ask if the relative spike-timing between pairs of cells became less reliable. The second used a general linear model based analysis to ask whether the activity of simultaneously recorded neurons became any less predictive of the spiking activity of single neurons. Finally, the third approach used a reconstruction analysis to ask if the population activity was any less informative regarding the environmental position of the animal and whether theta sequences were impaired. The results of all three analyses paint a consistent picture: systemic cholinergic disruption did not degrade assembly integrity. These data demonstrate that place cell assemblies do not depend upon high quality phase precession.
This article was published in the following journal.
Intracellular protein crystallization occurs under various physiological and pathological settings, yet the underlying cellular processes remain enigmatic. After validating individual crystallization ...
The bundled structure of micron-sized pectin gel filaments was formed by quick shear-induced gelation of the filamentous domains of pectin-polyethylene glycol (PEG) assemblies. Highly concentrated pec...
Recent studies have highlighted the extraordinary cell type diversity that exists within mammalian organs, yet the molecular drivers of such heterogeneity remain elusive. To address this issue, much a...
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Structural modeling of a cell is an evolving strategic direction in computational structural biology. It takes advantage of new powerful modeling techniques, deeper understanding of fundamental princi...
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A cohort of 15 patients starting orthodontic treatment with fixed appliances will receive EXD-952 Ceramic Self-ligating brackets on all mandibular incisors and a different type of brackets...
This is a Phase II study for the use of T-cell replete reduced intensity conditioning (RIC) haploidentical donor allogeneic hematopoietic cell transplantation (HaploHCT) for individuals wi...
Patients with Parkinson's disease have internal rhythm dysfunction, which may affect the rhythmic movements such as walking. Poor regularity of the rhythmic movement may lead to freezing o...
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
The period of the CELL CYCLE following DNA synthesis (S PHASE) and preceding M PHASE (cell division phase). The CHROMOSOMES are tetraploid in this point.
The interval between two successive CELL DIVISIONS during which the CHROMOSOMES are not individually distinguishable. It is composed of the G phases (G1 PHASE; G0 PHASE; G2 PHASE) and S PHASE (when DNA replication occurs).
CELL CYCLE regulatory signaling systems that are triggered by DNA DAMAGE or lack of nutrients during G2 PHASE. When triggered they restrain cells transitioning from G2 phase to M PHASE.
Regulatory signaling systems that control the progression of the CELL CYCLE through the G1 PHASE and allow transition to S PHASE when the cells are ready to undergo DNA REPLICATION. DNA DAMAGE, or the deficiencies in specific cellular components or nutrients may cause the cells to halt before progressing through G1 phase.