Interestingly, clozapine treatment also improves synaptic plasticity of the STOP null animals by restoring long-term potentiation in the hippocampus.
All together, the pharmacological reactivity of STOP null mice to antipsychotics evokes the pharmacological response of humans to such LY2109761 in vivo drugs. Totally,
our study suggests that STOP null mice may provide a useful preclinical model to evaluate pharmacological properties of antipsychotic drugs.”
“Intracerebral microinjection is a commonly used technique for local delivery of biologically active agents. However, it is known that mechanical injury of the cortex can induce spreading depression (SD), a wave of transient cellular depolarization. We examined the effects of intracortical microinjections of a new selective I-h channel antagonist ORG 34167 and of different control treatments (saline and sham microinjections) on spontaneously occurring spike-wave discharges (SWDs) in WAG/Rij rats, a valid genetic model of absence epilepsy. Electroencephalographic (EEG) recording in awake rats has shown that both the drug and control microinjections are followed by long-term (for more than an hour) suppression of SWDs. dc-EEG recording in WAG/Rij rats has revealed that sham microinjections induce SD in 65% (31/48) cases. Number of SWDs decreased substantially for at least 90 min after
the sham injections which induced cortical SD but remained unchanged GSK1904529A molecular weight if SD was not triggered by microinjection. Depsipeptide These findings suggest that SD induced by intracortical microinjection may contribute to long-term suppression of non-convulsive
epileptic activity after this experimental procedure. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.”
“A novel spatial multiscale model of a colonic crypt is described, which couples the cell cycle (including cell division) with the mechanics of cell movement. The model is used to investigate the process of monoclonal conversion under two hypotheses concerning stem cell behavior. Under the first hypothesis, ‘stem-ness’ is an intrinsic cell property, and the stem cell population is maintained through asymmetric division. Under the second hypothesis, the proliferative behavior of each cell is governed by its microenvironment through a biochemical signalling cue, and all cell division is symmetric. Under each hypothesis, the model is used to run virtual experiments, in which a harmless labeling mutation is bestowed upon a single cell in the crypt and the mutant clonal population is tracked over time to check if and when the crypt becomes monoclonal. It is shown that under the first hypothesis, a stable structured cell population is not possible without some form of population-dependent feedback; in contrast, under the second hypothesis, a stable crypt architecture arises naturally.