Sentence examples for enduring activation from inspiring English sources

As a consequence, autocrine mechanisms are assumed to play a key role in synovial hyperplasia and the enduring activation of SFB [ 22].

The increased retention of MPs also controlled release and drove accumulation of polyIC within the LN and in LN-resident APCs, resulting in more enduring activation of DCs (Fig. 6b) (53).

Spontaneous neuronal activity at the beginning of experimental GlyR α3K185L expression period is mainly dependent on GABAAR activation (Supplementary Figure 2), suggesting that inability of chronically silent neurons with enduring GlyR α3K185L activation to participate in spontaneous neural network activity underlies neurodegeneration.

By challenging primary hippocampal neurons with these two different experimental neurotoxic strategies including enduring GlyR α3K185L activation associated with chronic inhibition of neuronal activity as it may occur in the hippocampus of TLE patients and NMDA-dependent excitotoxicity, our study provides compelling evidence for a protein structural role of KCC2 in neuroprotection.

In neurons with enduring GlyR α3K185L activation, Vrev was significantly more depolarized than in control neurons.

Reciprocally, co-expression of the KCC2-NTD, not of KCC2-CTD, rescued survival of neurons with enduring GlyR α3K185L activation.

Gramicidin-perforated patch clamp was used again to analyze the effects of co-expression of KCC2wt on membrane properties of neurons with enduring GlyR α3K185L activation.

Thus, co-expression of KCC2wt was not able to prevent persistent changes in intrinsic membrane properties of neurons with enduring GlyR α3K185L activation.

Moreover, upon acute glycine washout, Vrev and EGABA remained largely unchanged, and RN recovered only partially, similar to neurons with enduring GlyR α3K185L activation in the absence of KCC2wt.

Furthermore, RN of neurons with enduring GlyR α3K185L activation was significantly decreased compared to control neurons, indicating presence of open GlyR α3K185L channels in the plasma membranes of neurons exposed to 10  μM glycine.

Consequently, the calculated driving force of GABA responses was 4.9±2.9 mV in control neurons (n=12; Figure 5d), whereas it was close to 0 mV (−0.4±0.9 mV, n=12; Figure 5e) in neurons with enduring GlyR α3K185L activation.