Monthly Archives: April 2017

Live imaging confirmed that transport of labeled vesicles was blocked by BFA see more (data not shown). As Schwann cells do not myelinate in the presence of BFA (data not shown), we established microfluidic chambers, which allowed neurons to be … Continue reading →

Indeed, the finding that deafening alters the spontaneous action potential output of HVCX neurons OSI-744 ic50 in anesthetized birds hints that the output of this cell type may also be altered during singing. Although the exact role of HVCX neuron … Continue reading →

All patients were operated at the Academic Medical Center Amsterdam, a tertiary academic referral center. All patients gave informed consent for the procedure. Patients often were examined on multiple visits before consideration of surgical intervention to confirm the persistence of … Continue reading →

All synaptotagmin-controlled fusion reactions appear to require complexin as a cofactor (e.g., see Reim et al., 2001, Cai et al., 2008, Jorquera et al., 2012 and Cao et al., 2013). It seems likely that all Ca2+-triggered exocytosis depends on synaptotagmin Ca2+ sensors and complexins and that … Continue reading →

Although the functional analysis of cortico-thalamo-cortical communication is still in its early days, there is accumulating evidence in support of an essential involvement of “higher-order” thalamus in cortical processes. Responses of pulvinar and PoM neurons depend on input from cortex, … Continue reading →

For the case of opportunities, exploration is mandated by the (initially unexpected) potential gain, and this may be treated as a form of appetitive see more prediction error known as an exploration bonus. One, presumably model-free, realization of such a … Continue reading →

Within a block click here of 24 trials, the amount of reward was always large (0.25 or 0.3 ml) for the saccades to one direction and small (0 or 0.03 ml) for the saccades to the other direction. Even in the small-reward … Continue reading →

25 ± 0.11 versus 1.49 ± 0.12, p = 0.1642; PSD-95-positive, 0.89 ± 0.07 versus 1.01 ± 0.08, p = 0.2809; double-positive, 0.86 ± 0.07 versus 0.93 ± 0.08, p = 0.4911, two-tailed t test; Kif1a−/−: synaptophysin-positive, 1.03 ± 0.09 versus 1.06 ± 0.10, p = 0.8125; PSD-95-positive, 0.74 ± GSK1349572 0.05 versus … Continue reading →

, 2005), a likely possibility is that the internally generated amplitude signal described in vS1 cortex ( Fee et al., 1997) is relayed from vM1 cortex. We now come to the crux issue and ask if neurons in vS1 cortex code … Continue reading →

, 2009), possibly due to the effect of additional regulatory mechanisms—for example, it is possible that Syt1 may become inhibited by phosphorylation or that Syt7 may be constitutively activated by phosphorylation or by alternative splicing ( Sugita et al., 2001). The … Continue reading →