Is alcohol modulation of neuronal nicotinic acetylcholine receptors alpha subunit dependent?
The alpha3beta2 AChRs are insensitive to ethanol because ethanol is at the transition point from potentiation to inhibition among n-alcohols with different carbon-chain lengths. The differential action on the alpha4beta2 and alpha3beta2 AChRs may explain the differential action of ethanol on the central nervous system.
The present study is an initial step to more accurate speed modulation of RBPs to optimize the cardiac load control. To develop future control algorithms, the concept of high speed during diastole having a maximal unloading effect on the LV and high speed during systole increasing the pulse pressure is worth considering.