Topic: Xenopus laevis oocytes

Progression of Alzheimer’s disease is accompanied by the dysfunction of the cholinergic system and massive loss of cholinergic neurons containing the nicotinic acetylcholine receptors (nAChR). NAChR agonists protect neuronal cells against amyloid toxicity, eliminate the senile plaques, and improve learning and memory of transgenic mice. Moreover, nAChRs antagonists, that block the binding of Abeta to the receptor, inhibit Abeta-induced tau protein phosphorylation in neuronal cells. It means that the toxicity of Aβ is mediated through a direct interaction between Abeta and nAChRs. The most abun

Y-Aminobutyric acid type A (GABA-A) receptors are GABA-gated ion channels that are assembled of 5 (out of a set of 19) subunits, with six possible different alpha subunits. These differently assembled subunits lead to receptors with unique pharmacological and physiological properties that also show unique anatomical distribution. Animal models of several neuropsychiatric conditions suggest that compounds selectively activating, or positively modulating, cerebellar alpha6-containing GABA-A receptors can have highly beneficial effects on different diseases. For the case of essential tremor, flum