Comparative effects of aluminum and ouabain on synaptosomal choline uptake, acetylcholine release and (Na+/K+)ATPase

Potential therapeutic effect of nanobased formulation of rivastigmine on rat model of Alzheimer's disease

“…57 It has been shown that AChE activity and phospholipid composition of rat brain synaptic plasma membranes, as well as the Na + /K + -ATPase kinetics, were altered significantly with Al treatment. 58 Consistent with the previous finding of Silva et al, 59 we observed that AlCl 3 administration caused a significant increase in AChE activity, whereas activity of Na + /K + -ATPase was inhibited in rat cerebral cortex. It was suggested that allosteric interaction between Al and the peripheral anionic site of the enzyme might lead to increased enzymatic activity.…”

Acetylcholine Release and Choline Uptake by Cuttlefish (Sepia officinalis) Optic Lobe Synaptosomes

“…In conclusion, the results described here, together with preliminary data from earlier studies (2,5,(7)(8)(9)(10)(11)(12), provide further strong evidence that ACh performs an important physiological role in mediating neuronal signaling at synapses of the cuttlefish optic lobe. …”

“…Furthermore, recent work on cuttlefish optic lobe slices (11) has shown that mecamylamine hydrochloride, a nicotinic receptor antagonist, blocks excitatory postsynaptic currents, which are due to spontaneously released ACh. As far as we know, our recent paper (12) was the first to provide a brief insight into the release of ACh and the uptake of its precursor (Ch) in cuttlefish optic lobe. The present study further characterizes these major processes of cholinergic function, by analyzing the time-course of ACh release and Ch uptake and by comparing the effect of two secretagogues, KCl and veratridine, in pinched-off nerve terminals (synaptosomes) from cuttlefish optic lobes.…”

“…Once again, we wish to draw attention to the evidence, provided in our recent paper (12), that synaptosomal fractions isolated from cuttlefish optic lobe are suitable in vitro models to study neurotransmission. In particular, we have demonstrated that the uptake of Ch is inhibited by the selective inhibitor of the (Na ϩ /K ϩ )ATPase, ouabain, suggesting that the high-affinity Ch transporter of cuttlefish optic lobe also requires a transmembrane Na ϩ gradient to mediate active transport of Ch.…”

Does neurotransmission impairment accompany aluminium neurotoxicity?

“…In matter of fact, aluminium partially reverses the suppressive effects of verapamil on acetylCoA content and acetylcholine release [144]. On the other hand, aluminium effects match those of ouabain and seem to be proportional to the degree of (Na + /K + )ATPase inhibition, that holds down-regulation of choline uptake and acetylcholine release in rat brain synaptosomes [146]. Following intracerebroventricular injection of aluminium lactate, attenuation of baseline and K + depolarization induced acetylcholine release was also observed during in vivo microdialysis, which allows the collection of acetylcholine from brain extracellular fluid [147,148].…”