科研之友
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摘要
Background: Aluminum (Al) causes neurodegeneration and its toxic effects on cholinergic system in the brain is well documented. However, it is unknown whether and how Al changes oscillation patterns, driven by the cholinergic system, in the hippocampus.
Objective: We studied acute effects of Al on nicotinic acetylcholine receptors (nAChRs)-mediated modulation of persistent gamma oscillations in the hippocampus.
Method: The field potential recording was done in CA3 area of acute hippocampal slices.
Results: Carbachol-induced gamma oscillation peak power increased (1.32 +/- 0.09mV(2)/Hz, P<0.01) in control conditions (without Al) by application of 10 mu M nicotine as compared to baseline value normalized to 1. This nicotine-induced facilitation of gamma oscillation peak power was found to depend on non-alpha 7 nAChRs. In slices with Al pre-incubation for three to four hours, gamma oscillation peak power was reduced (5.4 +/- 1.8mV(2)/Hz, P<0.05) and facilitatory effect of nicotine on gamma oscillation peak power was blocked as compared to the control (18.06 +/- 2.1mV(2)/Hz) or one hour Al pre-incubated slices (11.3 +/- 2.5mV(2)/Hz). Intriguingly wash-out, after three to four hours of Al incubation, failed to restore baseline oscillation power and its facilitation by nicotine as no difference was observed in gamma oscillation peak power between Al wash-out slices (3.4 +/- 1.1mV(2)/Hz) and slices without washout (3.6 +/- 0.9mV(2)/Hz).
Conclusion: This study shows that at cellular level, exposure of hippocampal tissue to Al compromised nAChR-mediated facilitation of cholinergic hippocampal gamma oscillations. Longer in vitro Al exposure caused permanent changes in hippocampal oscillogenic circuitry and changed its sensitivity to nAChR-modulation. This study will help to understand the possible mechanism of cognitive decline induced by Al.
- 出版日期2018
