Zou Xin, Coyle Damien, Wong-Lin KongFatt, Maguire Liam
Intelligent Systems Research Centre, University of Ulster, Magee Campus, Derry, Northern Ireland, UK.
J Comput Neurosci. 2012 Jun;32(3):465-77. doi: 10.1007/s10827-011-0363-7. Epub 2011 Sep 21.
Alzheimer's disease (AD) progression is usually associated with memory deficits and cognitive decline. A hallmark of AD is the accumulation of beta-amyloid (Aβ) peptide, which is known to affect the hippocampal pyramidal neurons in the early stage of AD. Previous studies have shown that Aβ can block A-type K(+) currents in the hippocampal pyramidal neurons and enhance the neuronal excitability. However, the mechanisms underlying such changes and the effects of the hyper-excited pyramidal neurons on the hippocampo-septal network dynamics are still to be investigated. In this paper, Aβ-blocked A-type current is simulated, and the resulting neuronal and network dynamical changes are evaluated in terms of the theta band power. The simulation results demonstrate an initial slight but significant theta band power increase as the A-type current starts to decrease. However, the theta band power eventually decreases as the A-type current is further decreased. Our analysis demonstrates that Aβ blocked A-type currents can increase the pyramidal neuronal excitability by preventing the emergence of a steady state. The increased theta band power is due to more pyramidal neurons recruited into spiking mode during the peak of pyramidal theta oscillations. However, the decreased theta band power is caused by the spiking phase relationship between different neuronal populations, which is critical for theta oscillation, is violated by the hyper-excited pyramidal neurons. Our findings could provide potential implications on some AD symptoms, such as memory deficits and AD caused epilepsy.
阿尔茨海默病(AD)的进展通常与记忆缺陷和认知衰退相关。AD的一个标志是β-淀粉样蛋白(Aβ)肽的积累,已知其在AD早期会影响海马锥体神经元。先前的研究表明,Aβ可阻断海马锥体神经元中的A型钾电流并增强神经元兴奋性。然而,这种变化的潜在机制以及过度兴奋的锥体神经元对海马-隔区网络动力学的影响仍有待研究。在本文中,模拟了Aβ阻断的A型电流,并根据θ波段功率评估由此产生的神经元和网络动力学变化。模拟结果表明,随着A型电流开始下降,θ波段功率最初会有轻微但显著的增加。然而,随着A型电流进一步下降,θ波段功率最终会降低。我们的分析表明,Aβ阻断的A型电流可通过阻止稳态的出现来增加锥体神经元的兴奋性。θ波段功率增加是由于在锥体θ振荡峰值期间有更多的锥体神经元进入放电模式。然而,θ波段功率降低是由不同神经元群体之间的放电相位关系被过度兴奋的锥体神经元破坏所致,而这种相位关系对θ振荡至关重要。我们的研究结果可能为一些AD症状,如记忆缺陷和AD引起的癫痫,提供潜在的启示。