Although the role of corticopetal acetylcholine (ACh) in higher cognitive functions is increasingly recognized, the questions as (1) how ACh works in attention(s), memory dynamics and cortical state transitions, and also (2) why and how loss of ACh is involved in dysfunctions such as visual hallucinations in dementia with Lewy bodies and deficit of attention(s), are not well understood. From the perspective of a dynamical systems viewpoint, we hypothesize that transient ACh released under top-down attention serves to temporarily invoke attractor-like memories, while a background level of ACh reverses this process returning the dynamical nature of the memory structure back to attractor ruins (quasi-attractors). In fact, transient ACh loosens inhibitions of pyramidal neurons (PYRs) by PV+ fast spiking (FS) interneurons, while a baseline ACh recovers inhibitory actions of PV+ FS. Attentional ACh thus dynamically modifies brain's connectivity. The core of this process is in the depression of GABAergic inhibitory currents in PYRs due to muscarinic (probably M-2 subtype) presynaptic effects on GABAergic synapses of PV+ FS neurons.