Solving the binding problem
Cellular adhesive molecules and their control of the cortical quantum entangled network
Danko Georgiev, Medical University of Varna
Cogprints: 2 May 2003
The author proposes a model by which quantum coherence arises in the cytoskeleton, is transmitted to the synapse, and from there to neighbouring neurons via the neurexin-neuroligin complex in the synaptic cleft. This is suggested to bring a large group of neurons into quantum entanglement, and to provide a solution for the binding problem.
The article proposes a possible process to support quantum entanglement between neurons, based on neurexin and neuroligin. This involves the 20-30 nanometre wide synaptic cleft, which is filled with electron-dense material. The presynaptic side has an active zone containing vesicles of neurotransmitters. Apart from signalling processes, there is also an adhesive junction at the synapse formed by neurexins and neuroligins. These are brain specific molecules, which bind to one another, and are part of a family of molecules known as CAMS, which are often present at synapses. The author claims growing evidence for the role of CAMs in modulating both short and long lasting plasticity. Receptors required for longer term potentiation (LTP) may be linked to the modulation of the cell adhesion proteins. Adhesion proteins could modulate glutamate receptors, possibly by altering the width of the synaptic cleft, and the size of the pre and post synaptic active zones, and also by altering glial cell processing around the edge of the synapse. Neurexin and neuroligin appear well suited to link pre and postsynaptic signalling mechanisms. The C-termini of neuroligins are inside the postsynaptic neuron and bind to the PDZ, which is thought to act as a nexus for receptors and signalling molecules on the postsynaptic side. The C-termini of the neurexins binds to CASK another PDZ containing protein on the presynaptic side.
The author relates these structures to the proposal that the cytoskeleton is important to the processing of incoming information in the brain, and that macroscopic quantum coherence arises in the cytoskeleton. Beyond this, he is looking for a means by which coherence passes from one neuron to another. He has rejected the Hameroff proposal that this happens via gap junctions between dendrites.
There is a thickening of the cell membrane on both sides of the synapse. The postsynaptic density (PSD) has been proposed to be a protein lattice that organises receptors, ion channels and signalling molecules. The proteins in the lattice contain PDZ domains involving PSD-95 that can bind to many types of synaptic proteins, including receptors for the main excitatory synapse. CASK, a presynaptic protein and PSD-95 stabilise the synapse by interacting with neurexin and neuroligin cell adhesion molecules, or by indirectly linking synaptic proteins to the cytoskeleton. CASK is tethered to the cytoskeleton by an actin binding protein. The author suggests that the neurexin-neuroligin cell adhesion complex could be connected indirectly to the cytoskeleton and mediate interneuronal quantum entanglement across the syanptic cleft. This is suggested to allow coherence across a large group of neurons, as a way of solving the binding problem.