Ion channels are integral membrane proteins that help establish and control the small voltage gradient across the plasma membrane of living cells by allowing the flow of ions down their electrochemical gradient (1). They are present in the membranes that surround all
biological cells because their main function is to regulate the flow of ions across this membrane. Whereas some ion channels permit the passage of ions based on charge, others conduct based on a ionic species, such as sodium or potassium. Furthermore, in some ion channels, the
passage is governed by a gate which is controlled by chemical or electrical signals, temperature, or mechanical forces. There are a few main classifications of gated ion channels. There are voltage- gated ion channels, ligand-gated, other gating systems and finally those that are
classified differently, having more exotic characteristics. The first are voltage- gated ion channels
which open and close in response to membrane potential. These are then separated into sodium, calcium, potassium, proton, transient receptor, and cyclic nucleotide-gated channels; each of which is responsible for a unique role. Ligand-gated ion channels are also known as ionotropic receptors, and they open in response to specific ligand molecules binding to the extracellular domain of the receptor protein. The other gated classifications include activation and inactivation by second messengers, inward-rectifier potassium channels, calcium-activated potassium channels, two-pore-domain potassium channels, light-gated channels, mechano-sensitive ion channels and cyclic nucleotide-gated channels. Finally, the other classifications are based on less normal characteristics such as two-pore channels, and transient receptor potential channels (2). Shank proteins make up a family of scaffold proteins identified through their interaction with a variety of membrane and cytoplasmic proteins (3). Shank proteins at postsynaptic sites of excitatory synapses play roles in signal transmission into the postsynaptic neuron. Studies suggest that Shank2 is expressed in the neurons of the developing
retina, and could play a role in the neuronal differentiation of the developing retina (4). Other recent studies suggest that the disruption of glutamate receptors at the Shank-postsynaptic platform could contribute to the destruction of the postsynaptic density, which underlies the synaptic dysfunction and loss in Alzheimer