How does the binding of a ligand to a receptor cause it to become concentrated into a coated pit? Not all receptors that carry out receptor mediated endocytosis are found in coated pits prior to ligand binding yet they do end up in coated pits prior to becoming internalized

Explanation:

Binding of a ligand to its receptor produces a conformational change in the receptor initiating a sequence of reactions leading to a specific cellular response.  Clustering/gathering of receptor proteins within  coated pits is the first step of RME. This process may be  either spontaneous or induced by ligands. Some receptors,  such as those for LDL bearing cholesterol and transferrin bearing iron, appear to be  clustered in coated pits independent of prior ligand binding.  Other receptors, including those for EGF and insulin are evenly distributed over the plasma membrane.  

The rate of receptor diffusion on the  cell surface plasma membrane can explain their movement into coated pits.

Some studies have also suggested that  membrane lipids flow toward coated pit areas and that this way all membrane proteins may be carried passively to  coated pits, preferentially selecting for receptor proteins  mediating endocytosis. These proteins may then become "trapped" via specific signals in the  cytoplasmic tail (downstream effectors) which interact with structural components of  the coated pit which includes the adaptor proteins- AP-2.

i think its c. amphipod

voluntary muscles are controlled by the cerebellum.