Adherens junctions are formed by linking the actin cytoskeleton to transmembrane proteins known as cadherins. Cadherins are capable of interacting with other cadherins from neighboring cells on the exoplasmic face of the cell membrane. This interaction forms a physical link essentially connecting the actin cytoskeletons of the two adjacent cells, thus promoting force transduction.

Desmosomes are another type of cell junction that link the intermediate filaments of the cytoskeleton to cadherins.

Of the choices, only adherens junctions and hemidesmosomes are responsible for anchoring the extracellular matrix. This is accomplished by associating the actin cytoskeleton (for adherens junctions) or the intermediate filament cytoskeleton (for hemidesmosomes) with transmembrane proteins known as integrins. Integrins interact with the extracellular matrix.

Desmosomes are responsible for anchoring adjacent cells to one another by connecting their intermediate filament cytoskeletons with cadherins. Gap junctions connect the cytoplasm of adjacent cells and allow the free flow of small molecules between them. 

"Gap junctions prevent molecules and ions from traveling between cells in the extracellular space" is incorrect because this describes the function of tight junctions. Gap junctions electrically couple two cells by permitting the formation of small channels that connect two cells. 

Most of the other proteins listed are structural, but do not form any kind of pore or channel through which an electrical message can cross. Connexins are required for this function of gap junctions. 

While each of the proteins listed contribute to cell structure and function, the tight junction requires claudins and occludins to anchor the cytoskeleton of two adjacent cells to one another. These are the primary structural components of tight junctions. 

Gap junctions can be thought of as small tunnels between cells. They allow for the immediate transport of ions and molecules between the cells. Gap junctions are prominent in cardiac myocytes, and help spread action potentials via electrical synapses to coordinate the contraction of the heart.

The movement of substances between cells is most commonly controlled by tight junctions. These junctions can be regulated, which can alter how strongly they resist the movement of material between cells, like those in the digestive tract during absorption.

Second messengers are the molecules in a signal transduction pathway that will activate an intracellular response. Epinephrine is a hormone that will bind a receptor on the exoplasmic face of the cell, making is a first messenger. G subunits interact with adaptor proteins that will then stimulate the production of second messengers. Receptor tyrosine kinases are examples of receptor proteins that will bind first messengers. cAMP, however, is a widely used second messenger that is involved in the activation of many pathways and signal amplification in the cytosol.

A second messenger response is created in cells that use signal transduction, meaning that the signaling molecules attach to a receptor on the outside of the cell. Steroid hormones are largely nonpolar, and can enter the cell in order to affect cellular processes at the level of transcription. As a result, they do not need to rely on second messenger pathways in order to elicit a response.

The peak of an action potential signals the inactivation of sodium channels. This effectively prevents more sodium from entering the cell and halts the depolarization that was previously occurring, resulting in a maximum depolarization value. Potassium channels remain open, and are the cause for the membrane potential to start dropping (positive charge is leaving the cell). The sodium-potassium pump does not stop during this process. In fact, its continued function is essential for eventually restoring the resting membrane potential.