"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.

Neurotransmitters will bind their respective receptors on the post-synaptic membrane, which is a muscle in this case. This binding causes changes to other proteins on that membrane, which results in an opening of ion channels. The muscle then depolarizes due to the influx of positively charged ions, and this can be measured as a positive change in the muscle membrane potential. 

The sodium-potassium pump maintains the resting membrane potential by utilizing 1 ATP to transport 2 potassium ions into the cell, and pumping 3 sodium ions out, which makes the inside of the cell negative relative to the outside of the cell.