CVS Practice Test

When norepinephrine is released into the synaptic cleft, the primary process that occurs is its reabsorption back into the nerve terminal. This reuptake is facilitated by specific transporter proteins located on the presynaptic neuron. Reabsorption serves critical functions: it terminates the action of norepinephrine in the synaptic cleft, allowing for precise control of neurotransmission and enabling the neuron to reuse norepinephrine for future neurotransmission.

This process helps to maintain neurotransmitter balance and is essential for the normal functioning of the sympathetic nervous system. By reabsorbing norepinephrine, neurons can regulate the amount of neurotransmitter available and influence the intensity of the signal.

In contrast, norepinephrine does not undergo conversion to epinephrine directly within the synaptic cleft, nor is it degraded by acetylcholinesterase, which specifically breaks down the neurotransmitter acetylcholine. While norepinephrine can be stored in vesicles for future use, this occurs prior to its release into the synaptic cleft, rather than after its release. Thus, the primary fate of norepinephrine post-release is its reabsorption into the nerve terminal.