potentials. As expected, no neurotransmitters are secreted into the culture medium. If the axonal membrane then is artificially depolarized by making the medium «100 mM KCl, neurotransmitters are released from the cells because of the influx of Ca2+ through open voltage-gated Ca2+ channels. Indeed, patch-clamping experiments show that voltage-gated Ca2 + channels, like voltage-gated Na+ channels, open transiently upon depolarization of the membrane.

Two pools of neurotransmitter-filled synaptic vesicles are present in axon terminals: those "docked" at the plasma membrane, which can be readily exocytosed, and those in reserve in the active zone near the plasma membrane. Each rise in Ca2+ triggers exocytosis of about 10 percent of the docked vesicles. Membrane proteins unique to synaptic vesicles then are specifically internalized by endocytosis, usually via the same types of clathrin-coated vesicles used to recover other plasma-membrane proteins by other types of cells. After the endocytosed vesicles lose their clathrin coat, they are rapidly refilled with neurotransmitter. The ability of many neurons to fire 50 times a second is clear evidence that the recycling of vesicle membrane proteins occurs quite rapidly.

I Cocaine inhibits the transporters for norepineph-I rine, serotonin, and dopamine. Binding of cocaine Ii'iUiiihIl'm dopamine transporter inhibits reuptake of dopamine, thus prolonging signaling at key brain synapses; indeed, the dopamine transporter is the principal brain "cocaine receptor." Therapeutic agents such as the antidepres-sant drugs fluoxetine (Prozac) and imipramine block serotonin uptake, and the tricyclic antidepressant desipramine blocks norepinephrine uptake. I

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