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Cocaine also blocks the serotonin transporter and norepinephrine transporter, inhibiting reuptake of serotonin and norepinephrine from the synaptic cleft into the pre-synaptic axon terminal and increasing activation of serotonin receptors and norepinephrine receptors in the post-synaptic neuron, contributing to the mental and physical effects ...
These chemicals inhibit the action of DAT and, to a lesser extent, the other monoamine transporters, but their effects are mediated by separate mechanisms. Monoamine transporters are established targets for many pharmacological agents that affect brain function, including the psychostimulants cocaine and amphetamine. Cocaine and amphetamine ...
Axon terminals (also called terminal boutons, synaptic boutons, end-feet, or presynaptic terminals) are distal terminations of the branches of an axon. An axon, also called a nerve fiber, is a long, slender projection of a nerve cell that conducts electrical impulses called action potentials away from the neuron's cell body to transmit those ...
Cocaine is a relatively "balanced" inhibitor, although facilitation of dopaminergic neurotransmission is what has been linked to the reinforcing and addictive effects. In addition, cocaine has some serious limitations in terms of its cardiotoxicity [188] due to its local anesthetic activity. Thousands of cocaine users are admitted to emergency ...
The effect of these structural changes on behavior is uncertain and studies have produced conflicting results. Two studies [18] [19] have shown that an increase in dendritic spine density due to cocaine exposure facilitates behavioral sensitization, while two other studies [20] [21] produce contradicting evidence.
The impulse travels down the axon in one direction only, to the axon terminal where it signals other neurons. An action potential occurs when the membrane potential of a specific cell rapidly rises and falls. [1] This depolarization then causes adjacent locations to similarly depolarize.
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The repeated additions to the axon terminal membrane would eventually result in the uncontrolled growth of the axon terminal, which could lead to disastrous breakdown of the synaptic complex. The axon terminal compensates for this problem by reuptaking the vesicle by endocytosis and reusing its components to form new synaptic vesicles. [1]