As far as i know when you accept cocaine in your blood some cocaine molecules reach some synapses in your brain and fill some Reuptake tunnels preventing the cell to simply "do not know that fired neurotransmitters have achieved their task" and doing so the cell fires neurotransmitters again becuase "it" simple do not know that "it" have achieved its task. In this case cocaine molecules fill Reuptake tunnels in Dopamin Serotonin and Norepinephrine orientated neurons.But since the firing occurs when an electrical signal occur how the neurotransmitters are fired again when such electrical signal does not exist?

If im mistaken in my physiology knowledge explained above please correct me!


You are correct that cocaine "fills the tunnel" (the pharmacology terminology is that it "blocks the transporter"). But it is not an autoreceptor, so the reuptake transporter does not send a stop signal, it just removed neurotransmitter from the cleft. But once you've blocked it with cocaine, neurotransmitter is not being removed from the cleft so it has a much longer and stronger signaling effect on the post-synaptic neuron.

But cocaine can also block sodium channels, which assist in action potential propagation and that has more of a local anesthetic effect.

The effect you are thinking of would pertain to auto-receptors, not reuptake transporters. Autoreceptors tend to be more like the post-synaptic targets of the neurotransmitter.

  • $\begingroup$ so you say a single neurotransmitter can bind to a receptor many times and can do its task many times (like neurotransmitters are not limited) and by blocking the transporter all neurotransmitters in this case perform their task many times and new neurotransmitters are arriving just because this is the normal function of the brain ? $\endgroup$ – Flux Oct 1 '13 at 9:03
  • $\begingroup$ ligan-receptor kinetics have an "off-rate" and an "on-rate" so yes, they can bind more than once, but some receptors can become "desensitized" from being stimulated. Regardless, having more neurotransmitter in the vicinity of receptors leads to a larger chance per unit time of ligand finding receptor and activating it. $\endgroup$ – Keegan Keplinger Oct 4 '13 at 15:56
  • $\begingroup$ for example if i have a long dopamine flow like being on cocaine for 1 hour will this dopamine "attack" damage your brain? Because as far as i know cocaine consumption damage your brain or im wrong? $\endgroup$ – Flux Oct 4 '13 at 21:16
  • $\begingroup$ I'm not a medical expert, but I don't know of any damage to brain from cocaine. Of course, using cocaine, flooding your dopamine receptors, your body will compensate in the long run by reducing the number of receptors on the post-synaptic neuron (and it will require more cocaine next time). Once you quit doing cocaine, it will take a while to recover normal receptor levels. $\endgroup$ – Keegan Keplinger Oct 5 '13 at 0:46

Cocaine is cardiotoxic. After chronic exposure to high doses I would assume that primary damage would attack the cardiovascular system before levels of dopamine would be able to cause damage. Cocaine intoxication deaths have mostly been caused by this cardiotoxicity. Primarily, myocardial infarction, arrhythmia, heart failure, and sudden cardiac death are a result of overdose. Cocaine is a vasoconstrictor, which may be a leading cause to myocardial infarctions.


  • $\begingroup$ how does this answer the question? $\endgroup$ – AliceD Mar 31 '15 at 1:06
  • $\begingroup$ I am saying that you would most likely overdose and suffer cardiovascular consequences that result in death before it's possible to have brain damage as a result of too much dopamine in the post-synaptic cleft. $\endgroup$ – SpeedOfLight Mar 31 '15 at 17:20
  • $\begingroup$ That makes sense $\endgroup$ – AliceD Mar 31 '15 at 20:58

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