Effect of Chlorpromazine and Amphetamine on Neurotransmission

Author Paul Kenyon

In this simulation chlorpromazine is injected first and occupies postsynaptic receptor sites. Then amphetamine is injected. This mimics the arrival of an action potential at the nerve ending and causes the release a large number of DA molecules from the presynaptic neurone. But this released DA cannot activate the postsynaptic receptors because they are occupied by chlorpromazine molecules. Consequently, the postsynaptic neurone does not generate an action potential. The released DA is broken down by enzymes in the synaptic cleft, or is reabsorbed into the presynaptic neurone.

1. Bridging the information gap between neurones

Neurotransmitters are responsible for transmitting information across the synaptic gap between neurones.

Neurotransmitters are stored in synaptic vesicles. When action potentials are conducted down an axon:

  • synaptic vesicles attach themselves to the presynaptic membrane, then
  • break open and spill neurotransmitter into the synaptic cleft.

Neurotransmitters in the synaptic cleft :

  • attach to postsynaptic receptor sites and trigger an action potential in the postsynaptic membrane
  • some neurotransmitter attaches to presynaptic receptors (autoreceptors) located on the membrane (pre-synaptic membrane) of the cell that originally released them

2. Effect of pretreatment with chlorpromazine on amphetamine-induced release of DA

  • chlorpromazine binds to receptors in the postsynaptic membranes
  • this prevents neurotransmitters released by amphetamine from binding to these receptors
  • consequently the postsynaptic neurone cannot generate an action potential

Last updated 09/02/07
Copyright Dr. C.A.P. Kenyon 2000-07