Effect of Chlorpromazine on Neurotransmitter Release and Reuptake 

Author Paul Kenyon

Antipsychotic drugs such as chlorpromazine are thought to exert their theraputic effects by blocking DA receptors. Notice that chlorpromazine attaches to receptor sites in the postsynaptic membrane normally occupied by dopamine released from the presynaptic neuron.

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 chlorpromazine

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

Point to ponder
Why do you think are the consequences of chronic administration of chlorpromazine on neurotransmitter metabolism?

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