Neurotransmitters

First you don't block the neurotransmitters, you can block the re uptake of the neurotransmitters back into the pre-synaptic vesicles and this will cause the n.ts to remain in the synaptic cleft longer and be able to bind to receptors on the post synaptic neuron. A n.t exerts its effects on a cell or post synaptic neron by binding to the receptors on it. By blocking the reuptake of the n.t we are preventing the diffusion or reuptake of the available n.t in the synaptic cleft from going back into their vesicles and becoming dorminat, so by blocking this we INCREASE the amount and duration of n.t action on the receptors on the cells/postsynaptic neurons and because of this the effect is longer.

jackfackmasta's answer is right on! i would just add that neurotransmitters themselves can be acted upon in the synapse, although as the post noted, this action would not be called "blocking." like in the case of ach, ache binds directly to ach and breaks it down to choline and acetate, which are inert in the synapse. so even though ache effectively decreases the amount of ach in the synapse, it's not directly preventing the binding of ach with post-synaptic receptors. (that's the alternative route to termination of neurotransmitter activity, enzyme degradation, vs. reuptake.)

Thank you both so much!

i was just wondering the same thing! :)