Why does antagonising D2 receptors reduce positive schizophrenic symptoms?

[foldedelephants]

The title should say: why does antagonising D2 receptors reduce positive schizophrenic symptoms?
It doesn't make sense to me. If positive schizophrenic symptoms are caused by too much dopamine signalling in the mesolimbic system, and D2 receptors hyperpolarise the post synaptic neuron when activated, how does antagonising the D2 receptor reduce activity within the mesolimbic system?

 

[Posty McPostface]

The thing your missing is that there are two types of D2 receptors. There's D2 long and D2 short. Antagonism of only D2 short would result in your conclusion; but, most typical AP's work to antagonize D2 long receptors also. Also keep in mind that the newer atypical antipsychotics also target D2 autoreceptors, leading to reduced responsiveness of dopamine itself to the postsynaptic receptors or heightened response when there are low levels of DA (think aripiprazole).

As to answering your OP's question. Excessive activation of D2 receptors results in attaching significance to mundane and ordinary events leading often to the characteristic disorganized thoughts and psychotic symptoms seen in schizophrenics. Although there is some discussion currently taking place in the psychiatric and neurological community, it's still thought that reducing excessive dopamine activity is the best strategy for reducing positive symptoms (glutamate is being heavily investigated due to also being the most prominent excitatory neurotransmitter). There are other neurotransmitters at play, such as 5-HT, and the 5-HT2A&B&C receptors along with dysfunctions in the GABA system to moderate/regulate the aberrant excitatory activity seen in schizophrenics, which are still being investigated in relation to schizophrenia.

 

[Posty McPostface]

I'm surprised Wikipedia and Google have such lackluster information about the difference between D2-Long and D2-Short receptors, I suppose that could be worked on.