There are two PCP receptors as far as I know. Of course, many chemicals besides PCP bind to these receptors, but PCP is such an attention getting trio of letters.
The first PCP receptor is the NMDA non-competitive antagonist site. Located inside the channel of the ion channel that usually uses Glutamate or Asparatic Acid as it's neurotransmitter. Since as much of 80% of CNS neurons use Glutamate as an excitatory neurotransmitter, a large dose of PCP (which is several times the dose that most people would normally take) leaves the brain working at about 80% of capacity, which can be a good thing or a bad thing. Widespread inactivity in these areas is what causes the zombie like inactivity of PCP users, as well as the reduced emotional response to pain.
The other PCP receptor is the Dopamine Reuptake Site, or at least one of them. PCP also antagonizes this site, which means that dopamine never gets taken back into the pre-synaptic junction, and just sits at the post-synaptic site, which means that the dopamine receptor gets way overexcited. This is what causes PCP users to get manic and also to get hypertension.
The most interesting thing about these two sites is that one of them is inhibitory while the other is excitatory. Meaning that PCP users can become either zombie like or manic. A very interesting mix of yang and yin. Whether the endogenous NMDA antagonist that the body is believed to produce at times has the same effect on the dopamine reuptake site is unknown to me, and if it indeed does, the question of why the body would produce such a chemical with such different effects is an interesting one, to say the least.
In addition to these two, PCP obviously has some effect of receptors in the cerebellum, which causes the weird shuffling gait of PCP intoxication; but I don't have any information on what those receptors might be. | 
