Hypothalamic expression of the GCK gene plays an important role in the regulation of dietary glucose intake in particular, and overall feeding behavior in general. The primary hypothalamic cells expressing glucokinase are within the arcuate nucleus, ARC. Expression of the hypothalamic GCK gene increases specifically within the ARC in response to fasting. Manipulation of GCK expression within the ARC of experimental animals alters glucose intake. Increased GCK expression in the ARC results in increased glucose ingestion, whereas, decreased GCK expression results in reduced glucose ingestion. These observations indicate that ARC expression of GCK underlies the phenomenon of carbohydrate craving.
PCP has also been shown to cause schizophrenia-like changes in N -acetylaspartate and N -acetylaspartylglutamate levels in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.  It also induces symptoms in humans that mimic schizophrenia.  PCP not only produced symptoms similar to schizophrenia, it also yielded electroencephalogram changes in the thalamocortical pathway (increased delta decreased alpha) and in the hippocampus (increase theta bursts) that were similar to those in schizophrenia.  PCP induced augmentation of dopamine release may link the NMDA and DA hypothesis of schizophrenia.