neurons, acetylcholine release being induced by substance P (Arenas et al. 
1991 ; Petitet et al. 1991) released from D1 -containing striatonigral neurons 
and acting on substance P receptors that are expressed by cholinergic neurons 
(Gerfen 1991). These possible mechanisms mediating interactions among 
striatal neurons are not exhaustive. Thus, the direct action of dopamine on 
D1- and D2-containing striatonigral and striatopallidal neurons should be 
considered an important, but not the only, mechanism by which dopamine 
modulates the balance in the activity of these two striatal output pathways. 
Changes in levels of mRNA-encoding peptides in striatopallidal and 
striatonigral neurons provide an instructive assay of functional changes 
induced by pharmacologic manipulation of the striatal dopamine system. 
However, changes in peptide mRNA levels often take several days of repeated 
treatments to develop to significant levels. The induction of transcription factors 
such as c-fos in striatal neurons following a single pharmacologic treatment 
provide an assay that supplies information concerning the acute actions of 
dopamine receptor activation. Such studies have provided data that are 
consistent with data obtained by using peptide mRNA assays in identifying 
D1 receptor activation as specifically targeting striatonigral neurons (Robertson 
et al. 1990). The use of c-fos induction has also proved instructive in studying 
the acute actions of cocaine and amphetamine on striatal neurons (Graybiel 
et al. 1990). This approach, when combined with identification of the neurons 
in which the transcription factors are induced, promises to provide significant 
new information about the cellular and molecular actions of cocaine and other 
psychostimulant drugs. 
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