_ 60 -i 
O 
Morphine Cocaine 
■ G i 
0 A cyclase 
|| cA kinase (P) 
El cA kinase (S) 
FIGURE 2. Common adaptations in G proteins and the cAMP system in the 
NAc in response to chronic morphine and chronic cocaine. G r 
immunoreactivity of subunit; A cyclase , adenylate cyclase 
activity; cA kinase , cAMP-dependent protein kinase activity 
in particulate (P) and soluble (S) fractions. Data represent 
means±SEM (n=8 to 14). All changes shown in the figure are 
statistically significant by x 2 test. 
SOURCE: Data from Terwilligeretal. 1991a 
effects of chronic morphine action on NAc neurons have not yet been studied, 
similar effects compared with chronic cocaine would be predicted based on 
the biochemical findings. 
Morphine and cocaine were also shown to exert common chronic actions on 
several phosphoproteins in the VTA- NAc pathway, including increased levels 
of tyrosine hydroxylase in the VTA, lower levels of active tyrosine hydroxylase 
in the NAc, and lower levels of several forms of neurofilament proteins in the 
VTA (Beitner-Johnson and Nestler 1991; Beitner-Johnson et al., in press). 
Regulation of these morphine- and cocaine-regulated phosphoproteins 
(MCRPP), like the changes in the G proteins and the cAMP system, showed 
regional and pharmacological specificity. 
In addition to their regional and pharmacological specificity, further evidence to 
support the idea that morphine and cocaine regulation of G proteins, adenylate 
cyclase, cAMP-dependent protein kinase, and the various MCRPPs is related 
to drug reward mechanisms includes the findings that differences in these 
100 
