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Changes in PKA activity and G sα and G olfα levels after amphetamine‐ and cocaine‐induced behavioral sensitization
Author(s) -
Crawford Cynthia A.,
Choi Fiona Y.,
Kohutek Jodi L.,
Yoshida Shelly T.,
Mcdougall Sanders A.
Publication year - 2003
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.10301
Subject(s) - amphetamine , sensitization , nucleus accumbens , striatum , behavioral sensitization , chemistry , pharmacology , locomotor activity , dopamine , addiction , neuroscience , psychology , medicine
Neuroadaptations in the cAMP signal transduction system have been proposed to play a critical role in psychostimulant‐induced behavioral sensitization. Studies relevant to this hypothesis have provided conflicting evidence, however, because repeated cocaine and amphetamine treatment has been alternately reported to either increase or decrease protein kinase A (PKA) activity in the nucleus accumbens and dorsal striatum. In an attempt to reconcile these disparate findings, PKA activity and the stimulatory G‐protein subunits, G sα and G olfα , were measured after rats had received a sensitization‐inducing regimen of amphetamine or cocaine. Results showed that seven consecutive daily injections of amphetamine or cocaine produced locomotor sensitization and caused a reduction in accumbal PKA activity. A challenge injection of amphetamine on the test day also reduced dorsal striatal PKA activity. G sα levels were unaffected by psychostimulant exposure, while G olfα levels in the nucleus accumbens declined significantly after amphetamine or cocaine pretreatment. Because repeated amphetamine and cocaine treatment both induced behavioral sensitization and decreased accumbal PKA activity, it appears that psychostimulant‐induced increases in PKA activity are not necessary for the ultimate expression of behavioral sensitization. Synapse 51:241–248, 2004. © 2003 Wiley‐Liss, Inc.