“…However, following the co‐administration of ERK antisense/amphetamine, the partial reversal of pERK/pCREB/NPY/POMC/MC 3 receptor expression was about 30–50% compared to normal levels, implying the possibilities that (i) antisense ERK did not delete ERK completely (only 60% reduction), and (ii) ERK‐CREB signalling was not the only pathway involved in the induction of NPY/POMC gene expression in the amphetamine‐treated rats. Previous reports revealed that some transcription factors, such as AP‐1 (Hsieh et al, ), NF‐κB (Kuo et al, ) and STAT3 (Chu et al, ), and some cytoplasmic factors, such as PI3K (Chu et al, ), anti‐oxidative enzymes (Hsieh et al, ), PKC (Kuo et al, ) and PKA (Hsieh et al, ), were also activated and involved in regulating NPY/POMC gene expression during amphetamine treatment. Some previous reports revealed that ERK co‐operates with other transcription factors in the brain in the control of behaviour‐associated diseases.…”